angiogenesis
/ AN-jee-oh-JEN-uh-sis /
Imagine a small village that suddenly starts growing into a city. It quickly needs new roads to bring in food and carry away waste — without them, the outskirts starve. A growing tumor faces the same problem. Once it swells past about a millimeter or two across, the cells in the middle can no longer get enough oxygen and nutrients by simple diffusion from nearby blood vessels. Angiogenesis is the growing of new blood vessels, and tumors hijack this normal process to feed themselves.
More precisely, angiogenesis is the formation of new blood vessels that branch off from existing ones. It is a normal, useful process during growth and wound healing. A tumor that has run short of supply releases chemical signals — most famously a protein called VEGF (vascular endothelial growth factor) — that coax nearby blood vessels to sprout new branches toward the tumor. This 'angiogenic switch' is one of the hallmarks of cancer, because once the tumor has its own blood supply it can grow much larger and also gain a route for cells to escape into the bloodstream.
Angiogenesis matters as both a danger and a target. Because tumors depend on recruiting blood vessels, drugs called angiogenesis inhibitors (such as bevacizumab) try to block the VEGF signal and starve the tumor. A realistic caveat: these drugs slow many cancers but rarely cure them on their own, because tumors can adapt and find other ways to get blood, and the new vessels they build are often leaky and disorganized rather than neatly stopped.
A tiny tumor sits dormant for years because it cannot grow beyond the reach of nearby blood vessels. Then it flips the 'angiogenic switch,' pouring out VEGF; new vessels grow toward it, and within months the once-harmless cluster expands into a much larger, more dangerous mass.
Tumors recruit new blood vessels to grow past a tiny size.
Angiogenesis is a normal process the tumor hijacks; blocking it slows many cancers but rarely cures them alone, since tumors adapt.