Apoptosis: intrinsic and extrinsic pathways
The BCL-2 family and mitochondrial (intrinsic) pathway, death receptors and caspase-8 (extrinsic), how apoptosis differs from necrosis, the diseases of too little or too much apoptosis (follicular lymphoma, CLL, ALPS), and venetoclax pharmacology including the ramp-up and CYP3A4 arithmetic.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Apoptosis is regulated, energy-requiring cell death without inflammation. It deletes cells in development, ends immune responses and removes damaged cells.
- Two entry routes converge on the executioner caspases 3 and 7:
- Intrinsic (mitochondrial): internal stress, controlled by the BCL-2 family.
- Extrinsic (death receptor): Fas ligand, TNF or TRAIL, through caspase-8.
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Sources
- Venclexta (venetoclax) prescribing information, Table 8: CYP3A and P-gp inhibitorsDailyMed, US National Library of Medicine (AbbVie), accessed 2026-11-13
- Venclyxto (venetoclax) summary of product characteristicsEuropean Medicines Agency, accessed 2026-11-13
- Robbins and Cotran Pathologic Basis of Disease, 10th editionElsevier (Kumar V, Abbas AK, Aster JC), 2021
- Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011;144:646-74Cell, 2011
- Roberts AW, Davids MS, Pagel JM et al. Targeting BCL2 with venetoclax in relapsed chronic lymphocytic leukemia. N Engl J Med 2016;374:311-22New England Journal of Medicine, 2016
- Fischer K, Al-Sawaf O, Bahlo J et al. Venetoclax and obinutuzumab in patients with CLL and coexisting conditions (CLL14). N Engl J Med 2019;380:2225-36New England Journal of Medicine, 2019
- Agarwal SK, DiNardo CD, Potluri J et al. Management of venetoclax-posaconazole interaction in acute myeloid leukemia patients: evaluation of dose adjustments. Clin Ther 2017;39:359-67Clinical Therapeutics, 2017
- Last updated
- 14 November 2026
What changed
- 14 November 2026 Deploy to Cloudflare on push to main