Lifeboat Foundation

Our genetic code works a bit like DALL-E, apparently.

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Continue reading “B-Amyloid Protects The Brain Against Herpes Virus Infection: Amy Proal, PhD” »

The preprint, not yet peer-reviewed, is the latest from a global consortium that hunts down potential new genes. Ever since the Human Genome Project completed its first draft at the turn of the century, scientists have tried to decipher the genetic book of life. Buried within the four genetic letters—A, T, C, and G—and the proteins they encode is a wealth of information that could help tackle our most frustrating medical foes, such as cancer.

The Human Genome Project’s initial findings came as a surprise. Scientists found less than 30,000 genes that build our bodies and keep them running—roughly a third of that previously predicted. Now, roughly 20 years later, as the technologies that sequence our DNA or map proteins have become increasingly sophisticated, scientists are asking: “What have we missed?”

The new study filled the gap by digging into relatively unexplored portions of the genome. Called “non-coding,” these parts haven’t yet been linked to any proteins. Combining several existing datasets, the team zeroed in on thousands of potential new genes that make roughly 3,000 miniproteins.

Researchers think certain common viruses may trigger some autoimmune conditions—alone or in concert with other factors. A recent Office of Autoimmune Disease Research (OADR)-Office of Research on Women’s Health Science Talks series focused on understanding the triggers of autoimmunity and advancing research.

Almost 80 percent of people living with an autoimmune disease are women. It’s estimated there are 80–120 autoimmune diseases. These chronic and often debilitating diseases have no known cures. Some combination of genetics, immune regulation and the environment work together to form an “endotype” for each autoimmune disease patient, explained Dr. Judith James of the Oklahoma Medical Research Foundation.

Her presentation focused on lupus, or systemic lupus erythematosus (SLE), which disproportionately affects women. Nine women are diagnosed with SLE for every male. In SLE, the immune system attacks healthy tissue, causing inflammation and occasionally permanent damage.

One year of treatment with the targeted drug olaparib improves long-term survival in women with high-risk, early-stage breast cancer with mutations in BRCA1 or BRCA2 genes, new results from a major clinical trial show.

Ten years since the first patient was recruited, new findings from the phase III OlympiA trial – presented at San Antonio Breast Cancer Symposium (SABCS) 2024 – show that adding olaparib to standard treatment cuts the risk of cancer coming back by 35 per cent, and the risk of women dying by 28 per cent.

After six years, 87.5 per cent of patients who were treated with the drug were still alive compared with 83.2 per cent of those who were given the placebo pills.

Continue reading “Major trial shows prolonged benefit of olaparib in early-stage inherited breast cancer” »

Large-scale protein and gene profiling have massively expanded the landscape of cancer-associated proteins and gene mutations, but it has been difficult to discern whether they play an active role in the disease or are innocent bystanders.

In a study published in Nature Cancer, researchers at Baylor College of Medicine revealed a powerful and unbiased machine learning-based approach called FunMap for assessing the role of cancer-associated mutations and understudied proteins, with broad implications for advancing cancer biology and informing therapeutic strategies.

“Gaining functional information on the genes and proteins associated with cancer is an important step toward better understanding the disease and identifying potential therapeutic targets,” said corresponding author Dr. Bing Zhang, professor of molecular and human genetics and part of the Lester and Sue Smith Breast Center at Baylor.

Published in Nature Communications, a new study led by the University of Minnesota Medical School and Duke University found that a DNA sequencing test for advanced prostate cancer patients can distinguish between patients with poor and favorable prognoses.

The new blood-based test —called AR-ctDETECT—is designed to detect and analyze small fragments of tumor-derived DNA in the blood of certain patients with advanced, metastatic prostate cancer.

In this new study, the AR-ctDETECT test was used to analyze DNA from more than 770 blood samples from a phase 3 clinical trial of advanced prostate cancer patients. The test identified circulating tumor DNA (ctDNA) in 59% of patients with metastatic prostate cancer. Patients with detectable circulating tumor DNA had significantly worse overall survival compared to those without. These results demonstrate the potential of the AR-ctDETECT test to provide key genetic information to tailor treatments based on similar characteristics among patients.

New research reveals that centromeres, which are responsible for proper cell division, can rapidly reorganize over short time scales. Biologists at the University of Rochester are calling a discovery they made in a mysterious region of the chromosome known as the centromere a potential game-changer in the field of chromosome biology.

“We’re really excited about this work,” says Amanda Larracuente, the Nathaniel and Helen Wisch Professor of Biology, whose lab oversaw the research that led to the findings, which appear in PLOS Biology.

The discovery involves an intricate and seemingly carefully choreographed genetic tug-of-war between elements in the centromere, which is responsible for proper cell division. Instead of storing genes, centromeres anchor proteins that move chromosomes around the cell as it splits. If a centromere fails to function, cells may divide with too few or too many chromosomes.

CAR-T and NK cells engineered using a non-viral circular single-stranded DNA system show effective anti-tumor function.