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Summary: A groundbreaking study shows that the human hippocampus continues producing new neurons well into late adulthood. Researchers identified neural progenitor cells—the precursors to neurons—in adults up to 78 years old, confirming ongoing neurogenesis in the memory center of the brain.

Using advanced sequencing, imaging, and machine learning techniques, they traced how these cells develop and where they reside in the hippocampus. The findings may pave the way for regenerative therapies targeting cognitive and psychiatric disorders.

Key Facts:

• Neural progenitor cells persist in the hippocampus into late adulthood, enabling neurogenesis.
• Newly formed neurons localize to the dentate gyrus, a hub for memory and learning.
• Individual variation in neurogenesis could inform treatments for brain disorders.

Source: Karolinska Institute

A study in the journal Science presents compelling new evidence that neurons in the brain’s memory centre, the hippocampus, continue to form well into late adulthood.

The research from Karolinska Institutet in Sweden provides answers to a fundamental and long-debated question about the human brain’s adaptability.

The hippocampus is a brain region that is essential for learning and memory and involved in emotion regulation. Back in 2013, Jonas Frisén’s research group at Karolinska Institutet showed in a high-profile study that new neurons can form in the hippocampus of adult humans.

The researchers then measured carbon-14 levels in DNA from brain tissue, which made it possible to determine when the cells were formed.

Identifying cells of origin

However, the extent and significance of this formation of new neurons (neurogenesis) are still debated. There has been no clear evidence that the cells that precede new neurons, known as neural progenitor cells, actually exist and divide in adult humans.

“We have now been able to identify these cells of origin, which confirms that there is an ongoing formation of neurons in the hippocampus of the adult brain,” says Jonas Frisén, Professor of Stem Cell Research at the Department of Cell and Molecular Biology, Karolinska Institutet, who led the research.

From 0 to 78 years of age

In the new study, the researchers combined several advanced methods to examine brain tissue from people aged 0 to 78 years from several international biobanks. They used a method called single-nucleus RNA sequencing, which analyses gene activity in individual cell nuclei, and flow cytometry to study cell properties.

By combining this with machine learning, they were able to identify different stages of neuronal development, from stem cells to immature neurons, many of which were in the division phase.

To localise these cells, the researchers used two techniques that show where in the tissue different genes are active: RNAscope and Xenium. These methods confirmed that the newly formed cells were located in a specific area of the hippocampus called the dentate gyrus. This area is important for memory formation, learning and cognitive flexibility.

Hope for new treatments

The results show that the progenitors of adult neurons are similar to those of mice, pigs and monkeys, but that there are some differences in which genes are active. There were also large variations between individuals – some adult humans had many neural progenitor cells, others hardly any at all.

“This gives us an important piece of the puzzle in understanding how the human brain works and changes during life,” explains Jonas Frisén.

“Our research may also have implications for the development of regenerative treatments that stimulate neurogenesis in neurodegenerative and psychiatric disorders.”

The study was conducted in close collaboration with Ionut Dumitru, Marta Paterlini and other researchers at Karolinska Institutet, as well as researchers at Chalmers University of Technology in Sweden.

Funding: The research was funded by the Swedish Research Council, the European Research Council (ERC), the Swedish Cancer Society, the Knut and Alice Wallenberg Foundation, the Swedish Foundation for Strategic Research, the StratRegen programme, the EMBO Long-Term Fellowship, Marie Sklodowska-Curie Actions and SciLifeLab. Jonas Frisén is a consultant for the company 10x Genomics. See the scientific article for a complete list of potential conflicts of interest.

About this neurogenesis research news

Author: Press Office
Source: Karolinska Institute
Contact: Press Office – Karolinska Institute
Image: The image is credited to Neuroscience News

Original Research: Closed access.
“Identification of proliferating neural progenitors in the adult human hippocampus” by Jonas Frisén et al. Science

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Abstract

Identification of proliferating neural progenitors in the adult human hippocampus

Continuous adult hippocampal neurogenesis is involved in memory formation and mood regulation but is challenging to study in humans.

Difficulties finding proliferating progenitor cells called into question whether and how new neurons may be generated.

