Cancer

An investigational oral drug that targets RAS, the dominant oncogenic driver in pancreatic cancer, nearly doubled overall survival compared with common second-line chemotherapy regimens in patients with previously treated metastatic disease.

In the 500-patient phase 3 RASolute 302 trial, patients who received daraxonrasib, a RAS(ON) multi-selective inhibitor, lived a median of 13.2 months compared with 6.7 months for those who received chemotherapy. The drug also doubled progression-free survival, tripled the response rate, and delayed deterioration in both pain and quality of life.

“Results from RASolute 302 support daraxonrasib as a new standard of care for patients with previously treated metastatic pancreatic cancer,” said lead investigator Brian Wolpin, MD, MPH, director of the Hale Family Center for Pancreatic Cancer Research, Dana-Farber Cancer Institute in Boston, who presented the findings at the American Society of Clinical Oncology (ASCO) 2026. The study was also published simultaneously on May 31 in The New England Journal of Medicine.

Pancreatic ductal adenocarcinoma is one of the most lethal cancers, with most patients presenting with advanced disease at diagnosis. For those whose cancer progresses after first-line chemotherapy, no single standard second-line treatment has been established. Available regimens typically produce median progression-free survival of 3-4 months and a median overall survival of 6-7 months.

More than 90% of pancreatic cancers harbor activating RAS mutations — most commonly KRAS G12D and G12V — that drive tumor growth. The first approved KRAS inhibitors — sotorasib and adagrasib for certain lung and colorectal cancers — target KRAS G12C, which is rare in pancreatic cancer. So far, no RAS-targeted therapy has been approved for pancreatic cancer.

Daraxonrasib takes a broader approach. The oral agent can target a range of RAS variants, including mutant and wild-type RAS, by binding the active form of RAS and blocking downstream signaling.

In the phase 3 open-label RASolute 302 trial, researchers randomized 500 patients with previously treated metastatic pancreatic cancer 1:1 to receive daraxonrasib 300 mg orally once daily or investigator’s choice of chemotherapy. The most used regimens in the control arm were gemcitabine plus nab-paclitaxel (56.5%) and liposomal irinotecan plus fluorouracil and leucovorin (32.7%).

Patients were required to have an Eastern Cooperative Oncology Group performance status of 0 or 1. Documented RAS mutational status was required, and nearly 92% of patients had RAS G12 mutations.

The dual primary endpoints were overall survival and progression-free survival in the RAS G12 population. Key secondary endpoints included the same measures in the overall population as well as objective response rate and patient-reported quality of life. The median follow-up was 8.5 months.

In the RAS G12 population, daraxonrasib reduced the risk for death by 60% (hazard ratio [HR], 0.40; P < .001). The median overall survival was 13.2 months with daraxonrasib vs 6.6 months with chemotherapy. Results were nearly identical in the overall population: 13.2 vs 6.7 months (HR, 0.40; P < .001).

Progression-free survival in the RAS G12 population was 7.3 vs 3.5 months (HR, 0.45; P < .001). The objective response rate was 33.2% vs 11.8%.

Daraxonrasib significantly delayed deterioration in pain (median, 9.0 vs 3.7 months; HR, 0.51; P < .001) and global quality of life (5.6 vs 2.4 months; HR, 0.60; P < .001).

Treatment-related adverse events of grade ≥ 3 occurred in 43.6% of patients on daraxonrasib vs 57.5% of patients on chemotherapy. The most common high-grade events with daraxonrasib were rash (13.7%) and stomatitis (12.0%), whereas neutropenia (27.6%) and anemia (16.4%) were most common with chemotherapy.

One patient in the daraxonrasib arm died from treatment-related pneumonitis. Discontinuation due to adverse events occurred in 1.2% of patients on daraxonrasib vs 11.2% of patients on chemotherapy.

The median duration of treatment was 6.2 months with daraxonrasib vs 1.5-3.2 months across chemotherapy regimens, and 42% of patients on daraxonrasib remained on treatment at data cutoff, Wolpin said.

The open-label design is a limitation. About 15% of patients randomized to chemotherapy never received treatment, largely after learning their treatment assignment, although all were included in the intention-to-treat analysis.

Invited discussant Jennifer Knox, MD, a medical oncologist at Princess Margaret Cancer Center and professor of medicine at the University of Toronto in Toronto, Ontario, Canada, called daraxonrasib a game changer, describing the drug as “probably the most exciting strategy in five decades” for pancreatic cancer.

“It is an absolutely beautiful curve,” Knox said of the overall survival data, noting that the Kaplan-Meier curves separated early and continued to widen over time — a pattern rarely seen in pancreatic cancer trials where initial separation between treatment arms typically narrows as patients in both groups deteriorate.

Knox highlighted the pain and quality-of-life data as “the most important endpoints for our patients,” given the severity of the disease.

She pointed out, however, that the combination of rash and stomatitis will be “challenging” in practice, and called for improved supportive care and closer collaboration with dermatology as oncologists gain experience with this first-in-class drug.

Knox said RAS-targeted therapy “should dominate trials across the full spectrum of pancreatic cancer clinical presentations,” pointing to first-line combination trials already underway and noting that treating a larger, earlier population would have the greatest impact.

“This is the first glimpse at the real power of targeting RAS in pancreas cancer,” Knox said.

The study was funded by Revolution Medicines. Wolpin reported consulting or advisory roles with Revolution Medicines, Mirati Therapeutics, Ipsen, and others, and institutional research funding from Revolution Medicines, Agios, Amgen, AstraZeneca, Lilly, and Novartis. Knox reported receiving honoraria from Astellas Pharma, AstraZeneca, Incyte, and Ipsen, and consulting or advisory roles with AstraZeneca/MedImmune, Incyte, and Ipsen.

A version of this article was previously published on Medscape.com.

An investigational oral drug that targets RAS, the dominant oncogenic driver in pancreatic cancer, nearly doubled overall survival compared with common second-line chemotherapy regimens in patients with previously treated metastatic disease.

In the 500-patient phase 3 RASolute 302 trial, patients who received daraxonrasib, a RAS(ON) multi-selective inhibitor, lived a median of 13.2 months compared with 6.7 months for those who received chemotherapy. The drug also doubled progression-free survival, tripled the response rate, and delayed deterioration in both pain and quality of life.

“Results from RASolute 302 support daraxonrasib as a new standard of care for patients with previously treated metastatic pancreatic cancer,” said lead investigator Brian Wolpin, MD, MPH, director of the Hale Family Center for Pancreatic Cancer Research, Dana-Farber Cancer Institute in Boston, who presented the findings at the American Society of Clinical Oncology (ASCO) 2026. The study was also published simultaneously on May 31 in The New England Journal of Medicine.

Pancreatic ductal adenocarcinoma is one of the most lethal cancers, with most patients presenting with advanced disease at diagnosis. For those whose cancer progresses after first-line chemotherapy, no single standard second-line treatment has been established. Available regimens typically produce median progression-free survival of 3-4 months and a median overall survival of 6-7 months.

More than 90% of pancreatic cancers harbor activating RAS mutations — most commonly KRAS G12D and G12V — that drive tumor growth. The first approved KRAS inhibitors — sotorasib and adagrasib for certain lung and colorectal cancers — target KRAS G12C, which is rare in pancreatic cancer. So far, no RAS-targeted therapy has been approved for pancreatic cancer.

Daraxonrasib takes a broader approach. The oral agent can target a range of RAS variants, including mutant and wild-type RAS, by binding the active form of RAS and blocking downstream signaling.

In the phase 3 open-label RASolute 302 trial, researchers randomized 500 patients with previously treated metastatic pancreatic cancer 1:1 to receive daraxonrasib 300 mg orally once daily or investigator’s choice of chemotherapy. The most used regimens in the control arm were gemcitabine plus nab-paclitaxel (56.5%) and liposomal irinotecan plus fluorouracil and leucovorin (32.7%).

Patients were required to have an Eastern Cooperative Oncology Group performance status of 0 or 1. Documented RAS mutational status was required, and nearly 92% of patients had RAS G12 mutations.

The dual primary endpoints were overall survival and progression-free survival in the RAS G12 population. Key secondary endpoints included the same measures in the overall population as well as objective response rate and patient-reported quality of life. The median follow-up was 8.5 months.

In the RAS G12 population, daraxonrasib reduced the risk for death by 60% (hazard ratio [HR], 0.40; P < .001). The median overall survival was 13.2 months with daraxonrasib vs 6.6 months with chemotherapy. Results were nearly identical in the overall population: 13.2 vs 6.7 months (HR, 0.40; P < .001).

Progression-free survival in the RAS G12 population was 7.3 vs 3.5 months (HR, 0.45; P < .001). The objective response rate was 33.2% vs 11.8%.

Daraxonrasib significantly delayed deterioration in pain (median, 9.0 vs 3.7 months; HR, 0.51; P < .001) and global quality of life (5.6 vs 2.4 months; HR, 0.60; P < .001).

Treatment-related adverse events of grade ≥ 3 occurred in 43.6% of patients on daraxonrasib vs 57.5% of patients on chemotherapy. The most common high-grade events with daraxonrasib were rash (13.7%) and stomatitis (12.0%), whereas neutropenia (27.6%) and anemia (16.4%) were most common with chemotherapy.

One patient in the daraxonrasib arm died from treatment-related pneumonitis. Discontinuation due to adverse events occurred in 1.2% of patients on daraxonrasib vs 11.2% of patients on chemotherapy.

The median duration of treatment was 6.2 months with daraxonrasib vs 1.5-3.2 months across chemotherapy regimens, and 42% of patients on daraxonrasib remained on treatment at data cutoff, Wolpin said.

The open-label design is a limitation. About 15% of patients randomized to chemotherapy never received treatment, largely after learning their treatment assignment, although all were included in the intention-to-treat analysis.

Invited discussant Jennifer Knox, MD, a medical oncologist at Princess Margaret Cancer Center and professor of medicine at the University of Toronto in Toronto, Ontario, Canada, called daraxonrasib a game changer, describing the drug as “probably the most exciting strategy in five decades” for pancreatic cancer.

“It is an absolutely beautiful curve,” Knox said of the overall survival data, noting that the Kaplan-Meier curves separated early and continued to widen over time — a pattern rarely seen in pancreatic cancer trials where initial separation between treatment arms typically narrows as patients in both groups deteriorate.

Knox highlighted the pain and quality-of-life data as “the most important endpoints for our patients,” given the severity of the disease.

She pointed out, however, that the combination of rash and stomatitis will be “challenging” in practice, and called for improved supportive care and closer collaboration with dermatology as oncologists gain experience with this first-in-class drug.

Knox said RAS-targeted therapy “should dominate trials across the full spectrum of pancreatic cancer clinical presentations,” pointing to first-line combination trials already underway and noting that treating a larger, earlier population would have the greatest impact.

“This is the first glimpse at the real power of targeting RAS in pancreas cancer,” Knox said.

The study was funded by Revolution Medicines. Wolpin reported consulting or advisory roles with Revolution Medicines, Mirati Therapeutics, Ipsen, and others, and institutional research funding from Revolution Medicines, Agios, Amgen, AstraZeneca, Lilly, and Novartis. Knox reported receiving honoraria from Astellas Pharma, AstraZeneca, Incyte, and Ipsen, and consulting or advisory roles with AstraZeneca/MedImmune, Incyte, and Ipsen.

A version of this article was previously published on Medscape.com.

An investigational oral drug that targets RAS, the dominant oncogenic driver in pancreatic cancer, nearly doubled overall survival compared with common second-line chemotherapy regimens in patients with previously treated metastatic disease.

In the 500-patient phase 3 RASolute 302 trial, patients who received daraxonrasib, a RAS(ON) multi-selective inhibitor, lived a median of 13.2 months compared with 6.7 months for those who received chemotherapy. The drug also doubled progression-free survival, tripled the response rate, and delayed deterioration in both pain and quality of life.

“Results from RASolute 302 support daraxonrasib as a new standard of care for patients with previously treated metastatic pancreatic cancer,” said lead investigator Brian Wolpin, MD, MPH, director of the Hale Family Center for Pancreatic Cancer Research, Dana-Farber Cancer Institute in Boston, who presented the findings at the American Society of Clinical Oncology (ASCO) 2026. The study was also published simultaneously on May 31 in The New England Journal of Medicine.

Pancreatic ductal adenocarcinoma is one of the most lethal cancers, with most patients presenting with advanced disease at diagnosis. For those whose cancer progresses after first-line chemotherapy, no single standard second-line treatment has been established. Available regimens typically produce median progression-free survival of 3-4 months and a median overall survival of 6-7 months.

More than 90% of pancreatic cancers harbor activating RAS mutations — most commonly KRAS G12D and G12V — that drive tumor growth. The first approved KRAS inhibitors — sotorasib and adagrasib for certain lung and colorectal cancers — target KRAS G12C, which is rare in pancreatic cancer. So far, no RAS-targeted therapy has been approved for pancreatic cancer.

Daraxonrasib takes a broader approach. The oral agent can target a range of RAS variants, including mutant and wild-type RAS, by binding the active form of RAS and blocking downstream signaling.

In the phase 3 open-label RASolute 302 trial, researchers randomized 500 patients with previously treated metastatic pancreatic cancer 1:1 to receive daraxonrasib 300 mg orally once daily or investigator’s choice of chemotherapy. The most used regimens in the control arm were gemcitabine plus nab-paclitaxel (56.5%) and liposomal irinotecan plus fluorouracil and leucovorin (32.7%).

Patients were required to have an Eastern Cooperative Oncology Group performance status of 0 or 1. Documented RAS mutational status was required, and nearly 92% of patients had RAS G12 mutations.

The dual primary endpoints were overall survival and progression-free survival in the RAS G12 population. Key secondary endpoints included the same measures in the overall population as well as objective response rate and patient-reported quality of life. The median follow-up was 8.5 months.

In the RAS G12 population, daraxonrasib reduced the risk for death by 60% (hazard ratio [HR], 0.40; P < .001). The median overall survival was 13.2 months with daraxonrasib vs 6.6 months with chemotherapy. Results were nearly identical in the overall population: 13.2 vs 6.7 months (HR, 0.40; P < .001).

Progression-free survival in the RAS G12 population was 7.3 vs 3.5 months (HR, 0.45; P < .001). The objective response rate was 33.2% vs 11.8%.

Daraxonrasib significantly delayed deterioration in pain (median, 9.0 vs 3.7 months; HR, 0.51; P < .001) and global quality of life (5.6 vs 2.4 months; HR, 0.60; P < .001).

Treatment-related adverse events of grade ≥ 3 occurred in 43.6% of patients on daraxonrasib vs 57.5% of patients on chemotherapy. The most common high-grade events with daraxonrasib were rash (13.7%) and stomatitis (12.0%), whereas neutropenia (27.6%) and anemia (16.4%) were most common with chemotherapy.

One patient in the daraxonrasib arm died from treatment-related pneumonitis. Discontinuation due to adverse events occurred in 1.2% of patients on daraxonrasib vs 11.2% of patients on chemotherapy.

The median duration of treatment was 6.2 months with daraxonrasib vs 1.5-3.2 months across chemotherapy regimens, and 42% of patients on daraxonrasib remained on treatment at data cutoff, Wolpin said.

The open-label design is a limitation. About 15% of patients randomized to chemotherapy never received treatment, largely after learning their treatment assignment, although all were included in the intention-to-treat analysis.

Invited discussant Jennifer Knox, MD, a medical oncologist at Princess Margaret Cancer Center and professor of medicine at the University of Toronto in Toronto, Ontario, Canada, called daraxonrasib a game changer, describing the drug as “probably the most exciting strategy in five decades” for pancreatic cancer.

“It is an absolutely beautiful curve,” Knox said of the overall survival data, noting that the Kaplan-Meier curves separated early and continued to widen over time — a pattern rarely seen in pancreatic cancer trials where initial separation between treatment arms typically narrows as patients in both groups deteriorate.

Knox highlighted the pain and quality-of-life data as “the most important endpoints for our patients,” given the severity of the disease.

She pointed out, however, that the combination of rash and stomatitis will be “challenging” in practice, and called for improved supportive care and closer collaboration with dermatology as oncologists gain experience with this first-in-class drug.

