| ONDROUŠKOVÁ, Eva, Karel SOUČEK, Viktor HORVÁTH and Jan ŠMARDA. Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis. Leukemia Research. Elsevier, 2008, vol. 32, No 4, p. 599-609. ISSN 0145-2126. |
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@article{718339,
author = {Ondroušková, Eva and Souček, Karel and Horváth, Viktor and Šmarda, Jan},
article_number = {4},
keywords = {apoptosis; autophagy; programmed cell death},
language = {eng},
issn = {0145-2126},
journal = {Leukemia Research},
title = {Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis},
volume = {32},
year = {2008}
}
TY - JOUR
ID - 718339
AU - Ondroušková, Eva - Souček, Karel - Horváth, Viktor - Šmarda, Jan
PY - 2008
TI - Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis
JF - Leukemia Research
VL - 32
IS - 4
SP - 599-609
EP - 599-609
PB - Elsevier
SN - 01452126
KW - apoptosis
KW - autophagy
KW - programmed cell death
N2 - Loss of programmed cell death pathways is one of the features of malignancy that complicate the response of cancer cells to therapy. Activation of alternative death pathways offers a promising approach to enhance efficiency of cancer chemotherapy. We analysed programmed cell death pathways of v-myb-transformed BM2 monobolasts induced by arsenic trioxide, cycloheximide and camptothecin. We show that cell death is not executed by caspases but rather by alternative cell death pathways: camptothecin induces the lysosome-dependent cell death, arsenic trioxide induces autophagy, and most of cycloheximide-treated BM2 cells die by necrosis. The fact that alternative cell death pathways can be switched in cells with defects in activation and/or function of caspases suggests that understanding and targeting of these pathways could improve therapy on cancer cells suffering from defective apoptosis.
ER -
ONDROUŠKOVÁ, Eva, Karel SOUČEK, Viktor HORVÁTH and Jan ŠMARDA. Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis. \textit{Leukemia Research}. Elsevier, 2008, vol.~32, No~4, p.~599-609. ISSN~0145-2126.
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