Study also identifies potential path to making immunotherapy effective against the deadly, treatment-resistant cancer.
Category: biotech/medical – Page 11
Proliferation and Apoptosis Adaptor Protein 15 (PEA15), a Potential Oncogenic Regulator of VHL and HIF1A Identified through Proteomic Analysis in Hepatocellular Carcinoma
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Table Of Contents Proliferation and Apoptosis Adaptor Protein 15 (PEA15), a Potential Oncogenic Regulator of VHL and HIF1A Identified through Proteomic Analysis in Hepatocellular Carcinoma.
NIH-funded breakthrough shrinks CRISPR for precision delivery in the body
Smaller gene-editing system could expand treatment options for cancer, ALS and other diseases.
A National Institutes of Health (NIH)-funded research team has discovered an enhanced CRISPR gene-editing system that could enable targeted delivery inside the human body — a key step toward broader clinical use. Researchers identified a naturally occurring enzyme, Al3Cas12f, that is small enough to fit into adeno-associated virus vectors, a leading targeted delivery method for gene therapies. They then engineered an enhanced version that dramatically improved gene-editing performance in human cells.
The advance addresses a major limitation in CRISPR technology. Commonly used gene-editing proteins are too large for targeted delivery systems, restricting clinical applications to cells modified outside the body, such as blood and bone marrow.
Abstract: In ProstateCancer, treatment resistance and disease progression can be promoted by androgen receptor splice variants
Here, Johann de Bono, Luke Gaughan & team identify the protein TRA2B as being key for the synthesis of AR-Vs.
1Newcastle University Centre for Cancer, Paul O’Gorman Building, Framlington Place, Newcastle upon Tyne, United Kingdom.
2The Institute for Cancer Research, London, United Kingdom.
3The Royal Marsden NHS Foundation Trust, London, United Kingdom.
4Newcastle University Bioinformatics Service Unit, Medical School, Newcastle University, Newcastle, United Kingdom.
New toothpaste stops gum disease without killing good bacteria
Scientists have developed a new way to fight gum disease without wiping out the mouth’s helpful bacteria—a major shift from traditional treatments. Instead of killing everything, this targeted approach blocks only the harmful microbes that drive periodontitis, allowing beneficial bacteria to thrive and restore balance naturally.
Experimental Drug Can Reverse Osteoarthritis in Weeks, Animal Research Shows
The debilitating, chronic loss of joint cartilage known as osteoarthritis causes pain and bone decay for hundreds of millions of people every day, but new help may be on the way – in the form of a simple, single shot.
Based on ongoing animal experiments, injecting a carefully engineered, slow-release drug-delivery system into the damaged joint can coax the body’s own cartilage and bone cells to carry out an effective repair job in just a few weeks.
“In two years, we were able to go from a moonshot idea to developing these therapies to demonstrating that they reverse osteoarthritis in animals,” says chemical and biological engineer Stephanie Bryant, from the University of Colorado (UC) Boulder.
Previously unrecognized immune response could enhance defense against cancer
In a paradigm-breaking study, researchers have discovered a novel way the immune system, specifically Tcells, attack their target cells, reshaping long-held assumptions in immunology and demonstrating direct implications for the field of cancer immunology and bone marrow transplantation. The team consists of Dr. Pavan Reddy, director of the Dan L Duncan Comprehensive Cancer Center at Baylor College of Medicine (BCM) and his team, in collaboration with Drs. Arul Chinnaiyan, S P Hicks Endowed Professor of Pathology, and Marcin Cieslik, assistant professor of pathology, both from University of Michigan Rogel Cancer Center. The study is published in Nature Immunology.
Rewriting the rules of T cell biology The immune system relies on molecules called major histocompatibility complexes (MHC) to detect external “threats” to the body, including from cancerous or foreign (allogeneic) cells. Historically, MHC class I molecules were believed to present signals only to CD8+ T cells (“killer” T cells), while MHC II activated CD4+ T cells (“helper” T cells). This division of MHC class roles guided decades of immunology and cancer research.
In an example of collaborative work, Reddy’s graduate students Emma Lauder and Meng-Chih Wu from BCM and Chinnaiyan and Cieslik’s student Mahnoor Gondal, from University of Michigan, worked with colleagues on various components of the work that spanned several years. The work challenges this foundational MHC class-restricted dichotomy and reveals a previously unrecognized role for the class I pathway in CD4+ T cell–mediated immune defense.
How mRNA Vaccines Could Help Treat Cancer
Malignant tumors are sneaky. They tend to fly under the immune system’s radar because, unlike invaders such as viruses or bacteria, cancer cells arise from normal cells, so they bear many of the same familiar molecules on their surface.
(opens in new tab)Once tumors are established, they become even more adept at hiding out from the immune system. They might cloak themselves in proteins to block immune cells from entering them or undergo genetic changes to further reduce the chance that disease-fighting cells will notice anything is amiss.
The Fight For Slow And Boring Research
Great article. I should note that it actually has nothing to do with slow and boring research — it’s about the importance of scientists practicing good communication and public engagement to facilitate fundraising from non-governmental sources.
As federal research funding shrinks, scientists are looking to other sources of support. Can they learn to sell their work without selling out?
Since the middle of the twentieth century, the National Institutes of Health and the National Science Foundation have embodied an imperfect social contract: Federal agencies would fund basic research at scale, and in return, that research would serve the public good through medical advances, technological progress, and economic growth.
For scientists, this system created a reliable pathway: Do good work, write strong grants, and federal agencies would keep your lab running. It was never a perfectly fair system, but it was predictable enough that you could build a life around it. If your work was solid and your grants were strong, the system would fund you.
Affecting a Signaling Pathway Alleviates Alzheimer’s in Mice
A new study shows that the overexpression of somatostatin (SST), a neuropeptide produced in neurons and acting mostly on microglia, lowers inflammation and amyloid β burden, improving cognitive abilities in a mouse model of Alzheimer’s. Drugs affecting this pathway are already available [1].
The unusual suspect
In Alzheimer’s disease, many signaling pathways in the brain become dysregulated. Since going after the main hallmarks of the disease (amyloid β and tau protein accumulation) has only yielded modest results so far, scientists are exploring various secondary targets whose levels correlate with the disease.