Knox said RAS-targeted therapy “should dominate trials across the full spectrum of pancreatic cancer clinical presentations,” pointing to first-line combination trials already underway and noting that treating a larger, earlier population would have the greatest impact.

“This is the first glimpse at the real power of targeting RAS in pancreas cancer,” Knox said.

The study was funded by Revolution Medicines. Wolpin reported consulting or advisory roles with Revolution Medicines, Mirati Therapeutics, Ipsen, and others, and institutional research funding from Revolution Medicines, Agios, Amgen, AstraZeneca, Lilly, and Novartis. Knox reported receiving honoraria from Astellas Pharma, AstraZeneca, Incyte, and Ipsen, and consulting or advisory roles with AstraZeneca/MedImmune, Incyte, and Ipsen.

A version of this article was previously published on Medscape.com.

This transcript has been edited for clarity.

Hello, everyone. This is Dr Bishal Gyawali, from Queens University, Kingston, Canada. Today, I’m back with you to talk about some of the fallacies that I have seen in medicine, oncology, and the drug regulatory space. I wanted to clarify some of these fallacies.

In my last video, I talked about the FDA denying the approval of a new cancer drug. Let me start with one of the fallacies that is pertinent to that, which is that some people make an argument that patients are dying from a certain condition, such as cancer, or even any other disease besides cancer. That is an absolutely true statement, but that does not necessarily mean there should be a lower bar for drug approvals or we should be approving any drug that has a hint of benefit.

In fact, if we have increased mortality rates and our patients are dying from a certain condition, that means we actually need to have good drugs. We need to have drugs that prevent mortality. We need to have drugs that improve outcomes. Just having any drug out there, if we lower our threshold and are letting any drug be used in these patients because the argument is that people are dying, then in fact, it can have negative consequences.

First, there will be opportunity costs. If you can get any lousy drug into the market and make billions of dollars out of it, then there is no strong motivation to produce drugs that actually remarkably improve outcomes.

Second, patients will also be misled. It’s the patient’s opportunity cost in that they will use whatever time they have remaining to pursue these treatments that were not going to improve their outcomes anyway. This is time they could have better spent either in pursuing better treatments, if those treatments are out there, or to prioritize their time accordingly. This rather gives them a false hope, which can be harmful in the long term.

The first fallacy is that just because people are dying does not necessarily mean we should have more new drugs with a lower bar for approval.

The second fallacy I want to talk about, which is also related to this, is that if a certain cancer is rare, the bar for new drug approval should be quite low.

Of course, rare cancers are a special category, and rare cancers should be treated differently from a regulatory perspective. Absolutely. If the cancer is rare, we cannot have trials with large sample sizes to generate evidence. That problem is there, but that does not necessarily translate to the decision that we should approve anything, even something with a small hint of benefit.

There are other methods to make sure that, even in rare cancers, we can generate good-quality evidence. In fact, from an equity perspective, why should patients with rare cancer not deserve drugs that have good-quality evidence?

We can’t tell someone that, “Your cancer is rare, so you should get drugs that only have a benefit in terms of response rate whereas other cancers that are not rare will have drugs based on survival.”

Going back to the point about the difficulty in doing big trials in patients with rare cancers, that is absolutely true and there should be regulatory flexibility in this. I think accelerated approval is a pathway that allows for this regulatory flexibility, which allows access to these drugs early on based on earlier signals of benefit. You can continue to generate evidence in the future and confirm the clinical benefit.

There are also other nuances to this. One is that we should also make sure that this regulatory flexibility with rare cancers should not be misused. What do I mean by that? First, all rare cancers are not the same. There are some cancers that are ultra rare, and then there are some cancers that technically might fit the definition of rare, but trials are possible. Case in point: adrenocortical cancer. It is considered to be a very rare cancer, but there have been randomized trials in adrenocortical cancer.

Our efforts should be to maximize our collaboration globally so that a cancer that is rare locally will still not be so rare globally when we collect all these patients.

In certain situations, like let’s say, based on the molecular subtypes, any common cancer can be sliced and diced into a rare subtype: MSI-high, BRAF-negative, HER2-positive, right-sided colon cancer. If you start to slice cancers into these smaller and smaller molecular subtypes, you can consider anything as a rare cancer. That should not be misused as an excuse to get away from doing proper trials and generating adequate evidence for our patients.

The third fallacy I want to talk about is that increasing cancer incidence in a certain subgroup of population does not automatically translate into, “We should start screening this subgroup of population.”

A certain cancer — let’s say cancer X or cancer Y — is increasing in a young population, so therefore, we should lower the age of the screening of young populations. This cancer is increasing in this ethnic population, so therefore we should start screening this ethnic population more frequently. This cancer is increasing in this type of minority, so therefore, we should start screening this minority more.

No, it does not work like that. Increasing incidence will make us concerned, of course, but that does not necessarily translate into, “We should start screening them.” In order for a screening test to be useful, it has to fulfill a number of criteria.

The goal is not to detect cancers. The goal is to detect cancers that are not indolent enough that they would have never caused problems, nor speed up the diagnosis of aggressive cancers that are going to be lethal pretty soon anyway. The goal is to detect those cancers in the middle, so that by detecting early, we can intervene and improve the outcomes and improve the mortality from that cancer.

This type of intervention requires a thoughtful consideration of the increasing incidence of the cancer, of course, but also the utility of the screening test in that subgroup of population; the life expectancy of this subgroup of patients with and without cancer; the interventions available to address that increasing burden of cancer; and whether by intervening we are going to reduce the mortality rates.

Just because we can detect cancers does not mean we should detect cancers. That’s the third fallacy I wanted to talk about.

The fourth fallacy is related to when someone is asking for more evidence for anything. There is a new drug for this cancer,so what is the evidence? Or there is this new intervention that will detect ctDNA or whatever before the cancer relapses, or before the cancer even shows up as a screening test.

Whenever there is any treatment that is being promoted and someone asks for evidence, people sometimes try to make personal attacks by saying, “Oh, so, you’re okay with patients dying. You don’t want to save lives.”

Absolutely we want to save lives. That’s why we’re in this field, and that’s why we’re asking for more evidence. You should not consider someone who is asking for evidence as evil or that this person does not want this new drug, or this person does not want this innovation. No, that person actually wants to make sure that that innovation actually helps people. That’s why that person is asking for more evidence.

If we stop asking for evidence, then our whole practice becomes based on emotions, faith, and trust rather than science. You could extrapolate it to the other extreme, like if you are not asking for evidence. If it is interpreted as someone who is asking for evidence is evil, or someone who does not want patients to get new drugs, then you could extrapolate these to people also making claims about alternative medicines or ivermectin nowadays, and claiming that this cures cancer.

Science is science. You need to be the same no matter the circumstances. If you are asking for data for ivermectin, you should also be asking data for your cancer drug that you think is going to work. We should always ask for evidence.

Asking for evidence is not a sign that whoever is asking for evidence does not want the patient to have access to the drug. It is showing that the person who is asking for evidence actually wants to make sure that the patients who get this drug are actually being helped by the drug rather than being harmed.

I’m talking about 5 fallacies today. The final, fifth fallacy is that clinical expertise does not equal expertise in making public health decisions or even expertise in critical appraisal. Someone can be a fantastic breast cancer doctor, the best oncologist for breast cancer. That does not automatically make that person the best person to evaluate clinical trials of breast cancer drugs.

Someone can be a fantastic colon cancer doctor. That does not make that person automatically the best person to evaluate whether or not colonoscopy or colon cancer screening is indicated in a certain patient population.

These population-level decisions — including should this drug be approved, should this drug be funded, and should this screening test be made a public health measure, all of these public health decisions that are done at a population level — require different expertise in critical appraisal, clinical epidemiology, and public health.

Just because someone is a fantastic clinician does not make that person a fantastic public health expert. I see on social media often that a famous doctor with expertise in their domain, let’s say a famous neurosurgeon, might say, “I think brain tumors are increasing in incidence in young persons, so we should be targeting an MRI screening for everyone over the age of 30.”

I’m just making this up, but we see examples of things not dissimilar to this. Just because someone is a neurosurgeon does not make them an expert on brain tumor epidemiology, surveillance, or screening. We should separate clinical expertise from public health expertise.

Thank you.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello, everyone. This is Dr Bishal Gyawali, from Queens University, Kingston, Canada. Today, I’m back with you to talk about some of the fallacies that I have seen in medicine, oncology, and the drug regulatory space. I wanted to clarify some of these fallacies.

In my last video, I talked about the FDA denying the approval of a new cancer drug. Let me start with one of the fallacies that is pertinent to that, which is that some people make an argument that patients are dying from a certain condition, such as cancer, or even any other disease besides cancer. That is an absolutely true statement, but that does not necessarily mean there should be a lower bar for drug approvals or we should be approving any drug that has a hint of benefit.

In fact, if we have increased mortality rates and our patients are dying from a certain condition, that means we actually need to have good drugs. We need to have drugs that prevent mortality. We need to have drugs that improve outcomes. Just having any drug out there, if we lower our threshold and are letting any drug be used in these patients because the argument is that people are dying, then in fact, it can have negative consequences.

First, there will be opportunity costs. If you can get any lousy drug into the market and make billions of dollars out of it, then there is no strong motivation to produce drugs that actually remarkably improve outcomes.

Second, patients will also be misled. It’s the patient’s opportunity cost in that they will use whatever time they have remaining to pursue these treatments that were not going to improve their outcomes anyway. This is time they could have better spent either in pursuing better treatments, if those treatments are out there, or to prioritize their time accordingly. This rather gives them a false hope, which can be harmful in the long term.

The first fallacy is that just because people are dying does not necessarily mean we should have more new drugs with a lower bar for approval.

The second fallacy I want to talk about, which is also related to this, is that if a certain cancer is rare, the bar for new drug approval should be quite low.

Of course, rare cancers are a special category, and rare cancers should be treated differently from a regulatory perspective. Absolutely. If the cancer is rare, we cannot have trials with large sample sizes to generate evidence. That problem is there, but that does not necessarily translate to the decision that we should approve anything, even something with a small hint of benefit.

There are other methods to make sure that, even in rare cancers, we can generate good-quality evidence. In fact, from an equity perspective, why should patients with rare cancer not deserve drugs that have good-quality evidence?

We can’t tell someone that, “Your cancer is rare, so you should get drugs that only have a benefit in terms of response rate whereas other cancers that are not rare will have drugs based on survival.”

Going back to the point about the difficulty in doing big trials in patients with rare cancers, that is absolutely true and there should be regulatory flexibility in this. I think accelerated approval is a pathway that allows for this regulatory flexibility, which allows access to these drugs early on based on earlier signals of benefit. You can continue to generate evidence in the future and confirm the clinical benefit.

There are also other nuances to this. One is that we should also make sure that this regulatory flexibility with rare cancers should not be misused. What do I mean by that? First, all rare cancers are not the same. There are some cancers that are ultra rare, and then there are some cancers that technically might fit the definition of rare, but trials are possible. Case in point: adrenocortical cancer. It is considered to be a very rare cancer, but there have been randomized trials in adrenocortical cancer.

Our efforts should be to maximize our collaboration globally so that a cancer that is rare locally will still not be so rare globally when we collect all these patients.

In certain situations, like let’s say, based on the molecular subtypes, any common cancer can be sliced and diced into a rare subtype: MSI-high, BRAF-negative, HER2-positive, right-sided colon cancer. If you start to slice cancers into these smaller and smaller molecular subtypes, you can consider anything as a rare cancer. That should not be misused as an excuse to get away from doing proper trials and generating adequate evidence for our patients.

The third fallacy I want to talk about is that increasing cancer incidence in a certain subgroup of population does not automatically translate into, “We should start screening this subgroup of population.”

A certain cancer — let’s say cancer X or cancer Y — is increasing in a young population, so therefore, we should lower the age of the screening of young populations. This cancer is increasing in this ethnic population, so therefore we should start screening this ethnic population more frequently. This cancer is increasing in this type of minority, so therefore, we should start screening this minority more.

No, it does not work like that. Increasing incidence will make us concerned, of course, but that does not necessarily translate into, “We should start screening them.” In order for a screening test to be useful, it has to fulfill a number of criteria.

The goal is not to detect cancers. The goal is to detect cancers that are not indolent enough that they would have never caused problems, nor speed up the diagnosis of aggressive cancers that are going to be lethal pretty soon anyway. The goal is to detect those cancers in the middle, so that by detecting early, we can intervene and improve the outcomes and improve the mortality from that cancer.

This type of intervention requires a thoughtful consideration of the increasing incidence of the cancer, of course, but also the utility of the screening test in that subgroup of population; the life expectancy of this subgroup of patients with and without cancer; the interventions available to address that increasing burden of cancer; and whether by intervening we are going to reduce the mortality rates.

Just because we can detect cancers does not mean we should detect cancers. That’s the third fallacy I wanted to talk about.

The fourth fallacy is related to when someone is asking for more evidence for anything. There is a new drug for this cancer,so what is the evidence? Or there is this new intervention that will detect ctDNA or whatever before the cancer relapses, or before the cancer even shows up as a screening test.

Whenever there is any treatment that is being promoted and someone asks for evidence, people sometimes try to make personal attacks by saying, “Oh, so, you’re okay with patients dying. You don’t want to save lives.”

Absolutely we want to save lives. That’s why we’re in this field, and that’s why we’re asking for more evidence. You should not consider someone who is asking for evidence as evil or that this person does not want this new drug, or this person does not want this innovation. No, that person actually wants to make sure that that innovation actually helps people. That’s why that person is asking for more evidence.

If we stop asking for evidence, then our whole practice becomes based on emotions, faith, and trust rather than science. You could extrapolate it to the other extreme, like if you are not asking for evidence. If it is interpreted as someone who is asking for evidence is evil, or someone who does not want patients to get new drugs, then you could extrapolate these to people also making claims about alternative medicines or ivermectin nowadays, and claiming that this cures cancer.

Science is science. You need to be the same no matter the circumstances. If you are asking for data for ivermectin, you should also be asking data for your cancer drug that you think is going to work. We should always ask for evidence.

Asking for evidence is not a sign that whoever is asking for evidence does not want the patient to have access to the drug. It is showing that the person who is asking for evidence actually wants to make sure that the patients who get this drug are actually being helped by the drug rather than being harmed.

I’m talking about 5 fallacies today. The final, fifth fallacy is that clinical expertise does not equal expertise in making public health decisions or even expertise in critical appraisal. Someone can be a fantastic breast cancer doctor, the best oncologist for breast cancer. That does not automatically make that person the best person to evaluate clinical trials of breast cancer drugs.

Someone can be a fantastic colon cancer doctor. That does not make that person automatically the best person to evaluate whether or not colonoscopy or colon cancer screening is indicated in a certain patient population.

These population-level decisions — including should this drug be approved, should this drug be funded, and should this screening test be made a public health measure, all of these public health decisions that are done at a population level — require different expertise in critical appraisal, clinical epidemiology, and public health.

Just because someone is a fantastic clinician does not make that person a fantastic public health expert. I see on social media often that a famous doctor with expertise in their domain, let’s say a famous neurosurgeon, might say, “I think brain tumors are increasing in incidence in young persons, so we should be targeting an MRI screening for everyone over the age of 30.”

I’m just making this up, but we see examples of things not dissimilar to this. Just because someone is a neurosurgeon does not make them an expert on brain tumor epidemiology, surveillance, or screening. We should separate clinical expertise from public health expertise.

Thank you.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello, everyone. This is Dr Bishal Gyawali, from Queens University, Kingston, Canada. Today, I’m back with you to talk about some of the fallacies that I have seen in medicine, oncology, and the drug regulatory space. I wanted to clarify some of these fallacies.

In my last video, I talked about the FDA denying the approval of a new cancer drug. Let me start with one of the fallacies that is pertinent to that, which is that some people make an argument that patients are dying from a certain condition, such as cancer, or even any other disease besides cancer. That is an absolutely true statement, but that does not necessarily mean there should be a lower bar for drug approvals or we should be approving any drug that has a hint of benefit.

