Cancer
Walking may lower cardiovascular death risk for women with cancer history
Among postmenopausal women with a history of cancer, taking more daily steps and engaging in moderate-to-vigorous physical activity were both associated with a significantly reduced risk of death from cardiovascular disease, according to a new study.
Cancer survivors are at an increased risk of death from cardiovascular disease, according to a 2019 scientific statement from the Association. The statement also noted that exercise training is an essential part of cardiac rehabilitation and recovery after cancer treatment, and that exercise therapy can help to reduce cardiovascular toxicity during cancer treatment.
“Encouraging cancer survivors to be more active, sit less and take more steps every day could be a feasible approach for prolonging survivorship and reducing the risk of cardiovascular disease mortality,” said lead study author Eric Hyde, a research analyst at the University of California, San Diego.
“Our study helps us to better understand potential physical activity behaviours of postmenopausal women in relation to cancer survival.”
Researchers examined physical activity data from the Women’s Health Accelerometry Collaboration, a study combining two observational studies exploring the relationship among physical activity and sedentary behaviour with cancer incidence and death.
They assessed the potential associations of physical activity and sedentary behaviour with death from cardiovascular disease or all-cause mortality (death from any cause).
The study followed for about eight years nearly 2,500 post-menopausal women between the ages of 63 and 99 years. The analysis included participants diagnosed with breast or other cancers at least one year before enrolling in the studies.
Participants wore an accelerometer on the hip for at least 10 hours per day for up to one week. The device recorded daily physical activity, including light physical activity, moderate-to-vigorous physical activity, total physical activity and step counts. It also recorded sedentary behavior including total sitting time during awake hours.
After adjusting for age, race/ethnicity, various lifestyle and risk factors for cardiovascular disease, cancer type and years since cancer diagnosis, the study found that more daily steps and more moderate-to-vigorous physical activity were associated with a progressively lower risk of all-cause mortality; that the greatest benefit was seen among participants who logged 5,000–6,000 steps per day, and their risk of all-cause mortality was reduced by 40 per cent; and, each additional 2,500 steps per day was also incrementally associated with a 34 per cent reduction in risk of death from cardiovascular disease.
It also found that the greatest benefit from moderate-to-vigorous physical activity was seen among participants with at least one hour per day, which reduced all-cause mortality risk by 40% and cardiovascular disease mortality risk by 60 per cent. However, significant reductions in risk were also evident at amounts far below one hour per day, researchers noted.
Furthermore, every 102-minutes of sitting time per day was associated with a 12 per cent increased risk of all-cause mortality and a 30 per cent higher risk of death from cardiovascular disease.
“Risk reductions were even evident when participants walked fewer than 5,000 steps per day, half of the often touted 10,000 steps per day threshold,” Hyde said.
“Daily steps are an important measure because they are easily understood by the public, can be at any intensity level and are recorded on wearable devices like smartwatches that are increasingly being worn by all.”
Keith Diaz, the Florence Irving Associate Professor of Behavioral Medicine at Columbia University Medical Center in New York, noted that the study’s findings add to the understanding of how to manage health and promote longevity after a cancer diagnosis.
“While structured exercise remains the most efficient and effective way to improve your health, these findings highlight that walking – at any intensity – matters. The road to an active lifestyle is more accessible than we often assume, and the benefits are available to everyone, including people navigating life after cancer,” said Diaz, who was not involved in the study.
“Another key takeaway from this study is the impact of sedentary time. Many adults now spend the majority of their day sitting, not engaged in physical activity, and for cancer survivors, this issue is likely even more pronounced due to the physical toll of cancer treatment and recovery. These findings add to the growing body of evidence that prolonged sitting is a significant health risk—one that we must actively combat, particularly after a cancer diagnosis.”
Targeting CD1d altered immune cells slowed tumour growth and improved immunotherapy responses in mouse models of breast cancer, researchers found.
The findings suggest blocking the molecule could make the environment around breast tumours more favourable to anti-cancer immune responses.
Further work is needed to understand how these immune changes occur and how the approach could be safely used in patients.
Researchers from King’s College London, the Francis Crick Institute and University College London investigated how immune cells inside breast tumours influence cancer growth.
They focused on myeloid cells, a group of immune cells found in large numbers within tumours that can either support an immune attack against cancer or contribute to tumour growth and immune evasion.
The team examined CD1d, a molecule found on the surface of myeloid and other immune and tissue cells that helps regulate immune responses.
When CD1d was genetically removed from cells in a mouse model of breast cancer, the mice were more resistant to tumour growth. Researchers also saw changes in myeloid cell populations, including increased activity among cells that can help attack cancer.
The team then blocked CD1d using an antibody and again observed changes in myeloid cells and slower tumour growth. Blocking CD1d also improved responses to immunotherapy in the mouse model.
Researchers used single-cell RNA sequencing, a technique that examines gene activity in individual cells, to investigate the immune changes in more detail.
They identified a population of myeloid cells called monocytes that expressed genes associated with inflammation, an important part of the immune response. These cells were particularly important in restricting tumour growth in the mouse models.
A similar pattern of gene activity was identified in data from human breast cancer tumours. Its presence in myeloid cells was associated with positive responses to immunotherapy in breast cancer patients.
However, the findings in people were based on gene expression data and did not test CD1d-targeting treatment in patients.
Professor Patricia Barral, professor of immunobiology at King’s College London and senior author of the study, said: “Many breast cancers do not respond well to current immunotherapies.
“Our findings reveal a previously unrecognised mechanism by which immune cells within tumours are regulated.
“While CD1d is best known for helping immune cells recognise lipid molecules, we found that it also plays a role in shaping the behaviour of myeloid cells within tumours.
