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Category: genetics

Sleep and exercise may curb heart risk from mutant white blood cells

Healthy sleep and regular exercise can work to counteract genetic mutations in white blood cells that are associated with cardiovascular disease and are most common among older people, Mount Sinai researchers have found. In a study published in Nature, the team reported for the first time that sufficient sleep and exercise can help reduce the cancer-like cell expansion and atherosclerotic risk linked to mutations that spontaneously occur in white blood cells.

These mutations accumulate over our lifetimes and occur most often in hematopoietic stem cells, which are the cells in bone marrow that make blood cells, including macrophages and monocytes, immune cells that help defend the body. When these cells develop mutations, they start to proliferate, multiplying faster than they should, and become more inflammatory, irritating or damaging tissues in the body.

This condition, known as clonal hematopoiesis (CH), is detectable in a quarter of people over age 70 and half of people over 80, the researchers say, though it is infrequent in young, healthy people.

The Intelligence of Our Cells with Michael Levin

Each one of us have made the remarkable journey from matter to mind. The destination is our existence, one whole conscious being. The marvellous nature of our intelligence can be traced to the aptitude of every individual cell in our body. The whole is greater than the sum of its parts. What if we could rewire the code that separates self from world? Tadpoles with eyes growing from their tails, worms with two heads-is the manifestation of biology governed entirely by chance?

Michael Levin is an American developmental and synthetic biologist at Tufts University, where he is the Vannevar Bush Distinguished Professor. Levin is a director of the Allen Discovery Center at Tufts University and Tufts Center for Regenerative and Developmental Biology. He is also co-director of the Institute for Computationally Designed Organisms with Josh Bongard.

00:00 — Collective Intelligence 03:38 — Cognitive Light Cones 09:32 — Scaling of the light cone 12:07-Definition of Intelligent Life 13:53 — Free Energy Principle 15:02 — Cognitive Glue 17:56 — Bioelectricity vs Genetics 23:23 — Limb Regeneration in Humans 24:24 — Solving Cancer 28:02 — Length of Effects 29:09 — Alien Life 31:31 — Communicating with our body organs 35:13 — Tic Tac Toe with an Alien 38:41 — Training our body organs 40:06 — Non-Cellular intelligence 41:03 — Is everything intelligent in the universe? 45:11 — Collective vs Parts 47:10 — Mike’s message to extraterrestrials.

Sugar-coated CAR-T cells survive longer and shrink lymphoma tumors in mice

Scientists at Florida International University may have found a way to make a powerful cancer treatment work even better. The treatment, called CAR-T therapy, uses a patient’s own immune cells to fight cancer. Doctors remove special immune cells called T-cells from the body, genetically change them in a lab so they can recognize cancer, and then put them back into the patient to attack tumors. The therapy has already helped many people with serious blood cancers such as lymphoma and leukemia.

But there is still a problem: Cancer fights back. Tumors create a protective environment around themselves that can weaken or shut down immune cells before they finish destroying the cancer. In many cases, CAR-T cells do not survive long enough to completely wipe out the disease.

Now, FIU researchers say they may have found a way to help.

The World in 100 Years FULL EPISODE | Science Fiction Documentary

What will the world really look like in 100 years?

Forget flying cars, impossible megacities, and science-fiction fantasies. This documentary explores a realistic vision of life in the year 2,126 based on current trends in artificial intelligence, climate adaptation, biotechnology, energy, space exploration, economics, and human evolution.

How will cities change as the planet warms? What happens when AI becomes part of everyday life? Will humans live to 120 years? Will neural implants blur the line between biology and technology? Could Mars become a permanent home for thousands of people? And what happens to society when work, truth, privacy, and even human identity are redefined?

Travel one century into the future and discover a world that is both familiar and radically different from our own. A world shaped by the choices humanity is making right now.

From climate-engineered cities and fusion-powered civilizations to Martian settlements, artificial intelligence, genetic medicine, digital consciousness, and the search for life beyond Earth, this is a deep exploration of the most plausible future awaiting our species.

The future isn’t written.

Continue reading “The World in 100 Years FULL EPISODE | Science Fiction Documentary” | >

Scientists discover a two-stage aging process that may cause cancer and arthritis

Inherited genetic mutations may also stay silent for decades before increasing the risk of diseases such as cancer or fibrosis later in life.

Evolutionary Biology and Aging Research

The researchers say their model builds on long-standing evolutionary theories of aging. One influential idea is that natural selection becomes weaker later in life, allowing harmful biological processes to emerge with age because they have less impact on reproduction and survival earlier in life.

New antibody may boost KRAS-targeted lung cancer treatment after resistance emerges

An experimental antibody treatment that binds to a protein known as PCDH7 shrank tumors in preclinical models of non-small cell lung cancer (NSCLC), including those resistant to a targeted therapy, a study led by UT Southwestern Medical Center researchers showed. The findings, published in Science Advances, could eventually lead to a new class of drugs to treat NSCLC and potentially other cancers.