In fact, if we have increased mortality rates and our patients are dying from a certain condition, that means we actually need to have good drugs. We need to have drugs that prevent mortality. We need to have drugs that improve outcomes. Just having any drug out there, if we lower our threshold and are letting any drug be used in these patients because the argument is that people are dying, then in fact, it can have negative consequences.

First, there will be opportunity costs. If you can get any lousy drug into the market and make billions of dollars out of it, then there is no strong motivation to produce drugs that actually remarkably improve outcomes.

Second, patients will also be misled. It’s the patient’s opportunity cost in that they will use whatever time they have remaining to pursue these treatments that were not going to improve their outcomes anyway. This is time they could have better spent either in pursuing better treatments, if those treatments are out there, or to prioritize their time accordingly. This rather gives them a false hope, which can be harmful in the long term.

The first fallacy is that just because people are dying does not necessarily mean we should have more new drugs with a lower bar for approval.

The second fallacy I want to talk about, which is also related to this, is that if a certain cancer is rare, the bar for new drug approval should be quite low.

Of course, rare cancers are a special category, and rare cancers should be treated differently from a regulatory perspective. Absolutely. If the cancer is rare, we cannot have trials with large sample sizes to generate evidence. That problem is there, but that does not necessarily translate to the decision that we should approve anything, even something with a small hint of benefit.

There are other methods to make sure that, even in rare cancers, we can generate good-quality evidence. In fact, from an equity perspective, why should patients with rare cancer not deserve drugs that have good-quality evidence?

We can’t tell someone that, “Your cancer is rare, so you should get drugs that only have a benefit in terms of response rate whereas other cancers that are not rare will have drugs based on survival.”

Going back to the point about the difficulty in doing big trials in patients with rare cancers, that is absolutely true and there should be regulatory flexibility in this. I think accelerated approval is a pathway that allows for this regulatory flexibility, which allows access to these drugs early on based on earlier signals of benefit. You can continue to generate evidence in the future and confirm the clinical benefit.

There are also other nuances to this. One is that we should also make sure that this regulatory flexibility with rare cancers should not be misused. What do I mean by that? First, all rare cancers are not the same. There are some cancers that are ultra rare, and then there are some cancers that technically might fit the definition of rare, but trials are possible. Case in point: adrenocortical cancer. It is considered to be a very rare cancer, but there have been randomized trials in adrenocortical cancer.

Our efforts should be to maximize our collaboration globally so that a cancer that is rare locally will still not be so rare globally when we collect all these patients.

In certain situations, like let’s say, based on the molecular subtypes, any common cancer can be sliced and diced into a rare subtype: MSI-high, BRAF-negative, HER2-positive, right-sided colon cancer. If you start to slice cancers into these smaller and smaller molecular subtypes, you can consider anything as a rare cancer. That should not be misused as an excuse to get away from doing proper trials and generating adequate evidence for our patients.

The third fallacy I want to talk about is that increasing cancer incidence in a certain subgroup of population does not automatically translate into, “We should start screening this subgroup of population.”

A certain cancer — let’s say cancer X or cancer Y — is increasing in a young population, so therefore, we should lower the age of the screening of young populations. This cancer is increasing in this ethnic population, so therefore we should start screening this ethnic population more frequently. This cancer is increasing in this type of minority, so therefore, we should start screening this minority more.

No, it does not work like that. Increasing incidence will make us concerned, of course, but that does not necessarily translate into, “We should start screening them.” In order for a screening test to be useful, it has to fulfill a number of criteria.

The goal is not to detect cancers. The goal is to detect cancers that are not indolent enough that they would have never caused problems, nor speed up the diagnosis of aggressive cancers that are going to be lethal pretty soon anyway. The goal is to detect those cancers in the middle, so that by detecting early, we can intervene and improve the outcomes and improve the mortality from that cancer.

This type of intervention requires a thoughtful consideration of the increasing incidence of the cancer, of course, but also the utility of the screening test in that subgroup of population; the life expectancy of this subgroup of patients with and without cancer; the interventions available to address that increasing burden of cancer; and whether by intervening we are going to reduce the mortality rates.

Just because we can detect cancers does not mean we should detect cancers. That’s the third fallacy I wanted to talk about.

The fourth fallacy is related to when someone is asking for more evidence for anything. There is a new drug for this cancer,so what is the evidence? Or there is this new intervention that will detect ctDNA or whatever before the cancer relapses, or before the cancer even shows up as a screening test.

Whenever there is any treatment that is being promoted and someone asks for evidence, people sometimes try to make personal attacks by saying, “Oh, so, you’re okay with patients dying. You don’t want to save lives.”

Absolutely we want to save lives. That’s why we’re in this field, and that’s why we’re asking for more evidence. You should not consider someone who is asking for evidence as evil or that this person does not want this new drug, or this person does not want this innovation. No, that person actually wants to make sure that that innovation actually helps people. That’s why that person is asking for more evidence.

If we stop asking for evidence, then our whole practice becomes based on emotions, faith, and trust rather than science. You could extrapolate it to the other extreme, like if you are not asking for evidence. If it is interpreted as someone who is asking for evidence is evil, or someone who does not want patients to get new drugs, then you could extrapolate these to people also making claims about alternative medicines or ivermectin nowadays, and claiming that this cures cancer.

Science is science. You need to be the same no matter the circumstances. If you are asking for data for ivermectin, you should also be asking data for your cancer drug that you think is going to work. We should always ask for evidence.

Asking for evidence is not a sign that whoever is asking for evidence does not want the patient to have access to the drug. It is showing that the person who is asking for evidence actually wants to make sure that the patients who get this drug are actually being helped by the drug rather than being harmed.

I’m talking about 5 fallacies today. The final, fifth fallacy is that clinical expertise does not equal expertise in making public health decisions or even expertise in critical appraisal. Someone can be a fantastic breast cancer doctor, the best oncologist for breast cancer. That does not automatically make that person the best person to evaluate clinical trials of breast cancer drugs.

Someone can be a fantastic colon cancer doctor. That does not make that person automatically the best person to evaluate whether or not colonoscopy or colon cancer screening is indicated in a certain patient population.

These population-level decisions — including should this drug be approved, should this drug be funded, and should this screening test be made a public health measure, all of these public health decisions that are done at a population level — require different expertise in critical appraisal, clinical epidemiology, and public health.

Just because someone is a fantastic clinician does not make that person a fantastic public health expert. I see on social media often that a famous doctor with expertise in their domain, let’s say a famous neurosurgeon, might say, “I think brain tumors are increasing in incidence in young persons, so we should be targeting an MRI screening for everyone over the age of 30.”

I’m just making this up, but we see examples of things not dissimilar to this. Just because someone is a neurosurgeon does not make them an expert on brain tumor epidemiology, surveillance, or screening. We should separate clinical expertise from public health expertise.

Thank you.

A version of this article first appeared on Medscape.com.

A few days of fasting around chemotherapy sessions may improve treatment response and outcomes for some patients with advanced ovarian cancer, a small phase 2 trial suggests.

The study, of 36 patients with stage III or IV high-grade ovarian cancer, found that those randomly assigned to fast for 36 hours before chemotherapy and 24 hours afterward had stronger pathologic responses to chemotherapy and longer progression-free survival than patients who ate normally during treatment.

The findings, reported at a press briefing ahead the American Society of Clinical Oncology (ASCO) 2026, hint at a straightforward measure to potentially improve patients’ outcomes.

The working theory is that short-term fasting boosts chemotherapy response by lowering insulin and IGF-1 levels, both of which are implicated in tumor growth and chemotherapy resistance, said study presenter Claudia Marchetti, MD, of Agostino Gemelli University in Rome, Italy.

Speaking at the briefing, ASCO President Eric Small, MD, of the University of California San Francisco, called the study “a great example of a very simple intervention that has benefit and can be undertaken and implemented anywhere in the world.”

“It’s not an expensive new drug,” he said, “and yet it has the potential to really have an impact on this cancer.”

Ovarian cancer affects more than 324,000 women worldwide each year and causes more than 206,000 deaths annually. Around 80% of patients are diagnosed at an advanced stage, and up to 60% receive neoadjuvant chemotherapy to reduce tumor size and facilitate surgery.

Despite advances in surgery and chemotherapy, patients with advanced disease still face poor outcomes. There is, Marchetti said, “an urgent need for safe, low-cost, and easily implementable strategies that can enhance treatment efficacy and improve patient prognosis.”

Given evidence on the role of insulin in tumor growth and chemotherapy response, her team hypothesized that short bouts of fasting around the time of treatment might have benefits.

To test that idea, the researchers recruited 36 patients with newly diagnosed stage III or IV high-grade serous ovarian carcinoma who were not candidates for primary cytoreduction. All were in good general health, with a mean age of 62 years.

All patients received 3 rounds of carboplatin and paclitaxel before surgery. Prior to starting chemotherapy, half were randomly assigned to fast for 36 hours before and 24 hours after chemotherapy, whereas the other half ate normally throughout treatment.

Patients in the fasting group consumed no more than 350 calories per day during the fasting window. They were allowed to have unrestricted water, herbal tea, limited vegetable juice, and small amounts of light vegetable broth. (A ketogenic diet group had initially been planned but was closed early because of poor patient compliance.)

The study met its primary endpoint of change in insulin levels during chemotherapy, Marchetti reported. Baseline insulin levels were comparable between the 2 groups, but after 3 rounds of chemotherapy, they’d dipped by an average of 1.12 µIU/mL in the fasting group and increased by 9.76 µIU/mL in the control group (P = .01).

Fasting also improved clinical outcomes. Specifically, Marchetti said, 59% of fasting patients achieved a chemotherapy response score of 3 — indicating complete or near-complete tumor response before surgery — compared with 17% of patients in the control group.

Median progression-free survival was significantly longer in the fasting group, at 38 vs 24 months.

Importantly, Marchetti said, the fasting protocol was feasible, well tolerated, and safe: All patients assigned to the fasting group completed treatment, and rates of chemotherapy-related toxicities were similar between the 2 groups.

Additional analyses shed more light on the possible mechanisms underlying the fasting group’s improved outcomes: The researchers found that those patients tended to have lower levels of circulating suppressor granulocyte and monocyte populations that have been linked to tumor immune escape, which suggests, Marchetti said, fasting may have set the stage for a “more favorable immune environment” during chemotherapy.

However, she cautioned that much more research is needed. Her team is planning a larger multicenter trial to validate the current findings, and longer-term follow-up is necessary to see whether fasting ultimately impacts patients’ survival, Marchetti said.

In a statement, Eleonora Teplinsky, MD, an ASCO expert in gynecologic cancers, said these early findings are “encouraging, support earlier data, and highlight a promising area of cancer research.”

But she, too, emphasized the need for larger clinical trials to build on the results.

The study had no commercial funding. Marchetti disclosed having relationships with Arquer Diagnostics, AstraZeneca, Clovis Oncology, and other companies. Small disclosed having relationships with Janssen, Johnson & Johnson, and others. Teplinsky had no disclosures.

A version of this article first appeared on Medscape.com.

A few days of fasting around chemotherapy sessions may improve treatment response and outcomes for some patients with advanced ovarian cancer, a small phase 2 trial suggests.

The study, of 36 patients with stage III or IV high-grade ovarian cancer, found that those randomly assigned to fast for 36 hours before chemotherapy and 24 hours afterward had stronger pathologic responses to chemotherapy and longer progression-free survival than patients who ate normally during treatment.

The findings, reported at a press briefing ahead the American Society of Clinical Oncology (ASCO) 2026, hint at a straightforward measure to potentially improve patients’ outcomes.

The working theory is that short-term fasting boosts chemotherapy response by lowering insulin and IGF-1 levels, both of which are implicated in tumor growth and chemotherapy resistance, said study presenter Claudia Marchetti, MD, of Agostino Gemelli University in Rome, Italy.

Speaking at the briefing, ASCO President Eric Small, MD, of the University of California San Francisco, called the study “a great example of a very simple intervention that has benefit and can be undertaken and implemented anywhere in the world.”

“It’s not an expensive new drug,” he said, “and yet it has the potential to really have an impact on this cancer.”

Ovarian cancer affects more than 324,000 women worldwide each year and causes more than 206,000 deaths annually. Around 80% of patients are diagnosed at an advanced stage, and up to 60% receive neoadjuvant chemotherapy to reduce tumor size and facilitate surgery.

Despite advances in surgery and chemotherapy, patients with advanced disease still face poor outcomes. There is, Marchetti said, “an urgent need for safe, low-cost, and easily implementable strategies that can enhance treatment efficacy and improve patient prognosis.”

Given evidence on the role of insulin in tumor growth and chemotherapy response, her team hypothesized that short bouts of fasting around the time of treatment might have benefits.

To test that idea, the researchers recruited 36 patients with newly diagnosed stage III or IV high-grade serous ovarian carcinoma who were not candidates for primary cytoreduction. All were in good general health, with a mean age of 62 years.

All patients received 3 rounds of carboplatin and paclitaxel before surgery. Prior to starting chemotherapy, half were randomly assigned to fast for 36 hours before and 24 hours after chemotherapy, whereas the other half ate normally throughout treatment.

Patients in the fasting group consumed no more than 350 calories per day during the fasting window. They were allowed to have unrestricted water, herbal tea, limited vegetable juice, and small amounts of light vegetable broth. (A ketogenic diet group had initially been planned but was closed early because of poor patient compliance.)

The study met its primary endpoint of change in insulin levels during chemotherapy, Marchetti reported. Baseline insulin levels were comparable between the 2 groups, but after 3 rounds of chemotherapy, they’d dipped by an average of 1.12 µIU/mL in the fasting group and increased by 9.76 µIU/mL in the control group (P = .01).

Fasting also improved clinical outcomes. Specifically, Marchetti said, 59% of fasting patients achieved a chemotherapy response score of 3 — indicating complete or near-complete tumor response before surgery — compared with 17% of patients in the control group.

Median progression-free survival was significantly longer in the fasting group, at 38 vs 24 months.

Importantly, Marchetti said, the fasting protocol was feasible, well tolerated, and safe: All patients assigned to the fasting group completed treatment, and rates of chemotherapy-related toxicities were similar between the 2 groups.

Additional analyses shed more light on the possible mechanisms underlying the fasting group’s improved outcomes: The researchers found that those patients tended to have lower levels of circulating suppressor granulocyte and monocyte populations that have been linked to tumor immune escape, which suggests, Marchetti said, fasting may have set the stage for a “more favorable immune environment” during chemotherapy.

However, she cautioned that much more research is needed. Her team is planning a larger multicenter trial to validate the current findings, and longer-term follow-up is necessary to see whether fasting ultimately impacts patients’ survival, Marchetti said.

In a statement, Eleonora Teplinsky, MD, an ASCO expert in gynecologic cancers, said these early findings are “encouraging, support earlier data, and highlight a promising area of cancer research.”

But she, too, emphasized the need for larger clinical trials to build on the results.

The study had no commercial funding. Marchetti disclosed having relationships with Arquer Diagnostics, AstraZeneca, Clovis Oncology, and other companies. Small disclosed having relationships with Janssen, Johnson & Johnson, and others. Teplinsky had no disclosures.

A version of this article first appeared on Medscape.com.

A few days of fasting around chemotherapy sessions may improve treatment response and outcomes for some patients with advanced ovarian cancer, a small phase 2 trial suggests.

The study, of 36 patients with stage III or IV high-grade ovarian cancer, found that those randomly assigned to fast for 36 hours before chemotherapy and 24 hours afterward had stronger pathologic responses to chemotherapy and longer progression-free survival than patients who ate normally during treatment.

The findings, reported at a press briefing ahead the American Society of Clinical Oncology (ASCO) 2026, hint at a straightforward measure to potentially improve patients’ outcomes.

The working theory is that short-term fasting boosts chemotherapy response by lowering insulin and IGF-1 levels, both of which are implicated in tumor growth and chemotherapy resistance, said study presenter Claudia Marchetti, MD, of Agostino Gemelli University in Rome, Italy.

Speaking at the briefing, ASCO President Eric Small, MD, of the University of California San Francisco, called the study “a great example of a very simple intervention that has benefit and can be undertaken and implemented anywhere in the world.”

