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Acute changes in U937 nuclear Ca2+ preceding type 1 "apoptotic" programmed cell death due to MK 886

K M Anderson1, M Rubenstein, W A Alrefai

  • 1Hektoen Institute, Department of Biochemistry, Rush University Medical Center, University of Illinois and West Side V.A. Chicago, IL 60612, USA. marander427@MSN.com

Anticancer Research
|November 3, 2004
PubMed
Summary

MK 886, a 5-lipoxygenase inhibitor, triggers programmed cell death by increasing reactive oxygen species and nuclear calcium in U937 cells. This mechanism, involving mitochondria and Bcl-2, differs in solid cancer cells.

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