We analyzed the human hippocampus from birth through adulthood by single-nucleus RNA sequencing.

We identified all neural progenitor cell stages in early childhood. In adults, using antibodies against the proliferation marker Ki67 and machine learning algorithms, we found proliferating neural progenitor cells.

Furthermore, transcriptomic data showed that neural progenitors were localized within the dentate gyrus.

The results contribute to understanding neurogenesis in adult humans.

Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer’s disease.

Alzheimer’s is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It’s not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen.

Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it’s only been regarded as an energy backup for the liver and the muscles.

“This new study challenges that view, and it does so with striking implications,” says molecular biologist Pankaj Kapahi, from the Buck Institute. “Stored glycogen doesn’t just sit there in the brain, it is involved in pathology.”

Related: Insulin Isn’t Just Made by The Pancreas. Here’s Another Location Few Know About.

Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer’s.

Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers.

Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage.

“By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies,” says Buck Institute biologist Sudipta Bar.

The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP.

It’s a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments.

The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight loss, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen’s pathways, the researchers suggest.

“By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell’s inner chemistry to fight age-related decline,” says Kapahi.

“As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain’s hidden sugar code could unlock powerful tools for combating dementia.”

The research has been published in Nature Metabolism.

Combining zanidatamab-hrii (Ziihera) with chemotherapy as frontline treatment produced clinically meaningful and enduring activity in a small cohort of patients with HER2-positive advanced gastroesophageal adenocarcinoma, according to primary results from a phase 2 study (NCT03929666) published in Lancet Oncology.¹

The study treatment yielded a confirmed objective response rate (ORR) of 76.2% (95% CI, 60.5%-87.9%) among 42 evaluable patients, which included complete responses (CRs) in 3 patients (7%) and partial responses (PRs) in 29 (69%). The median duration of response (DOR) was 18.7 months (95% CI, 10.4-44.1), and the post hoc median time to first response was 1.3 months (IQR, 1.3-1.4).

Data showed a median progression-free survival (PFS) of 12.5 months (95% CI, 8.2-21.8), with estimated PFS rates of 57% (95% CI, 40%-70%) at 12 months and 31% (95% CI, 17%-46%) at 24 months. Additionally, treatment elicited a median overall survival (OS) of 36.5 months (95% CI, 23.6-not estimable [NE]), a 12-month OS rate of 87% (95% CI, 72%-94%), and a 24-month OS rate of 65% (95% CI, 49%-77%).

“[F]irst-line treatment with zanidatamab plus chemotherapy demonstrated rapid and durable antitumor activity with promising survival outcomes in patients with HER2-positive advanced gastroesophageal adenocarcinoma. Zanidatamab plus chemotherapy in the first-line setting was well tolerated with a manageable safety profile when incorporating antidiarrheal prophylaxis in the first 7 days of treatment,” lead study author Elena Elimova, MD, from the Department of Gastrointestinal Medical Oncology at Princess Margaret Cancer Centre in Toronto, Ontario, Canada, wrote with coauthors in the publication.¹ “If these results are confirmed in a large-scale, randomized, phase 3 trial, zanidatamab could represent a substantial advancement in the treatment of HER2-positive advanced gastroesophageal adenocarcinoma.”

In the open-label, multi-center phase 2 study, patients received zanidatamab in combination with capecitabine plus oxaliplatin (CAPOX), 5-fluorouracil (5-FU) plus cisplatin (FP), or leucovorin plus 5-FU and oxaliplatin (mFOLFOX6). In the CAPOX and FP groups, patients received zanidatamab at 30 mg/kg, 1800 mg with a weight of less than 70 kg, or 2400 mg with a weight of 70 kg or higher every 3 weeks. In the mFOLFOX6 group, patients received zanidatamab at 20 mg/kg, 1200 mg with a body weight under 70 kg, or 1600 mg with a weight of at least 70 kg every 2 weeks.

In part 1 of the trial, investigators evaluated the safety and tolerability of zanidatamab plus chemotherapy to determine a recommended phase 2 dose; the primary end points of this part were dose-limiting toxicities and dose reductions. In part 2 of the trial, the primary end point was investigator-assessed confirmed ORR per RECIST v1.1 criteria. Secondary efficacy endpoints across parts 1 and 2 of the trial included disease control rate, DOR, clinical benefit rate, PFS, and OS.

