New Cleveland Clinic research reveals that up to 5% of Americans – approximately 17 million people – carry genetic mutations or “variants” linked to increased cancer susceptibility, regardless of risk factors like personal or family cancer history.

Published in JAMA, the study suggests that these mutations may be more common than previously thought and highlights the potential for expanded genetic screening to identify more individuals at risk and improve early detection.

The research team, led by Joshua Arbesman, M.D., and Ying Ni, Ph.D., analyzed health records and genetic sequencing data from over 400,000 participants in the National Institute of Health’s All of Us Research Program, the country’s largest and most comprehensive genetic and healthcare database. 

When it comes to treating disease, one promising avenue is addressing the presence of senescent cells. These cells — also known as "zombie cells" — stop dividing but don't die off as cells typically do. They turn up in numerous diseases, including cancer and Alzheimer's disease, and in the process of aging. While potential treatments aim to remove or repair the cells, one hurdle has been finding a way to identify them among healthy cells in living tissue. In the journal Aging Cell, Mayo Clinic researchers report finding a new technique to tag senescent cells.

A major new study, which has recently begun recruiting, is hoped to lead to earlier detection of lung cancers.

People living in Leeds, Bath, Hull and Stoke-on-Trent will be among those approached to take part. The study is funded by National Institute for Health and Care Research (NIHR).

At the moment, chest X-ray is the test GPs are advised to use in almost for almost all symptoms to rule out or confirm a cancer. Symptoms can include a cough that persists for several weeks.

Worryingly, however, chest X-rays are not always conclusive. Indeed, it’s believed that they miss as many as 20 per cent of lung cancers.

More people in the UK die from lung cancer than from any other cancer - which is why earlier detection of the cases not diagnosed by X-ray could potentially save many lives.

Researchers strongly suspect that low-dose CT scans – far more accurate than X-rays - are likely to do just that. But until now, no one has yet done a large study comparing the two methods in patients with symptoms.

Within the last two months, a team of researchers and academics - from the Universities of Leeds, Sheffield, Exeter and Nottingham, plus Queen Mary University of London and University College London -  have started the process of recruiting 900 volunteers for the new study.

Scientists at the Keck School of Medicine of USC, working within the Southern California Superfund Research and Training Program for PFAS Assessment, Remediation and Prevention (ShARP) Center, have uncovered compelling evidence that exposure to perfluoroheptanoic acid (PFHpA), a lesser-known member of the PFAS family of “forever chemicals, is linked to a significantly higher risk and severity of metabolic dysfunction-associated steatotic liver disease (MASLD) in adolescents with obesity. The study, published in Communications Medicine (Nature Portfolio), integrates clinical data from adolescents undergoing bariatric surgery with advanced 3D liver models to reveal the biological mechanisms by which PFHpA may drive disease progression. The researchers examined blood samples from 137 adolescents enrolled in  Teen Longitudinal Assessment of Bariatric Surgery, the largest U.S. study of pediatric bariatric surgery. They found that adolescents with twice the amount of PFHpA in their blood faced an 80% greater likelihood of being diagnosed with MASLD compared to their peers with lower levels. Teens with higher exposures also showed more advanced liver injury, including inflammation and fibrosis—early signs of disease progression that can eventually lead to cirrhosis, liver failure, or even liver cancer. To strengthen these findings, the team tested PFAS on laboratory-grown liver spheroids using doses comparable to typical human exposure, showing that PFHpA disrupts critical biological pathways, including inflammation, oxidative stress and lipid metabolism. This dual approach allowed the researchers to connect exposure to mechanism, producing a distinctive molecular signature of PFHpA-related liver damage.