“It’s not an expensive new drug,” he said, “and yet it has the potential to really have an impact on this cancer.”

Ovarian cancer affects more than 324,000 women worldwide each year and causes more than 206,000 deaths annually. Around 80% of patients are diagnosed at an advanced stage, and up to 60% receive neoadjuvant chemotherapy to reduce tumor size and facilitate surgery.

Despite advances in surgery and chemotherapy, patients with advanced disease still face poor outcomes. There is, Marchetti said, “an urgent need for safe, low-cost, and easily implementable strategies that can enhance treatment efficacy and improve patient prognosis.”

Given evidence on the role of insulin in tumor growth and chemotherapy response, her team hypothesized that short bouts of fasting around the time of treatment might have benefits.

To test that idea, the researchers recruited 36 patients with newly diagnosed stage III or IV high-grade serous ovarian carcinoma who were not candidates for primary cytoreduction. All were in good general health, with a mean age of 62 years.

All patients received 3 rounds of carboplatin and paclitaxel before surgery. Prior to starting chemotherapy, half were randomly assigned to fast for 36 hours before and 24 hours after chemotherapy, whereas the other half ate normally throughout treatment.

Patients in the fasting group consumed no more than 350 calories per day during the fasting window. They were allowed to have unrestricted water, herbal tea, limited vegetable juice, and small amounts of light vegetable broth. (A ketogenic diet group had initially been planned but was closed early because of poor patient compliance.)

The study met its primary endpoint of change in insulin levels during chemotherapy, Marchetti reported. Baseline insulin levels were comparable between the 2 groups, but after 3 rounds of chemotherapy, they’d dipped by an average of 1.12 µIU/mL in the fasting group and increased by 9.76 µIU/mL in the control group (P = .01).

Fasting also improved clinical outcomes. Specifically, Marchetti said, 59% of fasting patients achieved a chemotherapy response score of 3 — indicating complete or near-complete tumor response before surgery — compared with 17% of patients in the control group.

Median progression-free survival was significantly longer in the fasting group, at 38 vs 24 months.

Importantly, Marchetti said, the fasting protocol was feasible, well tolerated, and safe: All patients assigned to the fasting group completed treatment, and rates of chemotherapy-related toxicities were similar between the 2 groups.

Additional analyses shed more light on the possible mechanisms underlying the fasting group’s improved outcomes: The researchers found that those patients tended to have lower levels of circulating suppressor granulocyte and monocyte populations that have been linked to tumor immune escape, which suggests, Marchetti said, fasting may have set the stage for a “more favorable immune environment” during chemotherapy.

However, she cautioned that much more research is needed. Her team is planning a larger multicenter trial to validate the current findings, and longer-term follow-up is necessary to see whether fasting ultimately impacts patients’ survival, Marchetti said.

In a statement, Eleonora Teplinsky, MD, an ASCO expert in gynecologic cancers, said these early findings are “encouraging, support earlier data, and highlight a promising area of cancer research.”

But she, too, emphasized the need for larger clinical trials to build on the results.

The study had no commercial funding. Marchetti disclosed having relationships with Arquer Diagnostics, AstraZeneca, Clovis Oncology, and other companies. Small disclosed having relationships with Janssen, Johnson & Johnson, and others. Teplinsky had no disclosures.

A version of this article first appeared on Medscape.com.

TOPLINE:

Telephone outreach by a nurse practitioner (NP) providing counseling and care coordination reduced the gaps in breast and cervical cancer screenings among women veterans in rural areas, according to a retrospective study.

METHODOLOGY:

• Researchers conducted a retrospective chart review of 55 women veterans who received interventions related to breast or cervical cancer screening at a rural Veterans Health Administration health care system.
• A Boost team, including an NP, a medical director, a program coordinator, and a program evaluation team, was established to provide care coordination and counseling for these participants.
• The NP conducted outreach by telephone to these participants receiving care at five community-based outpatient clinics located in rural counties and helped coordinate access to screening appointments through the Office of Community Care.
• Outcomes included the number of veterans due for breast or cervical cancer screening at the time of outreach and the number of mammograms and Pap smears completed in the 12-month period following the intervention.

TAKEAWAY:

• Of the 55 veterans who received Boost interventions related to cancer screening, 35 (64%) were due for breast cancer screening and 27 (49%) were due for cervical cancer screening before the intervention.
• Following the Boost intervention, the number of veterans due for breast cancer and cervical cancer screenings decreased to 18 (32%) and 16 (29%), respectively.
• Among veterans due for breast cancer screening, 29 (83%) received counseling regarding screening and 17 (59%) of counseled participants completed mammography; however, among those due for cervical cancer screening, 22 (81%) received counseling and 11 (50%) completed screening.
• None of the veterans who were due for screening but did not receive counseling completed their screening, demonstrating the critical role of clinician-provided education and counseling.

IN PRACTICE:

“We hope to expand Boost outreach from one NP working part-time across two health systems to a national partnership of licensed independent providers conducting clinician-initiated outreach to a broader and geographically more diverse group of veterans,” the authors wrote.

SOURCE:

This study was led by Lina Vadlamani, MD, MBA, San Francisco Internal Medicine Residency Program, University of California, San Francisco. It was published online on April 24, 2026, in Military Medicine.

LIMITATIONS:

This study was a secondary analysis in which participants were not randomly assigned, limiting causal inferences. Veterans who answered the phone and engaged with the NP were likely easier to reach and potentially more proactive about their health than those who did not engage, and this selection bias may have limited the generalizability of the findings.

DISCLOSURES:

This study was funded by the Department of Veterans Affairs, Veterans Health Administration, and Office of Rural Health. The authors reported having no relevant conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

Telephone outreach by a nurse practitioner (NP) providing counseling and care coordination reduced the gaps in breast and cervical cancer screenings among women veterans in rural areas, according to a retrospective study.

METHODOLOGY:

• Researchers conducted a retrospective chart review of 55 women veterans who received interventions related to breast or cervical cancer screening at a rural Veterans Health Administration health care system.
• A Boost team, including an NP, a medical director, a program coordinator, and a program evaluation team, was established to provide care coordination and counseling for these participants.
• The NP conducted outreach by telephone to these participants receiving care at five community-based outpatient clinics located in rural counties and helped coordinate access to screening appointments through the Office of Community Care.
• Outcomes included the number of veterans due for breast or cervical cancer screening at the time of outreach and the number of mammograms and Pap smears completed in the 12-month period following the intervention.

TAKEAWAY:

• Of the 55 veterans who received Boost interventions related to cancer screening, 35 (64%) were due for breast cancer screening and 27 (49%) were due for cervical cancer screening before the intervention.
• Following the Boost intervention, the number of veterans due for breast cancer and cervical cancer screenings decreased to 18 (32%) and 16 (29%), respectively.
• Among veterans due for breast cancer screening, 29 (83%) received counseling regarding screening and 17 (59%) of counseled participants completed mammography; however, among those due for cervical cancer screening, 22 (81%) received counseling and 11 (50%) completed screening.
• None of the veterans who were due for screening but did not receive counseling completed their screening, demonstrating the critical role of clinician-provided education and counseling.

IN PRACTICE:

“We hope to expand Boost outreach from one NP working part-time across two health systems to a national partnership of licensed independent providers conducting clinician-initiated outreach to a broader and geographically more diverse group of veterans,” the authors wrote.

SOURCE:

This study was led by Lina Vadlamani, MD, MBA, San Francisco Internal Medicine Residency Program, University of California, San Francisco. It was published online on April 24, 2026, in Military Medicine.

LIMITATIONS:

This study was a secondary analysis in which participants were not randomly assigned, limiting causal inferences. Veterans who answered the phone and engaged with the NP were likely easier to reach and potentially more proactive about their health than those who did not engage, and this selection bias may have limited the generalizability of the findings.

DISCLOSURES:

This study was funded by the Department of Veterans Affairs, Veterans Health Administration, and Office of Rural Health. The authors reported having no relevant conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

Telephone outreach by a nurse practitioner (NP) providing counseling and care coordination reduced the gaps in breast and cervical cancer screenings among women veterans in rural areas, according to a retrospective study.

METHODOLOGY:

• Researchers conducted a retrospective chart review of 55 women veterans who received interventions related to breast or cervical cancer screening at a rural Veterans Health Administration health care system.
• A Boost team, including an NP, a medical director, a program coordinator, and a program evaluation team, was established to provide care coordination and counseling for these participants.
• The NP conducted outreach by telephone to these participants receiving care at five community-based outpatient clinics located in rural counties and helped coordinate access to screening appointments through the Office of Community Care.
• Outcomes included the number of veterans due for breast or cervical cancer screening at the time of outreach and the number of mammograms and Pap smears completed in the 12-month period following the intervention.

TAKEAWAY:

• Of the 55 veterans who received Boost interventions related to cancer screening, 35 (64%) were due for breast cancer screening and 27 (49%) were due for cervical cancer screening before the intervention.
• Following the Boost intervention, the number of veterans due for breast cancer and cervical cancer screenings decreased to 18 (32%) and 16 (29%), respectively.
• Among veterans due for breast cancer screening, 29 (83%) received counseling regarding screening and 17 (59%) of counseled participants completed mammography; however, among those due for cervical cancer screening, 22 (81%) received counseling and 11 (50%) completed screening.
• None of the veterans who were due for screening but did not receive counseling completed their screening, demonstrating the critical role of clinician-provided education and counseling.

IN PRACTICE:

“We hope to expand Boost outreach from one NP working part-time across two health systems to a national partnership of licensed independent providers conducting clinician-initiated outreach to a broader and geographically more diverse group of veterans,” the authors wrote.

SOURCE:

This study was led by Lina Vadlamani, MD, MBA, San Francisco Internal Medicine Residency Program, University of California, San Francisco. It was published online on April 24, 2026, in Military Medicine.

LIMITATIONS:

This study was a secondary analysis in which participants were not randomly assigned, limiting causal inferences. Veterans who answered the phone and engaged with the NP were likely easier to reach and potentially more proactive about their health than those who did not engage, and this selection bias may have limited the generalizability of the findings.

DISCLOSURES:

This study was funded by the Department of Veterans Affairs, Veterans Health Administration, and Office of Rural Health. The authors reported having no relevant conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

Among women aged > 65 years who were at a high risk for cervical cancer and required screening, only 5.2% received appropriate screening. Women with a history of high-grade cervical dysplasia had a greater likelihood of appropriate screening.

METHODOLOGY:

• Researchers conducted a retrospective study to assess the rates of appropriate cervical cancer screening among 1787 women aged 66 years or older (median, 76 years; 96.3% White) who had a Medicare wellness visit or an annual gynecologic visit in a healthcare system in 2022.
• Data on age at the last cervical cancer screening, history of hysterectomy, human papillomavirus (HPV) status, and history of a diagnosis of cervical cancer or cervical dysplasia, high-grade dysplasia, and immune deficiency status were assessed.
• Participants were categorized into 2 groups: those at high risk for cervical cancer (prior high-grade cervical dysplasia or cancer, an immunocompromised status, or lack of two normal cytology results in the past 10 years; n = 250) and those at average risk (having no high-risk features and adequate prior screening or having a prior hysterectomy with no history of high-grade cervical dysplasia; n = 1537).
• The screening cessation criteria were based on adequate prior screening, defined as two prior negative cervical cancer screenings in the past 10 years, the absence of high-grade cervical dysplasia or cervical cancer, and no immune deficiency.

TAKEAWAY:

• Overall, 4.9% of patients had a history of inadequate prior screening; among women at high risk, 5.2% were appropriately screened.
• The odds of continued screening were greater for women with a history of a positive HPV test results (adjusted odds ratio [aOR], 3.4; P = .016), a history of high-grade cervical dysplasia (aOR, 3.8; P = .009), and those without prior hysterectomy (aOR, 2.2; P = .005).
• Among women at high risk for cervical cancer, those with a history of high-grade cervical dysplasia had increased odds of appropriate screening (aOR, 6.7; P = .002), whereas the odds decreased with every 5-year increase in age (aOR, 0.5; P = .031). Women with prior hysterectomy were less likely to be over-screened (aOR, 0.3; P < .001) than those without.
• Among the 79 women who underwent screening, 97.5% had normal cytology results; the remaining women had abnormal cytology results (atypical squamous cells of undetermined significance or atypical squamous cells); all patients with abnormal cytology results met high-risk criteria and were screened appropriately.

IN PRACTICE:

“[The study] findings suggest that most clinicians and patients are aware of recommendations to stop cervical cancer screening after age 65 years. However, there may be a lack of awareness regarding continued screening in high-risk patients or those with inadequate prior screening. The lack of prior screening history and results in the medical record suggests that providers may not understand the importance of these factors to inform cervical cancer screening in older patients,” the authors of the study wrote.

SOURCE:

The study was led by Daniel Rodriguez, BS, Kolschowsky Research and Education Institute, Sarasota Memorial Health Care System, Sarasota, Florida. It was published online on April 23, 2026, in the Journal of Lower Genital Tract Disease.

LIMITATIONS:

Screening history in electronic medical records may be incomplete.

DISCLOSURES:

The Sarasota Memorial Healthcare Foundation provided financial support for this research. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

Among women aged > 65 years who were at a high risk for cervical cancer and required screening, only 5.2% received appropriate screening. Women with a history of high-grade cervical dysplasia had a greater likelihood of appropriate screening.

METHODOLOGY:

• Researchers conducted a retrospective study to assess the rates of appropriate cervical cancer screening among 1787 women aged 66 years or older (median, 76 years; 96.3% White) who had a Medicare wellness visit or an annual gynecologic visit in a healthcare system in 2022.
• Data on age at the last cervical cancer screening, history of hysterectomy, human papillomavirus (HPV) status, and history of a diagnosis of cervical cancer or cervical dysplasia, high-grade dysplasia, and immune deficiency status were assessed.
• Participants were categorized into 2 groups: those at high risk for cervical cancer (prior high-grade cervical dysplasia or cancer, an immunocompromised status, or lack of two normal cytology results in the past 10 years; n = 250) and those at average risk (having no high-risk features and adequate prior screening or having a prior hysterectomy with no history of high-grade cervical dysplasia; n = 1537).
• The screening cessation criteria were based on adequate prior screening, defined as two prior negative cervical cancer screenings in the past 10 years, the absence of high-grade cervical dysplasia or cervical cancer, and no immune deficiency.

TAKEAWAY:

• Overall, 4.9% of patients had a history of inadequate prior screening; among women at high risk, 5.2% were appropriately screened.
• The odds of continued screening were greater for women with a history of a positive HPV test results (adjusted odds ratio [aOR], 3.4; P = .016), a history of high-grade cervical dysplasia (aOR, 3.8; P = .009), and those without prior hysterectomy (aOR, 2.2; P = .005).
• Among women at high risk for cervical cancer, those with a history of high-grade cervical dysplasia had increased odds of appropriate screening (aOR, 6.7; P = .002), whereas the odds decreased with every 5-year increase in age (aOR, 0.5; P = .031). Women with prior hysterectomy were less likely to be over-screened (aOR, 0.3; P < .001) than those without.
• Among the 79 women who underwent screening, 97.5% had normal cytology results; the remaining women had abnormal cytology results (atypical squamous cells of undetermined significance or atypical squamous cells); all patients with abnormal cytology results met high-risk criteria and were screened appropriately.

IN PRACTICE:

“[The study] findings suggest that most clinicians and patients are aware of recommendations to stop cervical cancer screening after age 65 years. However, there may be a lack of awareness regarding continued screening in high-risk patients or those with inadequate prior screening. The lack of prior screening history and results in the medical record suggests that providers may not understand the importance of these factors to inform cervical cancer screening in older patients,” the authors of the study wrote.

SOURCE:

The study was led by Daniel Rodriguez, BS, Kolschowsky Research and Education Institute, Sarasota Memorial Health Care System, Sarasota, Florida. It was published online on April 23, 2026, in the Journal of Lower Genital Tract Disease.

LIMITATIONS:

Screening history in electronic medical records may be incomplete.

