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The cell's built-in self-destruct programme, which tidily dismantles a damaged or unwanted cell without alarming its neighbours. Cancer cells disable it by mutating TP53 or overproducing BCL-2; chemotherapy and radiation work largely by inflicting enough damage to trigger it, and venetoclax removes the BCL-2 shield directly.
Apoptosis is triggered from inside (DNA damage sensed by p53, which tips the balance of BCL-2 family proteins and releases enzymes called caspases) or from outside (death signals from immune cells). Tumours resist it by mutating TP53, overexpressing BCL-2 or MCL-1, or losing the proteins that would push them over the edge; 'resisting cell death' is one of the hallmarks of cancer. Chemotherapy and radiation work largely by inflicting enough damage to trigger apoptosis, venetoclax removes the BCL-2 shield directly, and the calm, non-inflammatory nature of apoptosis is why it does not, by itself, alert the immune system, unlike immunogenic cell death.
In plain words · A protein that stops cells from self-destructing. Venetoclax removes that protection and has transformed leukaemia treatment.
Showing the target this term concerns: BCL-2.
Shares Levine 1997: p53, the cellular gatekeeper for growth and division, Tumour suppressor gene, p53 / RB / cell-cycle checkpoint, TP53.
Shares Levine 1997: p53, the cellular gatekeeper for growth and division, Tumour suppressor gene, TP53.
Shares Levine 1997: p53, the cellular gatekeeper for growth and division, Tumour suppressor gene, p53 / RB / cell-cycle checkpoint, TP53.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2, Venetoclax.
Shares Levine 1997: p53, the cellular gatekeeper for growth and division, Intrinsic apoptosis (BCL-2 family), BCL-2, p53 / RB / cell-cycle checkpoint.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2, Venetoclax.
Shares Immunogenic cell death, Intrinsic apoptosis (BCL-2 family), BCL-2, Venetoclax.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2, Venetoclax.