Patients 18 years and older with unresectable, locally advanced, recurrent, or metastatic HER2-expressing gastroesophageal adenocarcinoma and measurable disease per RECIST v1.1 guidelines were eligible for enrollment on the trial.² Other eligibility criteria included having an ECOG performance status of 0 or 1, adequate organ function, and adequate cardiac left ventricular function.

The median patient age was 58 years (IQR, 55-63), and most of the population was male (85%), White (61%), and not Hispanic (93%). Additionally, most patients had an ECOG performance status of 0 (57%), gastric anatomical subtype disease (41%), stage IV disease at initial diagnosis (83%), and measurable disease (93%). Prior neoadjuvant or adjuvant chemotherapy was reported in 11% of patients.

In a subgroup of patients with centrally confirmed HER2-positive disease (n = 41), zanidatamab-based therapy produced a confirmed ORR of 84% (n = 31/37; 95% CI, 68.0%-93.8%). Furthermore, the median PFS was 15.2 months (95% CI, 9.5-33.4) in this subgroup, and the median OS was 36.5 months (95% CI, 23.6-NE).

In a post hoc analysis of patients who enrolled on the trial before and after the implementation of antidiarrheal prophylaxis, 61% (n = 14/23; 95% CI, 38.5%-80.3%) and 95% (n = 18/19; 95% CI, 74.0%-99.9%) experienced confirmed responses. Those who received antidiarrheal prophylaxis experienced longer treatment duration and exposure.

Treatment-related adverse effects (TRAEs) affected 100% of patients, with the most common grade 3/4 TRAEs consisting of diarrhea (39%) and hypokalemia (22%). Additionally, 17% of patients had serious TRAEs, the most common of which was diarrhea (7%).

The median duration of grade 1/2 or grade 3 diarrhea was 6.5 days (IQR, 2-29) and 3 days (IQR, 2-5), respectively, among patients who enrolled on the trial before the implementation of antidiarrheal prophylaxis. The median durations were 3 days (IQR, 2-13) and 4.5 days (IQR, 3-8) among those who entered the trial following the implementation of antidiarrheal prophylaxis.

References

1. Elimova E, Ajani J, Burris H, et al. Zanidatamab plus chemotherapy as first-line treatment for patients with HER2-positive advanced gastro-oesophageal adenocarcinoma: primary results of a multicentre, single-arm, phase 2 study. Lancet Oncol. 2025;26(7):847-859. doi:10.1016/S1470-2045(25)00287-6
2. A safety and efficacy study of ZW25 (Zanidatamab) plus combination chemotherapy in HER2-expressing gastrointestinal cancers, including gastroesophageal adenocarcinoma, biliary tract cancer, and colorectal cancer. ClinicalTrials.gov. Updated March 13, 2025. Accessed July 1, 2025. https://tinyurl.com/y9d77aay

For decades, doctors have tackled heart disease by focusing on well-known risk factors—high blood pressure, high cholesterol, and diabetes. Medications like aspirin and statins have helped millions, yet heart disease remains the leading cause of death in the United States. Alarmingly, many people still suffer heart attacks even when these traditional risk factors are well-managed.

Now, researchers at the University of Michigan have identified a new piece of the puzzle that could explain why.

Their study highlights a protein called suPAR (soluble urokinase plasminogen activator receptor), produced by the immune system. Unlike cholesterol or blood pressure, suPAR appears to directly cause atherosclerosis—the buildup of plaque in the arteries that can lead to heart attacks and strokes.

Atherosclerosis affects more than a billion people worldwide. It occurs when fatty deposits accumulate along artery walls, restricting blood flow and increasing the risk of serious cardiovascular events.

SuPAR is produced in the bone marrow and acts like an inflammation “thermostat” in the body. Scientists already knew that people with elevated suPAR levels had a higher risk of heart disease, but this study is the first to show that suPAR may be a direct cause of the disease.

