J Lung Cancer.  2008 Dec;7(2):59-64. 10.6058/jlc.2008.7.2.59.

Alterations of the Apoptosis Genes and Their Products in Non-small Cell Lung Cancer Tissues

Affiliations
  • 1Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea. suhulee@catholic.ac.kr

Abstract

Apoptosis is a principal type of cell death, and it has a profound effect on the development of cancer. It is also well known that anti-cancer agents induce apoptosis, and defects in the apoptosis pathways reduce the treatment sensitivity. Of the many pathways that induce apoptosis, the mechanisms of the intrinsic and extrinsic apoptosis pathways are well established. Non-small cell lung cancer (NSCLC) is a leading cause of cancer death worldwide, yet the exact molecular mechanisms of its development remain unclear. Apoptosis deregulations may underlie the development and pathogenesis of NSCLC. This review discusses the general mechanisms of apoptosis, the constituents of the apoptosis machinery and the alterations of the apoptosis-related genes in NSCLC

Keyword

Non-small cell lung cancer; Apoptosis; Mutation; Expression

MeSH Terms

Apoptosis
Carcinoma, Non-Small-Cell Lung
Cell Death

Figure

  • Fig. 1. Current classification of cell death. Cell death can be categorized into programmed cell death and necrosis. The programmed cell death is further classified into type I (apoptosis) and type II (autophagy) programmed cell death. The interconnection of apoptosis, autophagy and necrosis remains unclear.

  • Fig. 2. Two apoptosis pathways. Apoptosis pathways are largely categorized in two pathways: the intrinsic and extrinsic pathways. The extrinsic apoptosis is initiated with activation of death receptors, while the intrinsic pathway is initiated from mitochondria. Initiator caspases in each pathway relay the apoptosis signal to effector caspases that eventually kill the cells.


Reference

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