For some tumours at least, a lack of host blood supply is not a problem.
Finding explains failure of drugs that target host vasculature.
Alla Katsnelson
Tumours don’t just rely on their host’s blood vessels for nourishment — they can make their own vasculature, according to two independent studies from the United States and Italy. The findings offer an explanation for why a class of drug once heralded as a game-changer in cancer treatment is proving less effective than had been hoped.
Almost four decades ago, Judah Folkman, a cell biologist at Harvard Medical School in Boston, Massachusetts, proposed that tumours were dependent on the blood vessels surrounding them, and that choking off that blood supply would kill the cancer1. Bevacizumab (Avastin), the first drug to block blood-vessel growth, was approved in 2004, but it and other ‘angiogenesis inhibitors’ have proved disappointing in the clinic, extending patients’ lives for at best a few months.