The research began with an analysis of over 5,000 people without known heart disease. Those with higher suPAR levels were significantly more likely to develop atherosclerosis, regardless of their cholesterol or blood pressure levels.

To find out why some people have higher suPAR levels, the team examined genetic data from 24,000 individuals. They identified a specific genetic variant in the PLAUR gene, which produces suPAR. People with this variant had both higher suPAR levels and a greater risk of developing atherosclerosis.

Using a method called Mendelian randomization—which leverages genetic data to explore cause-and-effect relationships—the researchers confirmed their findings in more than 500,000 participants from the UK Biobank and two additional datasets. The link between the PLAUR variant, elevated suPAR, and atherosclerosis was consistently strong.

To further validate their discovery, the team conducted experiments on mice. Those given high levels of suPAR developed significantly more plaque in their aortas—the main arteries leading from the heart—than mice with normal levels. This provided compelling evidence that suPAR actively contributes to artery damage.

What makes this discovery particularly significant is that suPAR is not affected by current heart disease treatments. Statins, for example, do not lower suPAR levels. This opens the door to a completely new treatment approach, targeting a mechanism not addressed by existing drugs.

Led by Dr. Salim Hayek, the researchers are now working on therapies aimed at safely reducing suPAR levels, with the goal of preventing or slowing the progression of heart disease.

This breakthrough may also shed light on the close link between heart and kidney disease. Prior studies have associated suPAR with kidney damage, and in the U.S., about 1 in 7 people have kidney disease—two-thirds of whom also have heart disease. In fact, more than 40% of heart disease patients show signs of kidney dysfunction. If suPAR contributes to both, targeting it could offer dual benefits.

Published in the Journal of Clinical Investigation, this study may redefine how doctors understand and treat heart disease—offering new hope to millions of people who continue to face it, despite following all the right steps.

We all have been bombarded with how magnesium supplements will cure our fatigue, leg pains and more. But do we all need magnesium, and should we take magnesium over the counter without any tests? Dr Rakesh Gupta, senior consultant, internal medicine, Indraprastha Apollo Hospitals, says: “While magnesium supplements are available over-the-counter (OTC), it’s not always advisable to take them without knowing your actual need. Magnesium is an essential mineral, but unnecessary supplementation can lead to side effects such as diarrhea, abdominal cramps, and in rare cases, toxicity-especially in people with kidney problems. In many cases, a balanced diet provides sufficient magnesium. If you’re experiencing symptoms like fatigue, muscle cramps, or irregular heartbeat, it’s better to consult a healthcare professional. They may recommend a blood test to check magnesium levels or assess your symptoms and dietary intake. Self-medicating with supplements, especially in high doses, isn’t safe or effective for everyone. It’s also important to consider interactions with other medications, such as antibiotics or diuretics. In short, while magnesium is vital, supplements should not be taken casually or as a blanket solution without understanding individual needs.

What does magnesium do in our bodies and what is the optimum source of intake?

Magnesium plays a crucial role in over 300 biochemical reactions in the body. It supports muscle and nerve function, regulates blood pressure, helps in energy production, maintains a healthy heartbeat, and is vital for bone health. It also plays a role in mood regulation and blood sugar control. The best and safest way to meet your magnesium needs is through food. Good dietary sources include green leafy vegetables (like spinach), nuts (especially almonds and cashews), seeds, legumes, whole grains, and bananas. Dark chocolate and certain fish like mackerel also contain magnesium. The recommended dietary allowance (RDA) for adults is around 310-420 mg per day depending on age and sex. When intake is through food, the risk of excess is low, and the absorption is more balanced. Supplements may be necessary only for those with confirmed deficiency, poor diet, or absorption issues.

What are the symptoms of magnesium deficiency and how can we check for the deficiency?

