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Bcl-2: an antidote to programmed cell death.

S J Korsmeyer1

  • 1Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, Missouri 63110.

Cancer Surveys
|January 1, 1992
PubMed
Summary

The bcl-2 gene acts as a novel oncogene by regulating programmed cell death, not cell proliferation. Overexpression of bcl-2 in transgenic mice leads to extended cell survival and tumor development, highlighting its role in cancer.

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Area of Science:

  • Molecular biology
  • Cell biology
  • Oncology

Background:

  • Cellular homeostasis relies on a balance between proliferation and cell death.
  • Neoplasia involves dysregulation of cell growth regulators.
  • The bcl-2 gene was identified at the t(14;18) breakpoint in B cell lymphomas.

Purpose of the Study:

  • To investigate the role of the bcl-2 gene as a regulator of programmed cell death.
  • To explore the function of bcl-2 in B cell lymphomas and normal tissues.
  • To examine the impact of bcl-2 overexpression on cell survival, immune responses, and tumor development.

Main Methods:

  • Identification of the bcl-2 gene at a chromosomal breakpoint.
  • Localization studies of Bcl-2 protein to mitochondria.
  • Generation and analysis of transgenic mice overexpressing bcl-2 in B cell lineage and thymus.

Main Results:

  • Bcl-2 blocks programmed cell death and is localized to mitochondria.
  • Bcl-2 is expressed in progenitor and long-lived cells, and in surviving B cells in germinal centers and thymocytes.
  • Overexpression of bcl-2 in transgenic mice resulted in extended cell survival, prolonged immune responses, B cell memory, and tumor development.

Conclusions:

  • Bcl-2 represents a new category of oncogenes that regulate programmed cell death.
  • Alterations in bcl-2 and other cell death regulatory genes are crucial in neoplasia.
  • Interference with programmed cell death by oncogenes like bcl-2 can promote tumor formation by increasing cell lifespan and opportunities for genetic aberrations.

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