Intrinsic and extrinsic pathways of apoptosis: Role in cancer development and prognosis

Adv Protein Chem Struct Biol. 2021:125:73-120. doi: 10.1016/bs.apcsb.2021.01.003. Epub 2021 Apr 15.

Abstract

Apoptosis, also named programmed cell death, is a fundament process required for morphogenetic homeostasis during early development and in pathophysiological conditions. It is come into existence in 1972 by work of Kerr, Wyllie and Currie and later on investigated during the research on development of the C. elegans. Trigger by several stimuli, apoptosis is necessary during the embryonic development and aging as homeostatic mechanism to control the cell population and also play a key role as defense mechanism against the immune responses and elimination of damaged cells. Cancer, a genetic disease, is a growing burden on the health and economy of both developing and developed countries. Every year there is tremendously increasing in the number of new cancer cases and mortality rate. Although, there is a significant improvement have been made in biotechnological and bioinformatic fields however, the therapeutic advantages and cancer etiology is still under explored. Several studies determined the deregulation of different apoptotic components during the cancer development and progression. Apoptosis relies on activation of distinct signaling pathways that are often deregulated in cancer. Thus, exploring the single or more than one apoptotic component underlying their expression in carcinogenesis could help to track the disease progression. Current book chapter will provide the several evidences supporting the use of different apoptotic components as prognosis and prediction markers in various human cancer types.

Keywords: Apoptosis; Cancer; Execution pathway; Extrinsic pathway; Intrinsic pathway; Prognosis.

Publication types

  • Review

MeSH terms

  • Apoptosis* / genetics
  • Apoptosis* / immunology
  • Carcinogenesis* / genetics
  • Carcinogenesis* / immunology
  • Humans
  • Neoplasms* / diagnosis
  • Neoplasms* / genetics
  • Neoplasms* / immunology
  • Prognosis
  • Signal Transduction* / genetics
  • Signal Transduction* / immunology