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   <subfield code="a">The role of the mitochondria in mediating cytotoxicity of anti-cancer therapies</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Dao Nguyen, Mustafa Hussain]</subfield>
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   <subfield code="a">Optimal cytotoxic anticancer therapy, at the cellular level, requires effective and selective induction of cell death to achieve a net reduction of biomass of malignant tissues. Standard cytotoxic chemotherapeutics have been developed based on the observations that mitotically active cancer cells are more susceptible than quiescent normal cells to chromosomal, microtubular or metabolic poisons. More recent development of molecularly targeted drugs for cancer focuses on exploiting biological differentials between normal and transformed cells for selective eradication of cancers. The common thread of &quot;standard” and &quot;novel” cytotoxic drugs is their ability to activate the apoptosis-inducing machinery mediated by mitochondria, also known as the intrinsic death signaling cascade. The aim of this article is to provide an overview of the role of the mitochondria, an energy-generating organelle essential for life, in mediating death when properly activated by cytotoxic stresses.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2007</subfield>
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   <subfield code="a">Mitochondria</subfield>
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   <subfield code="a">Bcl2 superfamily</subfield>
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   <subfield code="a">Bax : Bcl2-associated X protein</subfield>
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   <subfield code="a">Bak : Bcl2-antagonist/killer</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Bcl2 : B cell lymphoma protein 2</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Bid : Bcl2 inhibitory domain</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Bad : Bcl2 antagonist of cell death</subfield>
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   <subfield code="a">Bim : Bcl2-interacting mediator of cell death</subfield>
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   <subfield code="a">Omni/HtrA2 : high temperature requirement protein A2</subfield>
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   <subfield code="a">Puma/Bbc3 : p53-upregulated modulator of apoptosis/Bcl2-binding component 3</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Smac/Diablo : second mitochondria derived activator of caspases/direct inhibitor of apoptosis binding protein with low isoelectric point</subfield>
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   <subfield code="a">TRAIL : Tumor necrosis factor related apoptosis inducing ligand</subfield>
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   <subfield code="a">MOMP : mitochondria outer membrane permeability</subfield>
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   <subfield code="a">JNK : Jun N-terminus kinase</subfield>
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   <subfield code="a">ANT : adenine nucleotide transporter</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">VDAC : voltage-dependent anion channel</subfield>
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   <subfield code="a">Nguyen</subfield>
   <subfield code="D">Dao</subfield>
   <subfield code="u">Section of Thoracic Oncology, Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Room 4W-4-3940, 10 Center Drive, 29892, Bethesda, MD, USA</subfield>
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