DISCLOSURES:

The Sarasota Memorial Healthcare Foundation provided financial support for this research. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

Among women aged > 65 years who were at a high risk for cervical cancer and required screening, only 5.2% received appropriate screening. Women with a history of high-grade cervical dysplasia had a greater likelihood of appropriate screening.

METHODOLOGY:

• Researchers conducted a retrospective study to assess the rates of appropriate cervical cancer screening among 1787 women aged 66 years or older (median, 76 years; 96.3% White) who had a Medicare wellness visit or an annual gynecologic visit in a healthcare system in 2022.
• Data on age at the last cervical cancer screening, history of hysterectomy, human papillomavirus (HPV) status, and history of a diagnosis of cervical cancer or cervical dysplasia, high-grade dysplasia, and immune deficiency status were assessed.
• Participants were categorized into 2 groups: those at high risk for cervical cancer (prior high-grade cervical dysplasia or cancer, an immunocompromised status, or lack of two normal cytology results in the past 10 years; n = 250) and those at average risk (having no high-risk features and adequate prior screening or having a prior hysterectomy with no history of high-grade cervical dysplasia; n = 1537).
• The screening cessation criteria were based on adequate prior screening, defined as two prior negative cervical cancer screenings in the past 10 years, the absence of high-grade cervical dysplasia or cervical cancer, and no immune deficiency.

TAKEAWAY:

• Overall, 4.9% of patients had a history of inadequate prior screening; among women at high risk, 5.2% were appropriately screened.
• The odds of continued screening were greater for women with a history of a positive HPV test results (adjusted odds ratio [aOR], 3.4; P = .016), a history of high-grade cervical dysplasia (aOR, 3.8; P = .009), and those without prior hysterectomy (aOR, 2.2; P = .005).
• Among women at high risk for cervical cancer, those with a history of high-grade cervical dysplasia had increased odds of appropriate screening (aOR, 6.7; P = .002), whereas the odds decreased with every 5-year increase in age (aOR, 0.5; P = .031). Women with prior hysterectomy were less likely to be over-screened (aOR, 0.3; P < .001) than those without.
• Among the 79 women who underwent screening, 97.5% had normal cytology results; the remaining women had abnormal cytology results (atypical squamous cells of undetermined significance or atypical squamous cells); all patients with abnormal cytology results met high-risk criteria and were screened appropriately.

IN PRACTICE:

“[The study] findings suggest that most clinicians and patients are aware of recommendations to stop cervical cancer screening after age 65 years. However, there may be a lack of awareness regarding continued screening in high-risk patients or those with inadequate prior screening. The lack of prior screening history and results in the medical record suggests that providers may not understand the importance of these factors to inform cervical cancer screening in older patients,” the authors of the study wrote.

SOURCE:

The study was led by Daniel Rodriguez, BS, Kolschowsky Research and Education Institute, Sarasota Memorial Health Care System, Sarasota, Florida. It was published online on April 23, 2026, in the Journal of Lower Genital Tract Disease.

LIMITATIONS:

Screening history in electronic medical records may be incomplete.

DISCLOSURES:

The Sarasota Memorial Healthcare Foundation provided financial support for this research. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

Women who undergo surgery for breast cancer often hear that they should take it easy with exercise during recovery. But new research looking at intense strength training puts that advice into question.

The study, of nearly 200 women who’d undergone lumpectomy or mastectomy, found that a 3-month weight-training program helped patients make substantial gains in strength, mobility, balance, and body composition.

And while previous studies have examined resistance exercise during breast cancer surgery recovery, this program pumped up the intensity: Most women progressed to deadlifting 100 to 200 pounds, even though few had ever performed strength training before.

“Most of these patients can do a lot more than we think,” said principal investigator Colin Champ, MD, director of the Exercise Oncology and Resiliency Center at Allegheny Health Network in Pittsburgh.

The findings were presented at The American Society of Breast Surgeons (ASBrS) Annual Meeting, held in Seattle from April 29 to May 3.

Pumping Up the Intensity

For the analysis, Champ and his colleagues pooled the results of 3 small prospective studies of their strength conditioning program, including one that previously reported no worsening in patients’ lymphedema, and instead, showed signs of improvement.

The researchers evaluated program participants’ physical and functional gains and whether any of those parameters differed by the extent of their breast cancer surgery.

In total, there were 197 participants, including 85 who’d undergone mastectomies and 112 who’d had lumpectomies; 26 patients also had axillary lymph node dissection.

All of the women attended the same 3-month supervised strength-training program, starting at various points in their recovery process. Nearly half started at 3 months postdiagnosis.

According to Champ, the program addresses a full range of motion, with the exercise intensity building over a short period — similar to what professional athletes do in early training. The specific exercises include split squats, dumbbell presses, and dumbbell rows, done 3 days per week, for about 45-60 minutes.

Most participants, Champ said, start with deadlifting around 70 pounds (lifting weight from the floor to hip level). “If you can carry groceries, you can deadlift 60 or 70 pounds,” he noted.

Each month, the weight and sets increase, while the repetitions decrease.

“We just had a woman in her 70s who deadlifted about 200 pounds” as the program progressed, Champ said.

Benefits Regardless of Surgery Type

Women in the current analysis underwent baseline and post-program testing of body composition and functional parameters, including strength, mobility, and balance. Mastectomy patients (median age, 51 years) were younger than lumpectomy patients (median age, 59 years). They were also more likely to have had chemotherapy (45% vs 27%).

Overall, Champ’s team found that both surgery groups showed statistically significant improvements in muscle and body fat percentages over the course of the program, with muscle mass increasing by 1 percentage point on average and body fat declining by 1.5 percentage points.

Similarly, functional movement scores, grip strength, loads lifted, and balance skills also improved, with comparable benefits regardless of surgery type or whether lymph node dissection was performed.

By the end of the program’s third week, Champ said, most women could deadlift 100-pound weights. And by the 3-month mark, many were able to lift 200-pound loads.

Champ called the results empowering, and he hopes they help reframe the traditional mindset that intense strength training is too heavy a lift after breast cancer surgery.

A surgical oncologist who was not involved in the study agreed.

“This gives us something concrete to say to patients,” said Tina Hieken, MD, of the Mayo Clinic in Rochester, Minnesota. “We have more data to say it’s safe for you to exercise.’’

Hieken, who chaired the meeting’s scientific program committee, also noted that the findings pertain to women of all baseline fitness levels.

For her part, Hieken already encourages patients to walk for exercise and spend time outdoors — in part for the mental well-being benefits.

With patients facing so much uncertainty after a cancer diagnosis, she said, “this is something an individual can take control of.”

Champ and Hieken had no disclosures.

A version of this article first appeared on Medscape.com.

Women who undergo surgery for breast cancer often hear that they should take it easy with exercise during recovery. But new research looking at intense strength training puts that advice into question.

The study, of nearly 200 women who’d undergone lumpectomy or mastectomy, found that a 3-month weight-training program helped patients make substantial gains in strength, mobility, balance, and body composition.

And while previous studies have examined resistance exercise during breast cancer surgery recovery, this program pumped up the intensity: Most women progressed to deadlifting 100 to 200 pounds, even though few had ever performed strength training before.

“Most of these patients can do a lot more than we think,” said principal investigator Colin Champ, MD, director of the Exercise Oncology and Resiliency Center at Allegheny Health Network in Pittsburgh.

The findings were presented at The American Society of Breast Surgeons (ASBrS) Annual Meeting, held in Seattle from April 29 to May 3.

Pumping Up the Intensity

For the analysis, Champ and his colleagues pooled the results of 3 small prospective studies of their strength conditioning program, including one that previously reported no worsening in patients’ lymphedema, and instead, showed signs of improvement.

The researchers evaluated program participants’ physical and functional gains and whether any of those parameters differed by the extent of their breast cancer surgery.

In total, there were 197 participants, including 85 who’d undergone mastectomies and 112 who’d had lumpectomies; 26 patients also had axillary lymph node dissection.

All of the women attended the same 3-month supervised strength-training program, starting at various points in their recovery process. Nearly half started at 3 months postdiagnosis.

According to Champ, the program addresses a full range of motion, with the exercise intensity building over a short period — similar to what professional athletes do in early training. The specific exercises include split squats, dumbbell presses, and dumbbell rows, done 3 days per week, for about 45-60 minutes.

Most participants, Champ said, start with deadlifting around 70 pounds (lifting weight from the floor to hip level). “If you can carry groceries, you can deadlift 60 or 70 pounds,” he noted.

Each month, the weight and sets increase, while the repetitions decrease.

“We just had a woman in her 70s who deadlifted about 200 pounds” as the program progressed, Champ said.

Benefits Regardless of Surgery Type

Women in the current analysis underwent baseline and post-program testing of body composition and functional parameters, including strength, mobility, and balance. Mastectomy patients (median age, 51 years) were younger than lumpectomy patients (median age, 59 years). They were also more likely to have had chemotherapy (45% vs 27%).

Overall, Champ’s team found that both surgery groups showed statistically significant improvements in muscle and body fat percentages over the course of the program, with muscle mass increasing by 1 percentage point on average and body fat declining by 1.5 percentage points.

Similarly, functional movement scores, grip strength, loads lifted, and balance skills also improved, with comparable benefits regardless of surgery type or whether lymph node dissection was performed.

By the end of the program’s third week, Champ said, most women could deadlift 100-pound weights. And by the 3-month mark, many were able to lift 200-pound loads.

Champ called the results empowering, and he hopes they help reframe the traditional mindset that intense strength training is too heavy a lift after breast cancer surgery.

A surgical oncologist who was not involved in the study agreed.

“This gives us something concrete to say to patients,” said Tina Hieken, MD, of the Mayo Clinic in Rochester, Minnesota. “We have more data to say it’s safe for you to exercise.’’

Hieken, who chaired the meeting’s scientific program committee, also noted that the findings pertain to women of all baseline fitness levels.

For her part, Hieken already encourages patients to walk for exercise and spend time outdoors — in part for the mental well-being benefits.

With patients facing so much uncertainty after a cancer diagnosis, she said, “this is something an individual can take control of.”

Champ and Hieken had no disclosures.

A version of this article first appeared on Medscape.com.

Women who undergo surgery for breast cancer often hear that they should take it easy with exercise during recovery. But new research looking at intense strength training puts that advice into question.

The study, of nearly 200 women who’d undergone lumpectomy or mastectomy, found that a 3-month weight-training program helped patients make substantial gains in strength, mobility, balance, and body composition.

And while previous studies have examined resistance exercise during breast cancer surgery recovery, this program pumped up the intensity: Most women progressed to deadlifting 100 to 200 pounds, even though few had ever performed strength training before.

“Most of these patients can do a lot more than we think,” said principal investigator Colin Champ, MD, director of the Exercise Oncology and Resiliency Center at Allegheny Health Network in Pittsburgh.

The findings were presented at The American Society of Breast Surgeons (ASBrS) Annual Meeting, held in Seattle from April 29 to May 3.

Pumping Up the Intensity

For the analysis, Champ and his colleagues pooled the results of 3 small prospective studies of their strength conditioning program, including one that previously reported no worsening in patients’ lymphedema, and instead, showed signs of improvement.

The researchers evaluated program participants’ physical and functional gains and whether any of those parameters differed by the extent of their breast cancer surgery.

In total, there were 197 participants, including 85 who’d undergone mastectomies and 112 who’d had lumpectomies; 26 patients also had axillary lymph node dissection.

All of the women attended the same 3-month supervised strength-training program, starting at various points in their recovery process. Nearly half started at 3 months postdiagnosis.

According to Champ, the program addresses a full range of motion, with the exercise intensity building over a short period — similar to what professional athletes do in early training. The specific exercises include split squats, dumbbell presses, and dumbbell rows, done 3 days per week, for about 45-60 minutes.

Most participants, Champ said, start with deadlifting around 70 pounds (lifting weight from the floor to hip level). “If you can carry groceries, you can deadlift 60 or 70 pounds,” he noted.

Each month, the weight and sets increase, while the repetitions decrease.

“We just had a woman in her 70s who deadlifted about 200 pounds” as the program progressed, Champ said.

Benefits Regardless of Surgery Type

Women in the current analysis underwent baseline and post-program testing of body composition and functional parameters, including strength, mobility, and balance. Mastectomy patients (median age, 51 years) were younger than lumpectomy patients (median age, 59 years). They were also more likely to have had chemotherapy (45% vs 27%).

Overall, Champ’s team found that both surgery groups showed statistically significant improvements in muscle and body fat percentages over the course of the program, with muscle mass increasing by 1 percentage point on average and body fat declining by 1.5 percentage points.

Similarly, functional movement scores, grip strength, loads lifted, and balance skills also improved, with comparable benefits regardless of surgery type or whether lymph node dissection was performed.

By the end of the program’s third week, Champ said, most women could deadlift 100-pound weights. And by the 3-month mark, many were able to lift 200-pound loads.

Champ called the results empowering, and he hopes they help reframe the traditional mindset that intense strength training is too heavy a lift after breast cancer surgery.

A surgical oncologist who was not involved in the study agreed.

“This gives us something concrete to say to patients,” said Tina Hieken, MD, of the Mayo Clinic in Rochester, Minnesota. “We have more data to say it’s safe for you to exercise.’’

Hieken, who chaired the meeting’s scientific program committee, also noted that the findings pertain to women of all baseline fitness levels.

For her part, Hieken already encourages patients to walk for exercise and spend time outdoors — in part for the mental well-being benefits.

With patients facing so much uncertainty after a cancer diagnosis, she said, “this is something an individual can take control of.”

Champ and Hieken had no disclosures.

A version of this article first appeared on Medscape.com.

Dual checkpoint blockade allowed 70.6% of patients with microsatellite instability-high (MSI-H) resectable gastric or gastroesophageal junction adenocarcinoma (G/GEJAC) to avoid surgery in a small cohort of the INFINITY study.

MSI-H tumors account for roughly 10% of early G/GEJACs. They respond well to immunotherapy, with high rates of pathologic complete responses. The Italian INFINITY trial set out to test whether some patients with these tumors might not need gastrectomy.

The trial treated MSI-H patients with durvalumab 1500 mg once a month for 3 months along with 1 300-mg dose of the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) blocker tremelimumab on day 1. The 18 patients in cohort 1 proceeded to surgery, with a 60% pathologic complete response rate. An additional 18 patients in cohort 2 were the subject of a presentation at the American Association for Cancer Research (AACR) Annual Meeting 2026. These patients were assessed for clinical complete response; if present, they went on to surveillance; if not, they had surgery.

To qualify for a clinical complete response and surveillance, patients were required to have negative findings on CT and PET scans; tumor-informed circulating tumor DNA (ctDNA); and upper endoscopy with ultrasound, including bite-on-bite biopsies and nodal sampling. Surveillance afterward included CT, endoscopy with biopsies, and ctDNA every 12 weeks for up to 2 years.

Among 17 evaluable patients, 1 withdrew consent during immunotherapy, 13 (76%) had a clinical complete response and started surveillance, and the other 4 went to surgery. One patient in the surveillance group had a local regrowth after 4 months, underwent salvage surgery, and remained disease-free. At a median follow-up of 27.1 months, there were no additional progression events.

Overall, 12 of the 17 patients (70.6%) were gastrectomy-free at 2 years without additional treatment. Progression-free survival was 94.1%, and all patients were alive.

“The results are very encouraging,” lead investigator Alberto Leone, MD, said while presenting the results at the AACR annual meeting.

“Nonoperative management could be a safe and effective strategy for patients achieving a clinical complete response after only 3 months of dual immunotherapy,” said Leone, who is a gastrointestinal medical oncologist at the Istituto Nazionale dei Tumori, Milan, Italy. “However, the optimal strategy needs to be established in larger randomized trials.”

Study discussant Yelena Janjagian, MD, gastrointestinal medical oncologist at Memorial Sloan Kettering Cancer Center in New York City, said the findings were important, particularly given that 70.6% of patients avoided a potentially life-altering gastrectomy.

In addition to surgery, the study also calls into question the need for chemotherapy, long the backbone of management alongside surgery, she said. To replace it, however, “it appears that dual checkpoint blockade will be required for a chemotherapy-free approach to achieve organ preservation.”