“Overcoming resistance to molecularly targeted therapies is a critical unmet need for lung cancer patients. We are excited that these antibodies may open another therapeutic avenue for lung cancer, especially for patients whose cancers have become resistant to KRAS inhibitors,” said Kathryn O’Donnell, Ph.D., associate professor of molecular biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. O’Donnell co-led the study with first author Nicole Novaresi, Ph.D., a postdoctoral researcher in the O’Donnell Lab, and collaborators at the University of Texas Health Science Center at Houston.

NSCLC accounts for about 85% of lung cancer cases in the U.S. and is the leading cause of cancer-related deaths. The O’Donnell Lab focuses on identifying and characterizing proteins on the surface of NSCLC and other cancer cells because of their potential as therapeutic targets. In 2017, O’Donnell and her colleagues identified PCDH7 as a driver of NSCLC, especially in tumors with mutations in a gene called KRAS. Found in about 25% of NSCLC cases, these mutations cause uncontrolled cell proliferation that propels tumor growth.

How the body remembers the tumor?

While we tend to quickly forget having been ill or having received a vaccine, the immune system remembers remarkably well. It has memory B cells – “trained” immune cells that circulate throughout the body in search of harmful invaders they have encountered previously; these cells can rapidly deploy targeted weapons when faced with a pathogen again. Now, researchers report that activated memory B cells can also recognize an internal enemy: cancer cells.

In patients with ovarian cancer, the researchers identified memory cells that are capable of homing in on the tumor, springing into action and producing effective antibodies against it. The new study, whose findings were published in Immunity, advances the development of vaccines and therapies based on immune memory against cancer.

The immune system’s arsenal contains hundreds of millions of B cell clones, each producing a unique antibody against a specific pathogen. These antibodies are proteins that identify their target and either neutralize it or recruit other immune cells to attack it. When a clone encounters its target for the first time, its antibody binds weakly and elicits a limited response. But some of these cells enter “training camps” – structures called germinal centers in the lymph nodes – where they undergo genetic changes and rigorous selection, emerging with much more effective antibodies. Some of these trained cells immediately become active antibody producers; others develop into memory cells that remain inactive, circulating between the blood and the lymph nodes, but able to rapidly snap into action if the body is exposed again to the pathogen.

Faster biological aging consistently linked to poverty and discrimination

The study, published in Nature Human Behaviour, demonstrates that social inequality, such as poverty and racism, is related to biological aging measured in the epigenome, also known as “epigenetic clocks.” Epigenetic clocks analyze patterns of chemical marks on DNA to estimate a person’s biological age or the rate at which their body is aging. These tools are increasingly used by scientists to study how environmental exposures, lifestyle and social conditions affect health across the life course.

Previous individual studies have shown that epigenetic clocks are sensitive to socioeconomic and racial or ethnic disparities. However, because multiple types of epigenetic clocks exist, it has remained unclear which measures best capture the effects of social determinants of health, at which stages of life socioeconomic exposures most affect epigenetic aging, and whether associations differ by sex or by technical factors such as the tissue in which epigenetic data are collected. This study integrates findings across many independent studies, offering a comprehensive test of whether these associations are consistent and robust.

Faulty protein cleanup gene tied to severe early-onset neurological disorders

Though protein clumps associated with Alzheimer’s and Parkinson’s were discovered more than a century ago, researchers remain largely unable to prevent them from forming or eliminate them from the brain. And though a variety of therapies have taken aim at tau tangles, beta-amyloid plaques and Lewy bodies, among other notorious aggregates, none have been very effective at stopping disease progression.

Rockefeller’s Hermann Steller and his team in the Strang Laboratory of Apoptosis and Cancer Biology have long been focused on understanding how the cell’s protein-degrading machines, called proteasomes, are regulated. His lab discovered that a transporter protein termed PI31 shuttles proteasomes over long distances from the nerve cell body to synapses. When this system fails, synapses become depleted of degradative capacity, and proteins that should have been eliminated accumulate. As a result, synaptic communication breaks down, protein clumps form and neuronal health deteriorates.

Now a new study in Nature Communications, led by researchers from University College London and contributed to by Steller’s lab, has identified mutations in PSMF1, the gene that produces PI31, that cause the protein to malfunction. Moreover, the scientists demonstrated that these mutations cause a spectrum of severe, very early-onset neurological disorders.

Making CAR T Cells Safer

Research from CCR scientists points toward a strategy for making chimeric antigen receptor (CAR) T-cell therapy, the cell-based immunotherapy that has revolutionized the treatment of some blood cancers, safer and more effective for treating solid tumors.

The study, led by Grégoire Altan-Bonnet, Ph.D., Deputy Chief of the Laboratory of Integrative Cancer Immunology, Naomi Taylor, M.D., Ph.D., Senior Investigator in the Pediatric Oncology Branch, and Paul François, Ph.D., at the University of Montréal, shows how adding certain receptors to CAR T cells can prevent the cells from attacking healthy tissue while simultaneously enhancing their activity against cancer cells. The findings appeared April 10, 2025, in Cell.

CAR T-cell therapy reprograms patients’ immune cells to be effective cancer killers using genetically engineered chimeric antigen receptors (CARs) that are added to their T cells. CARs are designed to recognize molecules on the surface of cancer cells called antigens, which can usually be found on some healthy cells, too. This leads to manageable side effects for patients with blood cancer, but when CAR T cells designed to target solid tumors attack healthy tissue, the effects can be severe.

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