Magnesium deficiency can be subtle at first, but over time, it may present with symptoms like muscle cramps or twitches, fatigue, numbness or tingling, mood swings, irritability, poor sleep, and irregular heartbeat. In more severe cases, deficiency can lead to low calcium or potassium levels, which can further affect nerve and muscle function. However, because only about 1% of magnesium is found in the blood, standard blood tests may not always detect low tissue levels. A better assessment includes considering symptoms, dietary intake, medical history, and sometimes specialised tests like red blood cell magnesium levels. Chronic conditions such as diabetes, gastrointestinal disorders, alcoholism, and the use of certain medications can also raise the risk of deficiency. If you suspect low magnesium, consult your doctor rather than self-diagnosing. They can recommend appropriate tests or a trial of dietary changes before jumping to supplementation.

Who should avoid magnesium supplements?

Certain people should be cautious of magnesium supplements unless prescribed. Those  with kidney disease are at high risk, as their kidneys may not effectively remove excess magnesium, which can lead to toxicity. Symptoms of excess magnesium include nausea, low blood pressure, irregular heartbeat, confusion, and in extreme cases, coma. People on  medications like antibiotics (especially tetracyclines and quinolones), muscle relaxants, or diuretics should also be careful, as magnesium can interact with these drugs and affect absorption or efficacy. Those with heart block or certain digestive disorders that impair magnesium absorption should not take supplements without medical guidance. Pregnant or breastfeeding women should also follow prescribed limits. Magnesium from food is generally safe for everyone, but supplementation should be tailored to individual needs and medical history. Always talk to a healthcare provider before starting any new supplement, even if it’s available OTC.

A recent study conducted by the Well-Being and Cancer at Work (WeCanWork) project showed that men who worked in physically demanding jobs needed additional well-being support during and after cancer treatment.¹

Cathy Bradley, PhD, dean of the Colorado School of Public Health and deputy director of the University of Colorado Cancer Center, was an author on this study.² She spoke to CancerNetwork® about how these findings can be used to design future trials and support the needs of cancer survivors with physically demanding jobs.

The median survivor age was 51.48 years, 84.0% were White, and 25.6% reported having physically demanding jobs. Additional characteristics showed that 62.7% of survivors were married, 43.4% were college graduates, 73.7% worked full time, and 67.6% had an annual household income of less than $85,000.

The highest reported employer accommodations included allowing workers to change their start and stop time (84.2%), allowing more breaks and rest periods (73.7%), and giving shorter workdays (51.3%). However, the lowest reported employer accommodations included arranging transportation (5.3%), providing special equipment (13.2%), and providing rehabilitation services (15.8%).

The well-being scores highlighted that patients with physically demanding jobs had poorer wages (P <.001) and satisfaction with their benefits (P = .04), less autonomy (P = .03) and flexibility with work (P = .004), and greater financial insecurity (P = .002). Additionally, they experienced more negative job attitudes (P = .0003), workplace safety concerns (P <.001), less sleep (P = .05), and less support outside of work (P = .03).

What was the primary motivation behind initiating this study on cancer survivors and physically demanding jobs?

It’s based on prior evidence and work that people in physically demanding jobs have a harder time returning to work [after cancer]. We know that a lot of physically demanding jobs tend to be those without paid sick leave. They may not have health insurance. They may also be smaller employers, or if it’s something like a construction company, that doesn’t have to comply with the Family Medical Leave Act, or the Americans with Disabilities Act. We felt like this was an area of investigation that had not received enough [attention]. We wanted to understand that relationship, in particular. A lot of the prior work, and a lot of its mine, has been on women with breast cancer, and they, too, report that if they’re in physically demanding jobs, it’s harder for them to go back. Just not much work had been done on men, especially those in harder labor jobs.

What were some of the most surprising or significant findings from the study?

If [survivors] did have health insurance, they would continue to try hard to work and keep that financial barrier between them. Particularly, if they don’t have health insurance, they could be financially at risk. If they had health insurance, they were more likely to keep working at an hour threshold where they could qualify for health insurance. If they didn’t have these benefits, they were more likely to stop working.

It’s interesting because you wonder what sacrifices those with health insurance are making to continue to work. Maybe they have other benefits; if you work for an employer that offers health insurance, that employer may also offer accommodations or things like that. The reverse may be true. You also wonder if they’re doing it strictly for health insurance or trading off some of their health. Then, you think about people at the other end who are just leaving work because perhaps they don’t have the sick leave benefits or other things that would allow them to keep working. We just don’t know that underlying mechanism.

