DSTYK amplification enables lung cancer cells to evade T cell killing by sustaining ULK1-dependent suppression of TNF-α-induced apoptosis. Targeting ULK1 dismantles this survival pathway, restoring RIPK1-mediated cell death and sensitizing DSTYK-altered tumors to chemo-immunotherapy, revealing a promising therapeutic vulnerability in NSCLC.
Proton beam therapy continues to generate significant interest — and controversy — in prostate cancer. About 45 cancer centers in the US offer proton therapy to treat a variety of cancers, including prostate cancer.
The technology, however, faces ongoing debate about its role in prostate cancer. Despite the buzz, there is no randomized evidence demonstrating that proton therapy is superior to the current standard of care: intensity-modulated radiation therapy (IMRT). The core question has become: Is proton therapy for prostate cancer worth it?
Does the evidence line up with the buzz surrounding the use of proton therapy to treat prostate cancer?
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While it seems logical that age-related cognitive decline would be blamed on brain aging and degeneration (which, like anything in the brain, is notoriously hard to treat), there’s some evidence that processes elsewhere in the body influence the brain’s ability to form memories. In particular, neuronal pathways that sense the status of other organs in the body can influence cognitive functions in the brain.
Other studies have shown that our gut microbiome affects learning, memory, and behavior. But what we don’t yet understand is how these connections work—the specific molecules, microbes, and gut-brain communication involved—and whether we can use that knowledge to prevent or reverse age-related memory loss.
In our new work published today in Nature, we discovered that the aging gastrointestinal tract produces specific molecules that blunt the activity of a key gut-brain neuronal pathway, leading to age-related cognitive decline in mice.
Engineered cells are a high-value genetic asset that is key to many fields, including biotechnology, medicine, aging, and stem cell research, with the global market projected to reach $8.0 trillion USD by 2035. Yet the only ways to keep the cells safe are strong locks and watchful guards.
In Science Advances, a team of U.S. researchers present a new approach to genetically securing precious biological material. They created a genetic combination lock in which the locking or encryption process scrambled the DNA of a cell so that its important instructions were non-functional and couldn’t be easily read or used.
The unlocking, or decryption, process involves adding a series of chemicals in a precise order over time—like entering a password—to activate recombinases, which then unscramble the DNA to their original, functional form.
Researchers at Oregon Health & Science University have uncovered a key reason why immunotherapy has largely failed in pancreatic cancer—and identified a promising strategy to overcome that resistance. The study, published in the journal Immunity, shows that pancreatic tumors actively reshape their immune environment by co-opting regulatory immune cells that normally shut down tumor-killing cells. By reprogramming those cells, the research reveals a potential pathway to make immunotherapy effective against one of the deadliest and most treatment-resistant cancers.
“Pancreatic cancer is incredibly resistant to most therapies,” said the study’s senior author, Katelyn Byrne, Ph.D., assistant professor of cell, developmental and cancer biology in the OHSU School of Medicine and member of the OHSU Brenden-Colson Center for Pancreatic Care. “Even when we know the immune system is capable of long-lasting protection, it’s been very difficult to get that response to work in this disease.”
Immune checkpoint inhibitors and other immunotherapies have transformed care for cancers such as melanoma and lung cancer, but they have shown little benefit for pancreatic cancer. One major reason, Byrne said, is the presence of large numbers of regulatory T cells, or Tregs, inside pancreatic tumors.
In a recent Cell Press Blue paper, Zhang et al. identify two polyunsaturated lipids that selectively eliminate senescent cells by inducing ferroptosis, uncovering this iron-dependent cell death pathway as a vulnerability for senescent cells. Their findings position ferroptosis induction as a promising strategy for targeting senescence and aging-associated diseases.
Researchers at Oregon State University have pioneered a transformative approach for simultaneously targeting lung cancer and the debilitating muscle-wasting syndrome known as cachexia—a condition that plagues many lung cancer patients. Their groundbreaking work employs lipid nanoparticles (LNPs) as a delivery vehicle for messenger RNA (mRNA) therapeutics, addressing critical challenges in precision drug delivery for aggressive tumors deep within the lung tissue.
Lipid nanoparticles, microscopic carriers composed of fatty compounds like lipids, have revolutionized drug delivery with their ability to ferry genetic material directly into cells. In this study, the OSU team engineered LNPs comprised of DC-cholesterol and a specialized ionizable lipid, 113-O12B, which exhibited a remarkable ability to bind a blood serum protein called vitronectin. This binding triggers the formation of a protein corona on the nanoparticles, a dynamic interface that actively guides the LNPs to lung tissue, and more importantly, lung tumor microenvironments.
Vitronectin’s recruitment is no coincidence. It interacts with integrin receptors—cellular docking proteins highly expressed on lung cancer cells. These integrins act as biological gateways, facilitating enhanced uptake of the therapeutic nanoparticles by tumor cells while sparing healthy tissue. This receptor-mediated targeting marks a significant advance over conventional LNPs, which commonly accumulate in the liver, limiting their therapeutic index against lung malignancies.