Oncology & Targeted Therapeutics

apoptosis

Apoptosis is the body's built-in self-destruct program for cells. Rather than a cell bursting messily, it neatly dismantles itself: it shrinks, chops up its own DNA, packages its contents into tidy parcels, and is quietly cleared away. This orderly suicide is essential to normal life — it sculpts fingers from webbed hands in the embryo and removes cells that are damaged or dangerous.

Inside the cell, apoptosis runs through a cascade of protein-cutting enzymes called caspases, switched on along two main routes: an internal one triggered by stress or DNA damage and sensed at the mitochondria, and an external one triggered by death signals from outside. A family of guardian proteins decides whether the threshold for self-destruction has been crossed, balancing pro-death against pro-survival members.

Cancer is, in part, a failure of apoptosis: tumor cells accumulate damage that should kill them but they silence the suicide program and survive. Many anticancer drugs ultimately work by reawakening apoptosis — and some newer drugs directly tip the balance by blocking the pro-survival proteins that tumors lean on. The caveat is that nudging cells toward death must be tumor-selective, or healthy tissue suffers too.

Venetoclax blocks BCL-2, a pro-survival protein that leukemia cells overproduce to dodge apoptosis; with that brake removed, the cancer cells finally self-destruct.

Blocking a pro-survival protein lets apoptosis proceed in cancer cells.

Also called
programmed cell death程序性细胞死亡程序性細胞死亡