“Anti-PD-1 alone is not sufficient; we need CTLA-4 to expand and reactivate tumor-specific immunity,” Janjagian continued.

Ultimately, she expects immunotherapy to shift management of MSI-H cancers away from surgery, although some patients will still likely need an operation.

In addition to being MSI-H, patients in the study were mismatch repair deficient and Epstein-Barr virus-negative with T2/T3 tumors; T4 tumors were excluded.

Tumor-agnostic plasma ctDNA was positive at baseline in 13 patients and cleared in 11 after treatment. Higher baseline plasma ctDNA trended toward a lower likelihood of reaching a clinical complete response. Specificity was 100%, so when positive, the test was “very highly informative,” Leone said.

Three patients had grade 3 adverse events (hyperthyroidism, increased gamma-glutamyl transferase, and colitis) that resolved with steroids. There were no grade 4 events, treatment discontinuation, or deaths.

The work was funded by the GONO Foundation and AstraZeneca, the maker of durvalumab and tremelimumab. Leone reported having no disclosures. Janjagian reported having extensive industry ties, including travel funding, consulting fees, and research support from AstraZeneca.

M. Alexander Otto is a physician assistant with a master’s degree in medical science and a journalism degree from Newhouse. He is an award-winning medical journalist who worked for several major news outlets before joining Medscape. Alex is also an MIT Knight Science Journalism fellow. Email: aotto@medscape.net 

A version of this article first appeared on Medscape.com.

Dual checkpoint blockade allowed 70.6% of patients with microsatellite instability-high (MSI-H) resectable gastric or gastroesophageal junction adenocarcinoma (G/GEJAC) to avoid surgery in a small cohort of the INFINITY study.

MSI-H tumors account for roughly 10% of early G/GEJACs. They respond well to immunotherapy, with high rates of pathologic complete responses. The Italian INFINITY trial set out to test whether some patients with these tumors might not need gastrectomy.

The trial treated MSI-H patients with durvalumab 1500 mg once a month for 3 months along with 1 300-mg dose of the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) blocker tremelimumab on day 1. The 18 patients in cohort 1 proceeded to surgery, with a 60% pathologic complete response rate. An additional 18 patients in cohort 2 were the subject of a presentation at the American Association for Cancer Research (AACR) Annual Meeting 2026. These patients were assessed for clinical complete response; if present, they went on to surveillance; if not, they had surgery.

To qualify for a clinical complete response and surveillance, patients were required to have negative findings on CT and PET scans; tumor-informed circulating tumor DNA (ctDNA); and upper endoscopy with ultrasound, including bite-on-bite biopsies and nodal sampling. Surveillance afterward included CT, endoscopy with biopsies, and ctDNA every 12 weeks for up to 2 years.

Among 17 evaluable patients, 1 withdrew consent during immunotherapy, 13 (76%) had a clinical complete response and started surveillance, and the other 4 went to surgery. One patient in the surveillance group had a local regrowth after 4 months, underwent salvage surgery, and remained disease-free. At a median follow-up of 27.1 months, there were no additional progression events.

Overall, 12 of the 17 patients (70.6%) were gastrectomy-free at 2 years without additional treatment. Progression-free survival was 94.1%, and all patients were alive.

“The results are very encouraging,” lead investigator Alberto Leone, MD, said while presenting the results at the AACR annual meeting.

“Nonoperative management could be a safe and effective strategy for patients achieving a clinical complete response after only 3 months of dual immunotherapy,” said Leone, who is a gastrointestinal medical oncologist at the Istituto Nazionale dei Tumori, Milan, Italy. “However, the optimal strategy needs to be established in larger randomized trials.”

Study discussant Yelena Janjagian, MD, gastrointestinal medical oncologist at Memorial Sloan Kettering Cancer Center in New York City, said the findings were important, particularly given that 70.6% of patients avoided a potentially life-altering gastrectomy.

In addition to surgery, the study also calls into question the need for chemotherapy, long the backbone of management alongside surgery, she said. To replace it, however, “it appears that dual checkpoint blockade will be required for a chemotherapy-free approach to achieve organ preservation.”

“Anti-PD-1 alone is not sufficient; we need CTLA-4 to expand and reactivate tumor-specific immunity,” Janjagian continued.

Ultimately, she expects immunotherapy to shift management of MSI-H cancers away from surgery, although some patients will still likely need an operation.

In addition to being MSI-H, patients in the study were mismatch repair deficient and Epstein-Barr virus-negative with T2/T3 tumors; T4 tumors were excluded.

Tumor-agnostic plasma ctDNA was positive at baseline in 13 patients and cleared in 11 after treatment. Higher baseline plasma ctDNA trended toward a lower likelihood of reaching a clinical complete response. Specificity was 100%, so when positive, the test was “very highly informative,” Leone said.

Three patients had grade 3 adverse events (hyperthyroidism, increased gamma-glutamyl transferase, and colitis) that resolved with steroids. There were no grade 4 events, treatment discontinuation, or deaths.

The work was funded by the GONO Foundation and AstraZeneca, the maker of durvalumab and tremelimumab. Leone reported having no disclosures. Janjagian reported having extensive industry ties, including travel funding, consulting fees, and research support from AstraZeneca.

M. Alexander Otto is a physician assistant with a master’s degree in medical science and a journalism degree from Newhouse. He is an award-winning medical journalist who worked for several major news outlets before joining Medscape. Alex is also an MIT Knight Science Journalism fellow. Email: aotto@medscape.net 

A version of this article first appeared on Medscape.com.

Dual checkpoint blockade allowed 70.6% of patients with microsatellite instability-high (MSI-H) resectable gastric or gastroesophageal junction adenocarcinoma (G/GEJAC) to avoid surgery in a small cohort of the INFINITY study.

MSI-H tumors account for roughly 10% of early G/GEJACs. They respond well to immunotherapy, with high rates of pathologic complete responses. The Italian INFINITY trial set out to test whether some patients with these tumors might not need gastrectomy.

The trial treated MSI-H patients with durvalumab 1500 mg once a month for 3 months along with 1 300-mg dose of the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) blocker tremelimumab on day 1. The 18 patients in cohort 1 proceeded to surgery, with a 60% pathologic complete response rate. An additional 18 patients in cohort 2 were the subject of a presentation at the American Association for Cancer Research (AACR) Annual Meeting 2026. These patients were assessed for clinical complete response; if present, they went on to surveillance; if not, they had surgery.

To qualify for a clinical complete response and surveillance, patients were required to have negative findings on CT and PET scans; tumor-informed circulating tumor DNA (ctDNA); and upper endoscopy with ultrasound, including bite-on-bite biopsies and nodal sampling. Surveillance afterward included CT, endoscopy with biopsies, and ctDNA every 12 weeks for up to 2 years.

Among 17 evaluable patients, 1 withdrew consent during immunotherapy, 13 (76%) had a clinical complete response and started surveillance, and the other 4 went to surgery. One patient in the surveillance group had a local regrowth after 4 months, underwent salvage surgery, and remained disease-free. At a median follow-up of 27.1 months, there were no additional progression events.

Overall, 12 of the 17 patients (70.6%) were gastrectomy-free at 2 years without additional treatment. Progression-free survival was 94.1%, and all patients were alive.

“The results are very encouraging,” lead investigator Alberto Leone, MD, said while presenting the results at the AACR annual meeting.

“Nonoperative management could be a safe and effective strategy for patients achieving a clinical complete response after only 3 months of dual immunotherapy,” said Leone, who is a gastrointestinal medical oncologist at the Istituto Nazionale dei Tumori, Milan, Italy. “However, the optimal strategy needs to be established in larger randomized trials.”

Study discussant Yelena Janjagian, MD, gastrointestinal medical oncologist at Memorial Sloan Kettering Cancer Center in New York City, said the findings were important, particularly given that 70.6% of patients avoided a potentially life-altering gastrectomy.

In addition to surgery, the study also calls into question the need for chemotherapy, long the backbone of management alongside surgery, she said. To replace it, however, “it appears that dual checkpoint blockade will be required for a chemotherapy-free approach to achieve organ preservation.”

“Anti-PD-1 alone is not sufficient; we need CTLA-4 to expand and reactivate tumor-specific immunity,” Janjagian continued.

Ultimately, she expects immunotherapy to shift management of MSI-H cancers away from surgery, although some patients will still likely need an operation.

In addition to being MSI-H, patients in the study were mismatch repair deficient and Epstein-Barr virus-negative with T2/T3 tumors; T4 tumors were excluded.

Tumor-agnostic plasma ctDNA was positive at baseline in 13 patients and cleared in 11 after treatment. Higher baseline plasma ctDNA trended toward a lower likelihood of reaching a clinical complete response. Specificity was 100%, so when positive, the test was “very highly informative,” Leone said.

Three patients had grade 3 adverse events (hyperthyroidism, increased gamma-glutamyl transferase, and colitis) that resolved with steroids. There were no grade 4 events, treatment discontinuation, or deaths.

The work was funded by the GONO Foundation and AstraZeneca, the maker of durvalumab and tremelimumab. Leone reported having no disclosures. Janjagian reported having extensive industry ties, including travel funding, consulting fees, and research support from AstraZeneca.

M. Alexander Otto is a physician assistant with a master’s degree in medical science and a journalism degree from Newhouse. He is an award-winning medical journalist who worked for several major news outlets before joining Medscape. Alex is also an MIT Knight Science Journalism fellow. Email: aotto@medscape.net 

A version of this article first appeared on Medscape.com.

A personalized messenger RNA (mRNA) vaccine for pancreatic cancer continues to show promise for improving patient survival, according to 6-year follow-up results of a phase 1 clinical study.

Among the 8 out of 16 patients in the study who initially experienced an immune response to the vaccine, seven (87.5%) were still alive at follow-up, lead investigator Vinod P. Balachandran, MD, reported at the American Association for Cancer Research (AACR) Annual Meeting 2026.

Of the eight patients who did not respond, two (25%) were still alive, with a median survival time of 3.4 years. “This suggests that personalized vaccines can stimulate the immune system in some pancreatic cancer patients, and that these patients continue to do well for several years after vaccination,” said Balachandran, director of the Olayan Center for Cancer Vaccines at Memorial Sloan Kettering Cancer Center in New York City.

The findings suggest that this vaccine has the potential to improve outcomes in patients with pancreatic cancer, which is one of the deadliest cancers, he said.

The 5-year survival rate for pancreatic cancer is currently 13%, according to the American Cancer Society’s Cancer Statistics 2026 report.

Initial results of the trial evaluating the individualized neoantigen vaccine — autogene cevumeran, which is being developed by BioNTech and Genentech — were published in Nature in February 2025.

After pancreatic cancer surgery and chemo-immunotherapy, patients with pancreatic ductal adenocarcinoma (PDAC) received a vaccine personalized to each patient based on unique changes in their tumor DNA.

The eight patients with vaccine-induced T cells had prolonged recurrence-free survival (RFS; median not reached), whereas nonresponders had a median RFS of 13.4 months, the authors had reported in the Nature paper.

This correlation was not confounded by other factors, including those associated with the patient, tumor, treatment, and host immune fitness, Balachandran noted.

In the responders, the T-cell clones had “high magnitude and exceptional longevity,” with an average estimated lifespan of 7.7 years, he said.

A fundamental challenge in developing cancer vaccines has been generating durable functional T cells specific for tumor antigens, and these findings suggest that mRNA-lipoplex vaccines against somatic mutation-derived neoantigens like autogene cevumeran may help overcome this challenge in pancreatic cancer, he and his colleagues concluded in the Nature paper.

The latest findings presented at the AACR annual meeting further underscore the potential of this approach.

At the 6-year follow-up, median RFS was “still not reached” in the vaccine responders vs 1.1 year in the nonresponders, he noted.

“This translates to a difference in overall survival,” he said. “Seven of eight [responders to the vaccine] are still alive 4.5-6 years after surgery.”

And of the 2 of 8 nonresponders still alive, one appears to be mounting a subclinical vaccine-induced T-cell response, he added, noting that this “suggests that inducible vaccine immunity may also impact survival in PDAC.”

“The implication here, we believe, is that even if a cancer has very mutational by-products [like PDAC], these mutational by-products can empower potent and composite immunity,” he said. “This is important because it could potentially expand vaccine eligibility to many cancers.”

Currently, there are about 50 neoantigen vaccine trials in solid tumors ongoing worldwide, he noted.

Memorial Sloan Kettering reports that Genentech and BioNTech are now testing autogene cevumeran in a larger patient population at numerous sites worldwide.

Balachandran reported receiving research support from Genentech, Merck Sharp & Dohme, and AbbVie.

Sharon Worcester, MA, is an award-winning medical journalist based in Birmingham, Alabama, writing for Medscape, MDedge, and other affiliate sites. She currently covers oncology, but she has also written on a variety of other medical specialties and healthcare topics. She can be reached at sworcester@mdedge.com or on X: @SW_MedReporter.

A version of this article first appeared on Medscape.com.

A personalized messenger RNA (mRNA) vaccine for pancreatic cancer continues to show promise for improving patient survival, according to 6-year follow-up results of a phase 1 clinical study.

Among the 8 out of 16 patients in the study who initially experienced an immune response to the vaccine, seven (87.5%) were still alive at follow-up, lead investigator Vinod P. Balachandran, MD, reported at the American Association for Cancer Research (AACR) Annual Meeting 2026.

Of the eight patients who did not respond, two (25%) were still alive, with a median survival time of 3.4 years. “This suggests that personalized vaccines can stimulate the immune system in some pancreatic cancer patients, and that these patients continue to do well for several years after vaccination,” said Balachandran, director of the Olayan Center for Cancer Vaccines at Memorial Sloan Kettering Cancer Center in New York City.

The findings suggest that this vaccine has the potential to improve outcomes in patients with pancreatic cancer, which is one of the deadliest cancers, he said.

The 5-year survival rate for pancreatic cancer is currently 13%, according to the American Cancer Society’s Cancer Statistics 2026 report.

Initial results of the trial evaluating the individualized neoantigen vaccine — autogene cevumeran, which is being developed by BioNTech and Genentech — were published in Nature in February 2025.

After pancreatic cancer surgery and chemo-immunotherapy, patients with pancreatic ductal adenocarcinoma (PDAC) received a vaccine personalized to each patient based on unique changes in their tumor DNA.

The eight patients with vaccine-induced T cells had prolonged recurrence-free survival (RFS; median not reached), whereas nonresponders had a median RFS of 13.4 months, the authors had reported in the Nature paper.

This correlation was not confounded by other factors, including those associated with the patient, tumor, treatment, and host immune fitness, Balachandran noted.

In the responders, the T-cell clones had “high magnitude and exceptional longevity,” with an average estimated lifespan of 7.7 years, he said.

A fundamental challenge in developing cancer vaccines has been generating durable functional T cells specific for tumor antigens, and these findings suggest that mRNA-lipoplex vaccines against somatic mutation-derived neoantigens like autogene cevumeran may help overcome this challenge in pancreatic cancer, he and his colleagues concluded in the Nature paper.

The latest findings presented at the AACR annual meeting further underscore the potential of this approach.

At the 6-year follow-up, median RFS was “still not reached” in the vaccine responders vs 1.1 year in the nonresponders, he noted.

“This translates to a difference in overall survival,” he said. “Seven of eight [responders to the vaccine] are still alive 4.5-6 years after surgery.”

And of the 2 of 8 nonresponders still alive, one appears to be mounting a subclinical vaccine-induced T-cell response, he added, noting that this “suggests that inducible vaccine immunity may also impact survival in PDAC.”

“The implication here, we believe, is that even if a cancer has very mutational by-products [like PDAC], these mutational by-products can empower potent and composite immunity,” he said. “This is important because it could potentially expand vaccine eligibility to many cancers.”

Currently, there are about 50 neoantigen vaccine trials in solid tumors ongoing worldwide, he noted.

Memorial Sloan Kettering reports that Genentech and BioNTech are now testing autogene cevumeran in a larger patient population at numerous sites worldwide.

Balachandran reported receiving research support from Genentech, Merck Sharp & Dohme, and AbbVie.