How did these findings challenge or confirm existing understandings of cancer survivorship and employment?

They challenge it in the way that we’ve started to believe that people just go back to work. We’re seeing that that isn’t necessarily the case, and that if they do, they need to have a lot of support.

Beyond the general impact, what are some of the specific challenges identified such as lower satisfaction with wages, less job autonomy, and financial insecurity for those in these job situations?

The challenges are around paid sick leave, being able to take time away, and accommodations. Being able to get them in physically demanding jobs may be hard. If you’re in a desk job in an organization, it might be easier to change, be more flexible, and come in at 10 AM instead of 8 AM. If you’re doing construction, you’re probably going to be on the job site around 5 AM; there aren’t a lot of alternatives. [The challenge is giving] the support that’s required for them, and to be able to give them time away from work or just to be off until they’re ready to come back.

How has the WeCanWork project evolved from a research study to its current implementation phase?

In studying this, we started to think about what is it that could be helpful to everybody. We’re not going to be able to get paid sick leave passed as a national policy, but what’s something that we can do? One component is to have oncology practices start thinking about referring patients to occupational medicine for assistance. That can be enormously beneficial in the sense that somebody who is in occupational medicine could sit down and work with the oncology team to understand exactly what it is that the person needs, like more time away from work. I’m thinking about women with breast cancer who have surgery, have lymphedema, and can’t lift. For somebody who’s doing physically demanding work and may only be able to put in a half day, they can negotiate on that patient’s behalf with the employer to say, “Here’s what this person needs [while being treated for] cancer.” Oncology practices have been disconnected from occupational medicine. They fill out disability forms, but that’s not the same as being able to work with that person, ensuring that they have rehabilitation, understanding their benefits, and advocating for them.

How does the study highlight the critical need for integrated support systems that bridge the gap between oncology care and the workplace?

Our goal is to provide evidence-based information to show that this is helpful to people, and that it helps them continue to work. If employers know they can keep a good employee, they might be more enthusiastic about [these accommodations]. I imagine insurers would be as well. Just for oncology, it’s to give them additional support. They don’t necessarily understand sick leave policies or what a person needs at work the [same] way they understand that chemotherapy slows tumor progression. They’re focused on a very different component. Our goal is to be able to show that evidence base; that it’s a worthwhile thing to do. Also, we’re trying to understand the billing [aspect]. What code could they use for the referral and to help get reimbursed?

The investigators called for additional longitudinal studies. What specific long-term implications do you hope to explore with such studies?

I can see, in the future, being able to study who goes back to work in the long term. How long do they stay at work? What happens when they get there? [We want] to understand that, both with men and women in a variety of different jobs. We tend to find that people who are in good jobs are okay; if they work for a big employer, and it’s a job that offers a whole array of benefits, they tend to find their way and be okay with that. What kind of things can we do to provide support for people who aren’t in that situation? Over half of Americans are employed in small businesses.

Is there anything else you would like to highlight?

This is just an ongoing area of inquiry that we need to spend more time with as we start to develop these new therapies to treat cancer. I’m thinking about these oral targeted agents; they have longer-term [adverse] effects, and we need to know how that affects somebody who’s employed over time, especially if they’re going to take them for a long time. It’s not just chemotherapy for 6 months and they’re [finished]. They take them to evidence of disease progression, and that could be years. We do have to keep people working because those drugs aren’t cheap. It’s an interesting dynamic, and like I said, a place for more study.

References

1. Schwatka NV, Dally M, Dye-Robinson A, et al. WeCanWork study: well-being of male cancer survivors working physically demanding jobs. BMC Public Health. 2025;25(1):2025. doi:10.1186/s12889-025-23147-8
2. Zarella O. New study reveals cancer survivors in physically demanding jobs face greater challenges. News release. Colorado School of Public Health. June 23, 2025. Accessed July 1, 2025. https://tinyurl.com/4k6hmk4u

In recent years, science has made one thing clear: exercise isn’t just about fitness, it’s a vital component in preventing and managing serious diseases including cancer. From cutting the risk of developing certain cancers to improving treatment outcomes and lowering the chances of recurrence, staying physically active has powerful, proven benefits.

