The research expands a new way of thinking about the complex interactions between antioxidants and cancer.
Category: biotech/medical – Page 27
A study in mice and human tissue shows that the antioxidant glutathione feeds cancer cells
Glutathione is considered an antioxidant due to its ability to repair cellular damage. The body produces it naturally, but it is also sold as an antioxidant supplement. A study in mice and human tissue, published in Nature, shows that cancer cells can break it down and use it as fuel—particularly the cysteine it contains—promoting tumour growth and survival. “Depriving tumours of extracellular glutathione or inhibiting its breakdown is potentially a viable therapeutic strategy for cancer patients,” the authors state.
Yeast βglucan supplementation supports immunometabolic antitumor responses and reverses obesityinduced dysfunction via trained hematopoiesis
Obesity is associated with profound immune dysregulation, driving chronic inflammation while compromising host defense against tumors. While trained immunity can enhance innate effector functions, it has thus far required parenteral administration of microbial ligands. Here, we show that incorporating a yeast-derived β-glucan supplement in mouse diets induces trained immunity via reprogramming of hematopoietic stem and progenitor cells. This dietary intervention leads to sustained production of metabolically enhanced monocytes and macrophages that rescue anti-tumor immunity in high-fat diet-induced obese mice, and corrects immune dysfunction sustained after weight loss. Our work reveals that yeast β-glucans act as functional “immuno-nutrients,” which remodel innate immunity and identifies the mucosal/bone-marrow axis as a target for dietary manipulations to restore immune resilience without impacting metabolism.
Keywords: CP: immunology; beta-glucan; dietary supplementation; hematopoiesis; immunometabolism; innate immunity; macrophage; monocyte; obesity; trained immunity; tumor immunity.
Copyright © 2026 The Authors. Published by Elsevier Inc. All rights reserved.
Newly discovered microprotein linked to type 2 diabetes, shows promise as a precision treatment
A previously unknown microprotein hidden within the human mitochondrial genome may help explain certain forms of type 2 diabetes and could point toward a new precision medicine approach to treating it, according to a new USC study.
Obesity and type 2 diabetes are among the fastest-growing threats to human health, yet their genetic underpinnings remain only partly understood. While most disease-gene research focuses on the larger set of DNA found in the nucleus within cells, the much smaller genome found in mitochondria—cells’ energy factories—is now known to encode a family of microproteins with wide-ranging biological effects.
The new study adds a striking example to that list, said Pinchas Cohen, the study’s senior author, USC Distinguished Professor and dean of the USC Leonard Davis School of Gerontology. The findings were published in the journal Theranostics.
Oil droplets remodel themselves, swallow their surroundings like living cells
NYU researchers have made microscopic oil droplets in water do something usually reserved for living cells: change shape in complex, controllable ways and even engulf their surroundings.
The findings, published in Nature Communications, show that some of life’s signature behaviors—like morphing into complex shapes and capturing material—can emerge from physics and chemistry alone, without genes, proteins or active cellular machinery.
One of life’s defining features is morphogenesis—the ability of cells and tissues to reshape themselves, form compartments and engulf material from their surroundings. These remarkable transformations normally rely on a sophisticated molecular toolkit.
Human study links reduced inflammation to later myopia onset
University of Oklahoma College of Medicine researcher Jody Summers, Ph.D., has long hypothesized that inflammation plays a role in the development of myopia, or nearsightedness, in which close-up vision is clear but distance vision is blurry. Her laboratory experiments have been convincing, and now she has preliminary human data to support the theory.
Summers, a professor of cell biology, and R. Michael Siatkowski, M.D., MBA, professor and chair of the Dean McGee Department of Ophthalmology at the OU College of Medicine, reviewed the medical records of nearly 200 patients age 22 or younger who received eye exams at OU Health Dean McGee Eye Institute. About half were healthy, while the rest had juvenile idiopathic arthritis (JIA) and were being treated with anti-inflammatory drugs. They were having exams because JIA, an autoimmune disease that causes chronic inflammation, can affect the eyes.
The research was presented at the 2026 ARVO Annual Meeting, held in Denver, CO, May 3–7, 2026.
Personalized gene therapy helps teen with rare form of severe epilepsy walk independently
SCN2A-related developmental epileptic encephalopathy (DEE) is a rare, severe form of childhood epilepsy and one of the most common causes of monogenic autism. The condition is caused by single mutations in the sodium voltage-gated channel alpha subunit (SCN2A) gene, which controls the flow of sodium ions into neurons. These mutations promote abnormal brain excitability, resulting in uncontrolled seizures along with developmental delays, autism, movement problems and gastrointestinal issues. Most of these mutations are de novo (not inherited from a parent) and arise spontaneously.
Traditional antiseizure medications are often ineffective and do not address the underlying genetic cause of SCN2A-related DEE.
Now, an international team of researchers led by the University of California San Diego and Rady Children’s Institute for Genomic Medicine has treated two children with the condition using gene therapy tailored to each child’s specific SCN2A mutation.
Tumors Dysregulate Immune Cells in the Thymus
The immune system is made up of a wide range of cells to fight off disease. Each cell works in an orchestrated fashion to achieve robust immunity. The immune response encompasses both the innate and adaptive responses. Innate immunity is the first barrier of protection in which cells circulate the body and target a broad range of infections. The adaptive immune response more specifically targets disease by priming cells that drive the second wave of protection. One of the major cell types within the adaptive immune response includes T cells, which function to identify and eliminate disease and infection.
T cells are critical for healthy immunity and have been the focus of many immune-based therapies. These cells specifically target infections by identifying biomarkers on the cell surface. They are activated by dendritic cells, which prepare them to identify disease. This not only protects healthy tissues from being eliminated but reduces toxic effects when the body is trying to limit disease progression. There are many different subsets of T cells, which correlate to function and can further improve the body’s health. In the context of cancer, T cells become inert or unable to properly function. Many researchers are investigating ways to overcome this phenomenon and boost T cell activity. Since T cells are developed in the thymus, scientists have sought to learn more about this process and find ways to improve T cell immunity.
A recent article in Science Advances, by Dr. Motoko Kimura and others, demonstrates how tumors can evade anti-cancer immunity by altering the development of T cells in the thymus. The research field has previously focused on ways the tumors alter T cell function within the tumor microenvironment, but little is known about other areas of the body. Due to the thymus’ role in T cell development Kimura and his team investigated how the thymus is influenced by solid tumors.