Sharon Worcester, MA, is an award-winning medical journalist based in Birmingham, Alabama, writing for Medscape, MDedge, and other affiliate sites. She currently covers oncology, but she has also written on a variety of other medical specialties and healthcare topics. She can be reached at sworcester@mdedge.com or on X: @SW_MedReporter.

A version of this article first appeared on Medscape.com.

A personalized messenger RNA (mRNA) vaccine for pancreatic cancer continues to show promise for improving patient survival, according to 6-year follow-up results of a phase 1 clinical study.

Among the 8 out of 16 patients in the study who initially experienced an immune response to the vaccine, seven (87.5%) were still alive at follow-up, lead investigator Vinod P. Balachandran, MD, reported at the American Association for Cancer Research (AACR) Annual Meeting 2026.

Of the eight patients who did not respond, two (25%) were still alive, with a median survival time of 3.4 years. “This suggests that personalized vaccines can stimulate the immune system in some pancreatic cancer patients, and that these patients continue to do well for several years after vaccination,” said Balachandran, director of the Olayan Center for Cancer Vaccines at Memorial Sloan Kettering Cancer Center in New York City.

The findings suggest that this vaccine has the potential to improve outcomes in patients with pancreatic cancer, which is one of the deadliest cancers, he said.

The 5-year survival rate for pancreatic cancer is currently 13%, according to the American Cancer Society’s Cancer Statistics 2026 report.

Initial results of the trial evaluating the individualized neoantigen vaccine — autogene cevumeran, which is being developed by BioNTech and Genentech — were published in Nature in February 2025.

After pancreatic cancer surgery and chemo-immunotherapy, patients with pancreatic ductal adenocarcinoma (PDAC) received a vaccine personalized to each patient based on unique changes in their tumor DNA.

The eight patients with vaccine-induced T cells had prolonged recurrence-free survival (RFS; median not reached), whereas nonresponders had a median RFS of 13.4 months, the authors had reported in the Nature paper.

This correlation was not confounded by other factors, including those associated with the patient, tumor, treatment, and host immune fitness, Balachandran noted.

In the responders, the T-cell clones had “high magnitude and exceptional longevity,” with an average estimated lifespan of 7.7 years, he said.

A fundamental challenge in developing cancer vaccines has been generating durable functional T cells specific for tumor antigens, and these findings suggest that mRNA-lipoplex vaccines against somatic mutation-derived neoantigens like autogene cevumeran may help overcome this challenge in pancreatic cancer, he and his colleagues concluded in the Nature paper.

The latest findings presented at the AACR annual meeting further underscore the potential of this approach.

At the 6-year follow-up, median RFS was “still not reached” in the vaccine responders vs 1.1 year in the nonresponders, he noted.

“This translates to a difference in overall survival,” he said. “Seven of eight [responders to the vaccine] are still alive 4.5-6 years after surgery.”

And of the 2 of 8 nonresponders still alive, one appears to be mounting a subclinical vaccine-induced T-cell response, he added, noting that this “suggests that inducible vaccine immunity may also impact survival in PDAC.”

“The implication here, we believe, is that even if a cancer has very mutational by-products [like PDAC], these mutational by-products can empower potent and composite immunity,” he said. “This is important because it could potentially expand vaccine eligibility to many cancers.”

Currently, there are about 50 neoantigen vaccine trials in solid tumors ongoing worldwide, he noted.

Memorial Sloan Kettering reports that Genentech and BioNTech are now testing autogene cevumeran in a larger patient population at numerous sites worldwide.

Balachandran reported receiving research support from Genentech, Merck Sharp & Dohme, and AbbVie.

Sharon Worcester, MA, is an award-winning medical journalist based in Birmingham, Alabama, writing for Medscape, MDedge, and other affiliate sites. She currently covers oncology, but she has also written on a variety of other medical specialties and healthcare topics. She can be reached at sworcester@mdedge.com or on X: @SW_MedReporter.

A version of this article first appeared on Medscape.com.

Women with epithelial ovarian cancer treated in the US Department of Defense (DoD) universal health care system demonstrate better 5-year survival compared with similar patients from the national population. The survival advantage persists across multiple age groups and disease stages, with particularly notable improvements in patients aged 35-49 years and those with stage III disease.

METHODOLOGY:

• Researchers compared 1504 patients with invasive stage I-IV epithelial ovarian carcinoma from the Automated Center Tumor Registry (ACTUR) for the DoD with 6016 matched patients from the 18-region Surveillance, Epidemiology, and End Results (SEER) program between 1987 and 2013.
• Patients from ACTUR were matched in a 1:4 ratio with SEER patients stratified for age, race, year of diagnosis, and histology, including serous carcinoma, clear cell carcinoma, mucinous carcinoma, and endometrioid carcinoma with adenocarcinoma subtypes.
• Five-year overall survival was evaluated using the Kaplan-Meier method and compared using log-rank test, with median follow-up time of 46 months in ACTUR and 44 months in SEER.
• Adjusted hazard ratio (AHR) and 95% CI for all-cause mortality were estimated from multivariable Cox proportional regression modeling controlling for age, race, year of diagnosis, region of diagnosis, stage, histology, and grade.

TAKEAWAY:

• Overall survival differs between registries: 5-year survival of 53.2% in ACTUR vs 47.7% in matched SEER cohort (log-rank P = .001).
• In the primary adjusted model, ACTUR is associated with a lower risk for all-cause mortality vs SEER (AHR, 0.83; 95% CI, 0.76-0.91; P < .0001).
• Subset results retain lower adjusted risk for death for ACTUR vs SEER among ages 35-49 years (AHR, 0.66; 95% CI, 0.52-0.83; P = .0005), ages ≥ 65 years (AHR, 0.82; 95% CI, 0.70-0.96; P = .016), and stage III cancer (AHR, 0.79; 95% CI, 0.69-0.91; P = .0015).
• Histology-stratified findings show lower adjusted risk for death in ACTUR vs SEER for clear cell carcinoma (AHR, 0.63; 95% CI, 0.43-0.93; P =.02) and for endometrioid and other adenocarcinomas (AHR, 0.68; 95% CI, 0.56-0.81; P < .0001).

IN PRACTICE:

"This study is envisioned to be a stepping stone to further investigations of survival and other cancer health outcomes starting with patients diagnosed between 2014 and 2024 with epithelial carcinoma of the ovary, fallopian tube, or primary peritoneum in the DoD Healthcare System versus the national population or other Healthcare Systems,” wrote the authors of the study. “Dedicated funding and support in the [Military Health System] are needed to invest in infrastructure, technology, security, education, and research.”

SOURCE:

The study was led by Kathleen M. Darcy, PhD, and Christopher M. Tarney, MD, from the Gynecologic Cancer Center of Excellence, Department of Gynecologic Surgery & Obstetrics, Uniformed Services University, Walter Reed National Military Medical Center in Bethesda, Maryland. It was published online in Military Medicine.

LIMITATIONS:

The retrospective cohort study design limits causal inference. Although groups were balanced by age, race, year, and region of diagnosis, other demographic factors and socioeconomic variables such as patient comorbidities, educational attainment, household income, and health insurance status were not available and may have affected results. The databases fundamentally differ in how data are acquired, with ACTUR following hospital-based Facility Oncology Registry Data Standards and SEER being a national population-based registry, potentially affecting data quality, consistency, and reliability of survival outcome comparisons. The inclusion of patients diagnosed only through 2013 represents a limitation as it does not allow for contemporary evaluation of survival outcomes, particularly given advances over the past decade including maximal cytoreductive effort to no residual disease, increased adoption of neoadjuvant chemotherapy, and introduction of targeted maintenance agents. The study could not incorporate details regarding residual disease status or control for specifics regarding surgical and medical management, including primary vs interval debulking surgery or the type and timing of agents utilized in first-line, maintenance, and recurrent disease settings. Data regarding circulating biomarkers including CA125, molecular subtypes or alterations, and stratification by homologous recombination deficiency vs proficiency status were not available. Epithelial carcinomas of the fallopian tube and primary peritoneum were excluded from this study, which now are commonly incorporated with ovarian carcinomas. Results may not be generalizable to other populations given the unique characteristics of the Military Health System beneficiary population.

DISCLOSURES:

This research received funding from the Uniformed Services University from the Defense Health Program to the Henry M. Jackson Foundation for the Advancement of Military Medicine Inc., including award HU0001-18-2-0032 to the Murtha Cancer Center Research Program and awards HU0001-19-2-0031 and HU0001-24-2-0047 to the Gynecologic Cancer Center of Excellence Program. All coauthors disclosed no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Women with epithelial ovarian cancer treated in the US Department of Defense (DoD) universal health care system demonstrate better 5-year survival compared with similar patients from the national population. The survival advantage persists across multiple age groups and disease stages, with particularly notable improvements in patients aged 35-49 years and those with stage III disease.

METHODOLOGY:

• Researchers compared 1504 patients with invasive stage I-IV epithelial ovarian carcinoma from the Automated Center Tumor Registry (ACTUR) for the DoD with 6016 matched patients from the 18-region Surveillance, Epidemiology, and End Results (SEER) program between 1987 and 2013.
• Patients from ACTUR were matched in a 1:4 ratio with SEER patients stratified for age, race, year of diagnosis, and histology, including serous carcinoma, clear cell carcinoma, mucinous carcinoma, and endometrioid carcinoma with adenocarcinoma subtypes.
• Five-year overall survival was evaluated using the Kaplan-Meier method and compared using log-rank test, with median follow-up time of 46 months in ACTUR and 44 months in SEER.
• Adjusted hazard ratio (AHR) and 95% CI for all-cause mortality were estimated from multivariable Cox proportional regression modeling controlling for age, race, year of diagnosis, region of diagnosis, stage, histology, and grade.

TAKEAWAY:

• Overall survival differs between registries: 5-year survival of 53.2% in ACTUR vs 47.7% in matched SEER cohort (log-rank P = .001).
• In the primary adjusted model, ACTUR is associated with a lower risk for all-cause mortality vs SEER (AHR, 0.83; 95% CI, 0.76-0.91; P < .0001).
• Subset results retain lower adjusted risk for death for ACTUR vs SEER among ages 35-49 years (AHR, 0.66; 95% CI, 0.52-0.83; P = .0005), ages ≥ 65 years (AHR, 0.82; 95% CI, 0.70-0.96; P = .016), and stage III cancer (AHR, 0.79; 95% CI, 0.69-0.91; P = .0015).
• Histology-stratified findings show lower adjusted risk for death in ACTUR vs SEER for clear cell carcinoma (AHR, 0.63; 95% CI, 0.43-0.93; P =.02) and for endometrioid and other adenocarcinomas (AHR, 0.68; 95% CI, 0.56-0.81; P < .0001).

IN PRACTICE:

"This study is envisioned to be a stepping stone to further investigations of survival and other cancer health outcomes starting with patients diagnosed between 2014 and 2024 with epithelial carcinoma of the ovary, fallopian tube, or primary peritoneum in the DoD Healthcare System versus the national population or other Healthcare Systems,” wrote the authors of the study. “Dedicated funding and support in the [Military Health System] are needed to invest in infrastructure, technology, security, education, and research.”

SOURCE:

The study was led by Kathleen M. Darcy, PhD, and Christopher M. Tarney, MD, from the Gynecologic Cancer Center of Excellence, Department of Gynecologic Surgery & Obstetrics, Uniformed Services University, Walter Reed National Military Medical Center in Bethesda, Maryland. It was published online in Military Medicine.

LIMITATIONS:

The retrospective cohort study design limits causal inference. Although groups were balanced by age, race, year, and region of diagnosis, other demographic factors and socioeconomic variables such as patient comorbidities, educational attainment, household income, and health insurance status were not available and may have affected results. The databases fundamentally differ in how data are acquired, with ACTUR following hospital-based Facility Oncology Registry Data Standards and SEER being a national population-based registry, potentially affecting data quality, consistency, and reliability of survival outcome comparisons. The inclusion of patients diagnosed only through 2013 represents a limitation as it does not allow for contemporary evaluation of survival outcomes, particularly given advances over the past decade including maximal cytoreductive effort to no residual disease, increased adoption of neoadjuvant chemotherapy, and introduction of targeted maintenance agents. The study could not incorporate details regarding residual disease status or control for specifics regarding surgical and medical management, including primary vs interval debulking surgery or the type and timing of agents utilized in first-line, maintenance, and recurrent disease settings. Data regarding circulating biomarkers including CA125, molecular subtypes or alterations, and stratification by homologous recombination deficiency vs proficiency status were not available. Epithelial carcinomas of the fallopian tube and primary peritoneum were excluded from this study, which now are commonly incorporated with ovarian carcinomas. Results may not be generalizable to other populations given the unique characteristics of the Military Health System beneficiary population.

DISCLOSURES:

This research received funding from the Uniformed Services University from the Defense Health Program to the Henry M. Jackson Foundation for the Advancement of Military Medicine Inc., including award HU0001-18-2-0032 to the Murtha Cancer Center Research Program and awards HU0001-19-2-0031 and HU0001-24-2-0047 to the Gynecologic Cancer Center of Excellence Program. All coauthors disclosed no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Women with epithelial ovarian cancer treated in the US Department of Defense (DoD) universal health care system demonstrate better 5-year survival compared with similar patients from the national population. The survival advantage persists across multiple age groups and disease stages, with particularly notable improvements in patients aged 35-49 years and those with stage III disease.

METHODOLOGY:

• Researchers compared 1504 patients with invasive stage I-IV epithelial ovarian carcinoma from the Automated Center Tumor Registry (ACTUR) for the DoD with 6016 matched patients from the 18-region Surveillance, Epidemiology, and End Results (SEER) program between 1987 and 2013.
• Patients from ACTUR were matched in a 1:4 ratio with SEER patients stratified for age, race, year of diagnosis, and histology, including serous carcinoma, clear cell carcinoma, mucinous carcinoma, and endometrioid carcinoma with adenocarcinoma subtypes.
• Five-year overall survival was evaluated using the Kaplan-Meier method and compared using log-rank test, with median follow-up time of 46 months in ACTUR and 44 months in SEER.
• Adjusted hazard ratio (AHR) and 95% CI for all-cause mortality were estimated from multivariable Cox proportional regression modeling controlling for age, race, year of diagnosis, region of diagnosis, stage, histology, and grade.

TAKEAWAY:

• Overall survival differs between registries: 5-year survival of 53.2% in ACTUR vs 47.7% in matched SEER cohort (log-rank P = .001).
• In the primary adjusted model, ACTUR is associated with a lower risk for all-cause mortality vs SEER (AHR, 0.83; 95% CI, 0.76-0.91; P < .0001).
• Subset results retain lower adjusted risk for death for ACTUR vs SEER among ages 35-49 years (AHR, 0.66; 95% CI, 0.52-0.83; P = .0005), ages ≥ 65 years (AHR, 0.82; 95% CI, 0.70-0.96; P = .016), and stage III cancer (AHR, 0.79; 95% CI, 0.69-0.91; P = .0015).
• Histology-stratified findings show lower adjusted risk for death in ACTUR vs SEER for clear cell carcinoma (AHR, 0.63; 95% CI, 0.43-0.93; P =.02) and for endometrioid and other adenocarcinomas (AHR, 0.68; 95% CI, 0.56-0.81; P < .0001).

IN PRACTICE:

"This study is envisioned to be a stepping stone to further investigations of survival and other cancer health outcomes starting with patients diagnosed between 2014 and 2024 with epithelial carcinoma of the ovary, fallopian tube, or primary peritoneum in the DoD Healthcare System versus the national population or other Healthcare Systems,” wrote the authors of the study. “Dedicated funding and support in the [Military Health System] are needed to invest in infrastructure, technology, security, education, and research.”

SOURCE:

The study was led by Kathleen M. Darcy, PhD, and Christopher M. Tarney, MD, from the Gynecologic Cancer Center of Excellence, Department of Gynecologic Surgery & Obstetrics, Uniformed Services University, Walter Reed National Military Medical Center in Bethesda, Maryland. It was published online in Military Medicine.

