Here are the top medical news for the day:
Unique Fat Tissue Discovery Promotes Longevity and Sustains Exercise in Aging
Rutgers Health researchers have made discoveries about brown fat that may open a new path to helping people stay physically fit as they age
A team from Rutgers New Jersey Medical School found that mice lacking a specific gene developed an unusually potent form of brown fat tissue that expanded lifespan and increased exercise capacity by roughly 30%. The team is working on a drug that could mimic these effects in humans.
“Exercise capacity diminishes as you get older, and to have a technique that could enhance exercise performance would be very beneficial for healthful aging,” said Stephen Vatner, university professor and director of the Cardiovascular Research Institute in the medical school’s Department of Cell Biology and Molecular Medicine and senior author of this research that is published in Aging Cell.
Unlike white fat, which stores energy, brown fat burns calories and helps regulate body temperature. This study revealed brown fat also plays a crucial role in exercise capacity by improving blood flow to muscles during physical activity.
To test whether the brown fat – rather than some other result from the missing genes –accounted for the benefits, the researchers transplanted the brown fat to normal mice. They noted that the recipients gained similar benefits within days. Transplants using regular brown fat from normal mice, by contrast, took eight weeks to produce much milder improvements.
In the meantime, techniques such as deliberate cold exposure can increase brown fat naturally. Studies have found such efforts to produce short-term benefits that range from enhanced immune system function to improved metabolic health, but Vatner said none of the studies have run long enough to find any effect on healthful aging.
He added that most people would prefer to increase brown fat levels by taking pills rather than ice baths and is optimistic about translating the newest finding into an effective medication.
Ref: Vatner DE, Zhang J, Vatner SF. Brown adipose tissue enhances exercise performance and healthful longevity. Aging (Albany NY). 2024 Dec 18; 16:13442-13451 . https://doi.org/10.18632/aging.206179
Breakthrough Discovery: How Cancer Outsmarts the Immune System
Research into immunotherapy against cancer typically focuses on better recognition of cancer cells by the body's own immune system.
Researchers at Amsterdam UMC and Moffitt Cancer Center have investigated how cancer affects the energy management of a patient’s T cells and showed for the first time that contact with chronic lymphocytic leukaemia (CLL) cells leads to a serious energy crisis in these cells. These findings are published in Cellular & Molecular Immunology.
CLL is the most common type of leukaemia in the Western world and mainly affects the elderly. Despite new therapies, the disease remains incurable, and treatments are becoming increasingly expensive.
"Our research revealed two things to us: firstly, that healthy T cells greatly increase their absorption of cholesterol and fats after they have identified their targets. Without this fuel, they are unable to proliferate. Secondly, and crucially, that this doesn't happen when T cells come into close contact with leukemia cells,” says Arnon Kater, professor of Translational Haematology at Amsterdam UMC.
This discovery brings us one step closer to making CAR T-cell treatment more successful for a greater number of patients. More importantly, it opens the door for exploring similar strategies in other cancers where immune cells struggle to sustain their attack. By addressing the energy crisis in T cells, we hope to enhance immunotherapy across a wider range of cancers,” he adds.
Hence, the researchers concluded that a faulty lipid regulation at the transcriptional level, results in altered lipid composition and utilization in CLL T cells, contributing to T-cell dysfunction at multiple levels, the most important being impaired lipid raft formation and proliferation due to lack of cholesterol and phospholipids, and compromised bioenergetics by lower FAO. Thus, altered lipid metabolism constitutes an integral explanation for altered T-cell function in CLL.
Ref: Jacobs, C.F., Peters, F.S., Camerini, E. et al. Cholesterol homeostasis and lipid raft dynamics at the basis of tumor-induced immune dysfunction in chronic lymphocytic leukemia. Cell Mol Immunol (2025). https://doi.org/10.1038/s41423-025-01262-1
Genetic Drivers of Aggressive Prostate Cancer, Study reveals
Scientists from UCLA, the University of Toronto and the University of Melbourne have uncovered new genetic clues that explain why some prostate cancers remain slow-growing while others become life-threatening.
The findings, published in Cancer Discovery, evaluated the roles of inherited genetic factors passed down from our parents and somatic mutations acquired during tumor formation. The research shows that germline and somatic variability work together to initiate and drive progression of prostate cancer. This discovery could one day help improve how doctors predict and treat aggressive cancers.
The interaction between inherited genetic factors and the timing of mutations in the tumor’s DNA is central to understanding how prostate cancer evolves,” said Dr. Paul Boutros, professor of urology and human genetics at the David Geffen School of Medicine at UCLA, director of cancer data science at the UCLA Health Jonsson Comprehensive Cancer Center and co-senior author of the study. “We found that prostate cancer follows a common evolutionary path, with different tumors branching off depending on early genetic changes and an individual’s inherited genetic background. Some tumors may become aggressive because of specific mutations, while others remain indolent. Both genetic randomness and inherited traits play a role in determining these outcomes.
Researchers used whole-genome sequencing to analyze the complete genomes of 666 localized prostate tumors — the largest whole-genome dataset of its kind — covering the full range from mild to aggressive cases. The researchers identified 223 regions of the genome frequently mutated in prostate tumors that help cancer grow and spread. Most of these were undetectable using traditional targeted sequencing methods deployed in clinical assays.
“This study offers a new way of thinking about prostate cancer risk assessment,” said Boutros, who also serves as the interim vice dean for research at the David Geffen School of Medicine at UCLA, and is the associate director of cancer informatics at the UCLA Institute for Precision Health. “By combining inherited genetic markers with tumor sequencing, we could one day more accurately predict which cancers are likely to become aggressive and uncover new ways to prevent aggressive prostate cancer before it develops.”
Ref: Takafumi N. Yamaguchi, Kathleen E. Houlahan et al. The Germline and Somatic Origins of Prostate Cancer Heterogeneity: Cancer Discov (2025). https://doi.org/10.1158/2159-8290.CD-23-0882
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