Dr. Arun Kumar Goel, Chairman (Surgical Oncology) at Andromeda Cancer Hospital, Sonipat talked to Firstpost on how regular movement can strengthen the immune system, regulate hormones, reduce inflammation and support long-term survival.  

How does regular physical activity impact cancer prevention?

Cancers such as breast cancer, uterine cancer, ovarian cancer, oesophageal cancer, pancreatic cancer, cancer of kidney, multiple myeloma, meningioma etc, can be associated with excess body weight/obesity. Regular physical activity helps in reducing the risk of developing certain types of cancer. It keeps body weight under control, boosts the immune system, improves hormone balance, and reduces inflammation—all of which help lower cancer risk.

Is there scientific evidence linking specific types of exercise to reduced cancer risk?

Yes. Studies show that aerobic exercises like walking, jogging, swimming and cycling as well as strength training, can lower the risk of some cancers. Among them, brisk walking for at least 30 minutes a day has shown significant benefits.

What are the most common cancers where exercise shows a strong preventive benefit?

Exercise is especially helpful in reducing the risk of: Breast cancer, Colon cancer, Endometrial (uterine) cancer, Prostate cancer, Lung cancer (in non-smokers), and many more.

Can moderate daily activity like walking or household chores also lower cancer risk?

Yes. Even regular household work, climbing stairs, or walking to the local market can contribute to better health and lower cancer risk. You don’t need to join a gym—being active in daily life makes a difference.

How safe is it for patients to exercise during cancer treatment like chemotherapy or radiation?

For most patients, gentle to moderate exercise is safe and often recommended during treatment. It should be done under medical guidance, especially if the patient feels weak or has specific health issues. We advise patients to remain active during the cancer treatments so that they do not gain excess weight during the treatment.

Does exercise help reduce the side effects of cancer treatments, such as fatigue or neuropathy?

Yes. Light exercise can help reduce tiredness (fatigue), nausea, constipation, depression, and even nerve pain (neuropathy). It also improves sleep and overall mood.

What are the biological pathways through which exercise influences tumor growth or immune function?

Exercise improves blood flow, enhances the body’s natural killer cells (which fight cancer), reduces growth factors that feed tumors, and helps the body repair damage faster. It also controls insulin and hormone levels.

Is there a link between exercise and inflammation, hormone regulation, or insulin resistance in cancer patients?

Yes. Exercise reduces chronic inflammation, balances hormones like estrogen and insulin, and improves the way the body uses sugar. These changes help prevent cancer and slow its progression.

Are there standard exercise guidelines for cancer patients or survivors, and how should they be customised?

Global guidelines suggest at least 150 minutes of moderate activity per week, plus two days of strength training. However, the plan should be personalised based on age, type of cancer, stage, current treatment, and energy levels.

Should the approach differ based on cancer type, stage, or treatment status?

Yes. Someone recovering from surgery needs a different routine than someone on chemotherapy. A patient with bone cancer or lung involvement may need supervised or lighter exercises. Always consult your cancer doctor or physiotherapist before starting.

How important is exercise in post-cancer recovery and preventing recurrence?

Physical activity plays a big role in recovery. It helps patients regain strength, reduce depression, and may lower the chances of cancer coming back, especially in breast, colon, and prostate cancers.

What role does physical activity play in improving long-term outcomes and survival rates?

Patients who remain active tend to live longer and have a better quality of life. They are less likely to face complications, and their chances of surviving the disease improve.

Are there any myths or misconceptions about exercise and cancer you would like to correct?

Yes. Some people think rest is best during cancer—this is not true. While rest is needed when one is exhausted, avoiding all activity can lead to weakness, loss of muscle, and poor recovery. Another myth is that exercise can “spread cancer”—this is false. Exercise is safe and helpful in most cases.

Are there cases where patients should avoid certain types of exercise during treatment or recovery?

Yes. Patients with low blood counts, severe fatigue, balance problems, or risk of fractures (e.g., bone metastasis) should avoid heavy or risky exercises. In such cases, exercises should be guided by a physiotherapist or oncology team.