LIMITATIONS:

The retrospective cohort study design limits causal inference. Although groups were balanced by age, race, year, and region of diagnosis, other demographic factors and socioeconomic variables such as patient comorbidities, educational attainment, household income, and health insurance status were not available and may have affected results. The databases fundamentally differ in how data are acquired, with ACTUR following hospital-based Facility Oncology Registry Data Standards and SEER being a national population-based registry, potentially affecting data quality, consistency, and reliability of survival outcome comparisons. The inclusion of patients diagnosed only through 2013 represents a limitation as it does not allow for contemporary evaluation of survival outcomes, particularly given advances over the past decade including maximal cytoreductive effort to no residual disease, increased adoption of neoadjuvant chemotherapy, and introduction of targeted maintenance agents. The study could not incorporate details regarding residual disease status or control for specifics regarding surgical and medical management, including primary vs interval debulking surgery or the type and timing of agents utilized in first-line, maintenance, and recurrent disease settings. Data regarding circulating biomarkers including CA125, molecular subtypes or alterations, and stratification by homologous recombination deficiency vs proficiency status were not available. Epithelial carcinomas of the fallopian tube and primary peritoneum were excluded from this study, which now are commonly incorporated with ovarian carcinomas. Results may not be generalizable to other populations given the unique characteristics of the Military Health System beneficiary population.

DISCLOSURES:

This research received funding from the Uniformed Services University from the Defense Health Program to the Henry M. Jackson Foundation for the Advancement of Military Medicine Inc., including award HU0001-18-2-0032 to the Murtha Cancer Center Research Program and awards HU0001-19-2-0031 and HU0001-24-2-0047 to the Gynecologic Cancer Center of Excellence Program. All coauthors disclosed no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Offering adjuvant therapy to patients with stage III melanoma offers no melanoma-specific or overall survival benefit, reveals extended follow-up from the first population-based national study to estimate the impact of the treatment.

Hildur Helgadottir, MD, PhD, presented the new findings at the 22nd European Association of Dermato-Oncology (EADO) Congress 2026 on April 24 and described the lead-up to the latest update on the study.

To investigate the impact of adjuvant treatment in patients with stage III melanoma, researchers initially conducted a study in which they used the Swedish Melanoma Registry (SweMR) to identify a precohort of those treated before the introduction of adjuvant therapy in 2018 and a postcohort of those treated subsequently, following both groups out to 2023, she explained.

The analysis revealed no significant difference in melanoma-specific survival between the two groups, at a hazard ratio of 0.92, nor in overall survival, at a hazard ratio of 0.93 (P = .60 for both). However, median follow-up differed between the groups, at 69 months vs 39 months for the precohort vs the postcohort.

Helgadottir, who is a senior research specialist at the Karolinska Comprehensive Cancer Center in Stockholm, Sweden, said that when the earlier results were presented at the European Society for Medical Oncology 2024, there was some criticism that the follow-up was not long enough and that there was no information on the actual adjuvant treatment received in the postcohort patients.

The researchers therefore extended their study out to 2024 to increase the median follow-up to 60 months vs 92 months in the postcohort group vs the precohort group.

They also focused patient selection on patients aged less than 75 years because exposure to adjuvant therapy in older patients was low and restricted the analysis to sentinel lymph node-positive stage IIIB-D cutaneous melanoma diagnosed between 2016 and 2020. This was because adjuvant exposure in stage IIIA disease was low, and patients with clinically detected stage III melanoma started to receive neoadjuvant therapy from 2022 onward.

The current analysis, which was recently published in the European Journal of Cancer, involved 287 patients in the precohort and 349 in the postcohort, who had a median age of 60.0 years and 61.0 years, respectively, and of whom 62.0% and 60.5%, respectively, were male. The groups were well balanced in terms of baseline disease characteristics.

Helgadottir explained that 73% of patients in the postcohort received some form of adjuvant treatment, with the majority treated with PD-1 inhibitors, and a smaller proportion given B-Raf serine-threonine kinase inhibitors. The main reasons for not giving adjuvant therapy were favorable tumor characteristics and the presence of comorbidities.

Five-year melanoma-specific survival rates in the precohorts and postcohorts were 71.4% vs 73.2%, at a hazard ratio adjusted for age, sex, and American Joint Committee on Cancer stage of 1.01 (P = .931). Five-year overall survival rates were 67.3% vs 70.1%, at an adjusted hazard ratio of 0.96 (P = .791).

Helgadottir showed that there were also no significant survival differences in any of the prespecified subgroups for neither melanoma-specific nor overall survival.

There were, again, no significant differences in survival outcomes between the two patient groups, she reported.

The latest results are similar to those from another study conducted in Netherlands and a Danish analysis, Helgadottir said.

Taken together, and “considering the side effects and the costs, it is possible that we will go back to closely following up our patients and treating only at relapse,” she said, “and optimally, of course, that will be already in the neoadjuvant setting.”

“And of course we will need biomarkers because there could be some patients that really need adjuvant treatment, but we need to identify these patients,” continued Helgadottir. Overall survival results from KEYNOTE-054, which compares pembrolizumab with placebo after resection of high-risk stage III melanoma, are awaited, she continued.

Helgadottir explained that adjuvant treatment for stage III melanoma was approved in Sweden in 2018, with treatments freely available to all Swedish residents.

The SweMR is a population-based national register that has near-complete and detailed data on primary cutaneous melanomas, including nodal status and satellite and in-transit disease, and is linked to the national Cause of Death Registry. Helgadottir noted, however, that the SweMR does not contain any information on relapses or the nature of the oncologic treatment received by patients with melanoma.

Following her presentation, she was challenged by an audience member as to whether, on the basis of her findings, she would go back to following up with patients and treating at relapses.

“Maybe we should do that and believe in our own data, and we do. But still, the gold standard must always be the randomized clinical trial,” Helgadottir responded. “So I think, although that we believe in this data, we also want to see the results of the randomized studies.”

The audience member commented that she can see in the data from her own institution that they treat fewer and fewer patients with melanoma with adjuvant therapy by discussing it more thoroughly and being stricter on who should receive it.

Helgadottir agreed, adding that “based on this experience, we did not introduce it to stage II patients because it’s always harder to go back” once a group of patients has started to receive a treatment.

The research was supported by Regional Cancer Centres in Sweden and with grants from the Swedish Cancer Society, Region Stockholm, and the Cancer Research Funds of Radiumhemmet. Helgadottir declared having relationships with Bristol Myers Squibb, Merck Sharp & Dohme, Pierre Fabre, and Novartis.

The trial was supported by SkinVision. The researchers declared having no relevant financial relationships.

This article was previously published by Medscape.

Offering adjuvant therapy to patients with stage III melanoma offers no melanoma-specific or overall survival benefit, reveals extended follow-up from the first population-based national study to estimate the impact of the treatment.

Hildur Helgadottir, MD, PhD, presented the new findings at the 22nd European Association of Dermato-Oncology (EADO) Congress 2026 on April 24 and described the lead-up to the latest update on the study.

To investigate the impact of adjuvant treatment in patients with stage III melanoma, researchers initially conducted a study in which they used the Swedish Melanoma Registry (SweMR) to identify a precohort of those treated before the introduction of adjuvant therapy in 2018 and a postcohort of those treated subsequently, following both groups out to 2023, she explained.

The analysis revealed no significant difference in melanoma-specific survival between the two groups, at a hazard ratio of 0.92, nor in overall survival, at a hazard ratio of 0.93 (P = .60 for both). However, median follow-up differed between the groups, at 69 months vs 39 months for the precohort vs the postcohort.

Helgadottir, who is a senior research specialist at the Karolinska Comprehensive Cancer Center in Stockholm, Sweden, said that when the earlier results were presented at the European Society for Medical Oncology 2024, there was some criticism that the follow-up was not long enough and that there was no information on the actual adjuvant treatment received in the postcohort patients.

The researchers therefore extended their study out to 2024 to increase the median follow-up to 60 months vs 92 months in the postcohort group vs the precohort group.

They also focused patient selection on patients aged less than 75 years because exposure to adjuvant therapy in older patients was low and restricted the analysis to sentinel lymph node-positive stage IIIB-D cutaneous melanoma diagnosed between 2016 and 2020. This was because adjuvant exposure in stage IIIA disease was low, and patients with clinically detected stage III melanoma started to receive neoadjuvant therapy from 2022 onward.

The current analysis, which was recently published in the European Journal of Cancer, involved 287 patients in the precohort and 349 in the postcohort, who had a median age of 60.0 years and 61.0 years, respectively, and of whom 62.0% and 60.5%, respectively, were male. The groups were well balanced in terms of baseline disease characteristics.

Helgadottir explained that 73% of patients in the postcohort received some form of adjuvant treatment, with the majority treated with PD-1 inhibitors, and a smaller proportion given B-Raf serine-threonine kinase inhibitors. The main reasons for not giving adjuvant therapy were favorable tumor characteristics and the presence of comorbidities.

Five-year melanoma-specific survival rates in the precohorts and postcohorts were 71.4% vs 73.2%, at a hazard ratio adjusted for age, sex, and American Joint Committee on Cancer stage of 1.01 (P = .931). Five-year overall survival rates were 67.3% vs 70.1%, at an adjusted hazard ratio of 0.96 (P = .791).

Helgadottir showed that there were also no significant survival differences in any of the prespecified subgroups for neither melanoma-specific nor overall survival.

There were, again, no significant differences in survival outcomes between the two patient groups, she reported.

The latest results are similar to those from another study conducted in Netherlands and a Danish analysis, Helgadottir said.

Taken together, and “considering the side effects and the costs, it is possible that we will go back to closely following up our patients and treating only at relapse,” she said, “and optimally, of course, that will be already in the neoadjuvant setting.”

“And of course we will need biomarkers because there could be some patients that really need adjuvant treatment, but we need to identify these patients,” continued Helgadottir. Overall survival results from KEYNOTE-054, which compares pembrolizumab with placebo after resection of high-risk stage III melanoma, are awaited, she continued.

Helgadottir explained that adjuvant treatment for stage III melanoma was approved in Sweden in 2018, with treatments freely available to all Swedish residents.

The SweMR is a population-based national register that has near-complete and detailed data on primary cutaneous melanomas, including nodal status and satellite and in-transit disease, and is linked to the national Cause of Death Registry. Helgadottir noted, however, that the SweMR does not contain any information on relapses or the nature of the oncologic treatment received by patients with melanoma.

Following her presentation, she was challenged by an audience member as to whether, on the basis of her findings, she would go back to following up with patients and treating at relapses.

“Maybe we should do that and believe in our own data, and we do. But still, the gold standard must always be the randomized clinical trial,” Helgadottir responded. “So I think, although that we believe in this data, we also want to see the results of the randomized studies.”

The audience member commented that she can see in the data from her own institution that they treat fewer and fewer patients with melanoma with adjuvant therapy by discussing it more thoroughly and being stricter on who should receive it.

Helgadottir agreed, adding that “based on this experience, we did not introduce it to stage II patients because it’s always harder to go back” once a group of patients has started to receive a treatment.

The research was supported by Regional Cancer Centres in Sweden and with grants from the Swedish Cancer Society, Region Stockholm, and the Cancer Research Funds of Radiumhemmet. Helgadottir declared having relationships with Bristol Myers Squibb, Merck Sharp & Dohme, Pierre Fabre, and Novartis.

The trial was supported by SkinVision. The researchers declared having no relevant financial relationships.

This article was previously published by Medscape.

Offering adjuvant therapy to patients with stage III melanoma offers no melanoma-specific or overall survival benefit, reveals extended follow-up from the first population-based national study to estimate the impact of the treatment.

Hildur Helgadottir, MD, PhD, presented the new findings at the 22nd European Association of Dermato-Oncology (EADO) Congress 2026 on April 24 and described the lead-up to the latest update on the study.

To investigate the impact of adjuvant treatment in patients with stage III melanoma, researchers initially conducted a study in which they used the Swedish Melanoma Registry (SweMR) to identify a precohort of those treated before the introduction of adjuvant therapy in 2018 and a postcohort of those treated subsequently, following both groups out to 2023, she explained.

The analysis revealed no significant difference in melanoma-specific survival between the two groups, at a hazard ratio of 0.92, nor in overall survival, at a hazard ratio of 0.93 (P = .60 for both). However, median follow-up differed between the groups, at 69 months vs 39 months for the precohort vs the postcohort.

Helgadottir, who is a senior research specialist at the Karolinska Comprehensive Cancer Center in Stockholm, Sweden, said that when the earlier results were presented at the European Society for Medical Oncology 2024, there was some criticism that the follow-up was not long enough and that there was no information on the actual adjuvant treatment received in the postcohort patients.

The researchers therefore extended their study out to 2024 to increase the median follow-up to 60 months vs 92 months in the postcohort group vs the precohort group.

They also focused patient selection on patients aged less than 75 years because exposure to adjuvant therapy in older patients was low and restricted the analysis to sentinel lymph node-positive stage IIIB-D cutaneous melanoma diagnosed between 2016 and 2020. This was because adjuvant exposure in stage IIIA disease was low, and patients with clinically detected stage III melanoma started to receive neoadjuvant therapy from 2022 onward.

The current analysis, which was recently published in the European Journal of Cancer, involved 287 patients in the precohort and 349 in the postcohort, who had a median age of 60.0 years and 61.0 years, respectively, and of whom 62.0% and 60.5%, respectively, were male. The groups were well balanced in terms of baseline disease characteristics.

Helgadottir explained that 73% of patients in the postcohort received some form of adjuvant treatment, with the majority treated with PD-1 inhibitors, and a smaller proportion given B-Raf serine-threonine kinase inhibitors. The main reasons for not giving adjuvant therapy were favorable tumor characteristics and the presence of comorbidities.

Five-year melanoma-specific survival rates in the precohorts and postcohorts were 71.4% vs 73.2%, at a hazard ratio adjusted for age, sex, and American Joint Committee on Cancer stage of 1.01 (P = .931). Five-year overall survival rates were 67.3% vs 70.1%, at an adjusted hazard ratio of 0.96 (P = .791).

Helgadottir showed that there were also no significant survival differences in any of the prespecified subgroups for neither melanoma-specific nor overall survival.

There were, again, no significant differences in survival outcomes between the two patient groups, she reported.

The latest results are similar to those from another study conducted in Netherlands and a Danish analysis, Helgadottir said.

Taken together, and “considering the side effects and the costs, it is possible that we will go back to closely following up our patients and treating only at relapse,” she said, “and optimally, of course, that will be already in the neoadjuvant setting.”

“And of course we will need biomarkers because there could be some patients that really need adjuvant treatment, but we need to identify these patients,” continued Helgadottir. Overall survival results from KEYNOTE-054, which compares pembrolizumab with placebo after resection of high-risk stage III melanoma, are awaited, she continued.

Helgadottir explained that adjuvant treatment for stage III melanoma was approved in Sweden in 2018, with treatments freely available to all Swedish residents.

The SweMR is a population-based national register that has near-complete and detailed data on primary cutaneous melanomas, including nodal status and satellite and in-transit disease, and is linked to the national Cause of Death Registry. Helgadottir noted, however, that the SweMR does not contain any information on relapses or the nature of the oncologic treatment received by patients with melanoma.

Following her presentation, she was challenged by an audience member as to whether, on the basis of her findings, she would go back to following up with patients and treating at relapses.

“Maybe we should do that and believe in our own data, and we do. But still, the gold standard must always be the randomized clinical trial,” Helgadottir responded. “So I think, although that we believe in this data, we also want to see the results of the randomized studies.”

The audience member commented that she can see in the data from her own institution that they treat fewer and fewer patients with melanoma with adjuvant therapy by discussing it more thoroughly and being stricter on who should receive it.

Helgadottir agreed, adding that “based on this experience, we did not introduce it to stage II patients because it’s always harder to go back” once a group of patients has started to receive a treatment.

The research was supported by Regional Cancer Centres in Sweden and with grants from the Swedish Cancer Society, Region Stockholm, and the Cancer Research Funds of Radiumhemmet. Helgadottir declared having relationships with Bristol Myers Squibb, Merck Sharp & Dohme, Pierre Fabre, and Novartis.

The trial was supported by SkinVision. The researchers declared having no relevant financial relationships.

This article was previously published by Medscape.