The most common screening test for prostate cancer — a measure of prostate-specific antigen, or PSA, levels — so often suggests cancer where there is none that clinical guidelines no longer recommend the test for men over 70 and leave the decision up to younger patients.

Scientists at Stanford Medicine and their collaborators aim to make PSA screening more accurate — by calibrating PSA levels to each man’s genetics. Applying this type of personalization could significantly reduce overdiagnosis and better predict aggressive disease. Their research was published June 1 in Nature Medicine.

In addition to the regular blood-based PSA test, such personalized screening would require a germline genetic test, typically done on saliva, blood or cheek swab samples, to look for inherited genetic variants that affect PSA levels.

In a recent study led by Ravi Salgia, M.D., Ph.D., the Arthur & Rosalie Kaplan Chair in Medical Oncology, a team of researchers from City of Hope, one of the largest cancer research and treatment organizations in the United States, and other institutions found that nongenetic mechanisms are important in lung cancer patients who develop a resistance to one cancer therapy. Their findings were published in the October 13 issue of the journal Science Advances.

The team’s study explored resistance to the anti-cancer medication sotorasib in patients with non-small cell lung cancer (NSCLC). Sotorasib inhibits a specific mutation of a protein, KRAS G12C, that causes unchecked cell growth.

The researchers’ findings suggest that, initially, most tumor cells are sensitive to sotorasib. But some cells can become tolerant to therapeutic treatment without resorting to genetic mutations or alterations by manipulating the KRAS-sotorasib interaction network. Furthermore, they found that if sotorasib treatment is withheld, the tumor cells revert to becoming sensitive again, implying that the phenomenon is reversible and thus is driven by nongenetic mechanisms.

According to this information covid 19 sars is a chimeric virus that evolves with other genetic material which gives us clues for a proper antidote. Also it shows why it is so dangerous.

Ben Hu denies he was sick in late 2019, or that his coronavirus work led to COVID-19, and newly declassified U.S. intelligence doesn’t substantiate allegations against him.

I dont really care where it comes from but we need Crispr tec to be where any alteration we do want causes Zero un intended alterations any where else 100% of the time, aim for by 2030–2035 window.

A diverse set of species, from snails to algae to amoebas, make programmable DNA-cutting enzymes called Fanzors—and a new study from scientists at MIT’s McGovern Institute for Brain Research has identified thousands of them. Fanzors are RNA-guided enzymes that can be programmed to cut DNA at specific sites, much like the bacterial enzymes that power the widely used gene-editing system known as CRISPR. The newly recognized diversity of natural Fanzor enzymes, reported Sept. 27 in the journal Science Advances, gives scientists an extensive set of programmable enzymes that might be adapted into new tools for research or medicine.

“RNA-guided biology is what lets you make programmable tools that are really easy to use. So the more we can find, the better,” says McGovern Fellow Omar Abudayyeh, who led the research with McGovern Fellow Jonathan Gootenberg.

CRISPR, an ancient bacterial defense system, has made it clear how useful RNA-guided enzymes can be when they are adapted for use in the lab. CRISPR-based genome editing tools developed by MIT professor and McGovern investigator Feng Zhang, Abudayyeh, Gootenberg, and others have changed the way scientists modify DNA, accelerating research and enabling the development of many experimental gene therapies.