“These findings suggest that targeting the immune cells that surround and support tumours could boost anti-cancer immunity and potentially improve treatment responses in the future.”
Researchers now plan to investigate how the immune changes occur and how they can be safely harnessed in patients.
They also want to examine whether targeting CD1d could enhance existing treatments and influence treatment responses in different cancer types.
The work was supported by UKRI BBSRC, Breast Cancer Now and the Cancer Research UK City of London Centre.
An experimental cancer drug reduced bone loss and body fat in mice modelling post-menopausal changes, early research suggests.
The compound, CADD522, appeared to strengthen bones and help the animals stay leaner after surgery designed to mimic hormonal changes seen after menopause.
The treatment remains at an early experimental stage and has so far only been tested in animals.
The study, led by the University of East Anglia, investigated CADD522, which was originally developed to block a protein involved in the growth and spread of several cancers.
Mice treated with the compound for eight weeks showed significant improvements in bone health. Scans found increased bone volume and better preservation of the honeycomb-like structures inside bones that are crucial for strength and resilience.
Blood tests suggested the treatment stimulated new bone growth without interfering with the body’s normal process of breaking down and rebuilding bone.
Dr Darrell Green, lead researcher from UEA’s Norwich Medical School, said: “Osteoporosis affects around one in three women over the age of 50, leaving sufferers vulnerable to painful fractures that can seriously impact quality of life.
“Current treatments exist, but many are plagued by side effects, safety concerns or inconvenient dosing schedules that make long-term use difficult.”
The researchers also found that mice receiving CADD522 weighed less than untreated mice despite eating the same amount of food.
They had less body fat and fewer fat deposits in their bone marrow, a process commonly seen after menopause and linked to declining bone health.
The team also examined brain tissue and found that the drug appeared to reverse several menopause-related changes in fatty acids.
Levels of omega-3 fats including DHA remained largely intact, while several other lipid abnormalities shifted back towards healthier patterns.
Green said: “We didn’t directly test for memory or thinking ability, but our work raises questions about whether this drug could one day help address wider menopause-related health problems.”
Safety experiments in mice, rats and dogs found that CADD522 could be taken orally and was well tolerated.
The compound also appeared to be metabolised more slowly in human tissue than in rodents, potentially improving its performance in people.
“This is still in the early stages and has so far only been tested in animals but we hope that the benefits will translate to humans to ultimately reduce fracture rates,” added Green.
The research was led by UEA in collaboration with the University of Maryland, the Scintillon Research Institute in San Diego and the University of Stirling.
Safety testing was funded by The Sir William Coxen Trust as part of the development of CADD522 as a childhood cancer treatment.
The FDA has granted accelerated approval to AstraZeneca drug Etcamah for certain adults with advanced breast cancer carrying an ESR1 mutation.
Etcamah, also known as camizestrant, was approved in combination with a CDK4/6 inhibitor, either abemaciclib, palbociclib or ribociclib.
The treatment is for adults with hormone receptor-positive, HER2-negative, locally advanced or metastatic breast cancer when an estrogen receptor-1 (ESR1) mutation is detected during aromatase inhibitor and CDK4/6 inhibitor therapy using an FDA-authorised test.
ESR1 mutations are acquired resistance mutations that tumours may develop during treatment with aromatase inhibitors, a type of endocrine therapy commonly used as a front-line treatment for locally advanced or metastatic breast cancer.
Fewer than 5 per cent of patients have the mutation when HR-positive metastatic breast cancer is diagnosed, according to the FDA. After disease progression on an aromatase inhibitor, nearly 40 per cent have the mutation.
Acting FDA commissioner Kyle Diamantas said: “Women living with metastatic breast cancer face an uphill battle as their tumors continuously evolve to escape treatment.
“We owe them every weapon in our arsenal.
“Today’s approval delivers a win to these patients by granting them a targeted therapy designed specifically to overcome resistance, giving them more time before their disease progresses.”
The accelerated approval programme allows earlier approval of drugs that treat serious conditions and fill an unmet medical need based on surrogate or intermediate endpoints.
For Etcamah, approval was based on how long patients lived without their disease worsening, measured from when the resistance mutation was first detected in their blood.
The FDA said it has not yet been confirmed whether intervening when the mutation is detected, rather than waiting until disease progression is confirmed, results in a clinically meaningful benefit. Confirmatory studies are therefore required to verify and describe clinical benefit.
Angelo de Claro, director of the FDA’s Oncology Center of Excellence, said: “I commend both the FDA and the sponsor for their commitment to advancing cancer care and securing this accelerated approval.
“This marks the first FDA approval of a cancer therapy guided by the detection of a resistance mutation in circulating tumor DNA (ctDNA) before imaging tests show that the disease is progressing.
“But additional evidence is needed to confirm clinical benefit.”
Circulating tumour DNA, or ctDNA, consists of small pieces of tumour DNA released into the blood and can allow earlier molecular detection of resistance mutations.
The FDA also authorised the Guardant360 CDx assay as a companion diagnostic to identify patients with breast cancer who have ESR1 mutations for treatment with camizestrant.
Efficacy was assessed in a clinical trial comparing a switch to Etcamah plus a CDK4/6 inhibitor with continued treatment using an aromatase inhibitor plus a CDK4/6 inhibitor.
Estimated median progression-free survival was 16 months in the Etcamah group, compared with 9.2 months in the aromatase inhibitor group.
Etcamah’s prescribing information includes a boxed warning about the risk of irregular heart rhythm when taken with certain other medicines. It also includes warnings about an abnormally slow heart rate and potential harm to an unborn baby.
The FDA convened its Oncologic Drugs Advisory Committee for the application on 30 April 2026.
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