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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Surviving apoptosis

A T M Vaughan1, C J Betti, M J Villalobos

  • 1Department of Radiation Oncology, Loyola University Medical Center, 2160 South First Avenue, Building 112, Maywood, Illinois 60153, USA. avaugha@lumc.edu

Apoptosis : an International Journal on Programmed Cell Death
|February 28, 2002
PubMed

Insights

Cells surviving apoptosis can still undergo DNA damage, leading to leukemogenic translocations. This challenges the notion that chromatin cleavage during apoptosis always results in cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Apoptosis involves chromatin cleavage by activated nucleases, like caspase-activated deoxyribonuclease (CAD).
  • Caspase activation and subsequent nuclease activity are not always lethal, as cells can survive transient apoptotic signaling.
  • Inhibitors of Apoptotic Programmed Cell Death Proteins (IAPs) can protect cells from nuclease-mediated damage.

Purpose of the Study:

  • To investigate the role of apoptosis-associated DNA damage in generating leukemogenic translocations.
  • To explore how cells surviving the apoptotic cascade can harbor DNA alterations.
  • To examine the MLL gene as a potential target for apoptosis-mediated translocations.

Main Methods:

  • Analysis of caspase activation and nuclease activity in cells undergoing transient apoptosis.
  • Investigation of Inhibitors of Apoptotic Programmed Cell Death Proteins (IAPs) in cell survival.
  • Identification of translocations within the MLL gene in relation to apoptotic nuclease attack.

Main Results:

  • Demonstration that cells can survive caspase activation and nuclease activity despite apoptotic morphology.
  • Identification of specific translocation breakpoints within the MLL gene at sites of apoptotic nuclease cleavage.
  • Evidence suggesting that MLL gene translocations can arise from DNA damage during a potentially survivable apoptotic event.

Conclusions:

  • Chromatin cleavage during apoptosis does not invariably lead to cell death.
  • Transient caspase activation followed by recovery can result in DNA damage and oncogenic translocations.
  • Apoptosis-mediated DNA damage, particularly in genes like MLL, represents a novel mechanism contributing to leukemogenesis.

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