Proteasome inhibitors trigger mutations via activation of caspases and CAD, but mutagenesis provoked...
Proteasome inhibitors trigger mutations via activation of caspases and CAD, but mutagenesis provoked by the HDAC inhibitors vorinostat and romidepsin is caspase/CAD-independent
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New York: Springer US
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English
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New York: Springer US
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Genotoxic anti-cancer therapies such as chemotherapy and radiotherapy can contribute to an increase in second malignancies in cancer survivors due to their oncogenic effects on non-cancerous cells. Inhibition of histone deacetylase (HDAC) proteins or the proteasome differ from chemotherapy in that they eliminate cancer cells by regulating gene expr...
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Proteasome inhibitors trigger mutations via activation of caspases and CAD, but mutagenesis provoked by the HDAC inhibitors vorinostat and romidepsin is caspase/CAD-independent
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TN_cdi_proquest_journals_2210797145
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https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_journals_2210797145
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ISSN
1360-8185
E-ISSN
1573-675X
DOI
10.1007/s10495-019-01543-x