health
In 2026, researchers finally solved a decades-old puzzle about how melanoma tumors manage to keep dividing indefinitely instead of dying like normal cells.
Pittsburgh researchers found TERT mutations alone, common in most melanomas, couldn't fully explain the tumors' unusually long telomeres, the protective chromosome caps that normally shorten each division and eventually stop it. The missing piece was TPP1: extra TPP1 combined with mutated TERT builds abnormally long telomeres, letting melanoma cells bypass the normal division limit.
There is no evidence melanoma hijacks a virus to repair DNA, and excess vitamin D receptors are unrelated to telomere length, neither matches the actual mechanism researchers found.
Telomeres are like the plastic tips on shoelaces, shortening with each division until a cell stops dividing, but cancer cells that keep rebuilding them, as here, sidestep that built-in limit on aging.
health
What has remained true about the H5N1 bird flu cases reported in Bangladesh, Cambodia, and India since mid-2025?What did Alexander Fleming discover when he noticed mold killing bacteria in a forgotten petri dish?What natural hormone do these drugs imitate to curb appetite and blood sugar?How does a CRISPR-based therapy achieve its effect?What are these wearable devices called?Which AI system achieved this protein-folding breakthrough?Which brain protein do these new Alzheimer's drugs target?What are these engineered immune cells commonly called?What is this community of microbes collectively called?What concept do scientists use to estimate the body's true wear from cells and molecules?What field tailors medicines to a person's genetic makeup?Which common heart-rhythm problem are these watches designed to flag?Quration — Quration Play