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Acquired vorinostat resistance shows partial cross-resistance to "second-generation" HDAC inhibitors and correlates with loss of histone acetylation and apoptosis but not with altered HDAC and HAT activities


Dedes, J. Acquired vorinostat resistance shows partial cross-resistance to "second-generation" HDAC inhibitors and correlates with loss of histone acetylation and apoptosis but not with altered HDAC and HAT activities. 2010, University of Zurich, Faculty of Medicine.

Abstract

Histonedeacetylase(HDAC)inhibitors such as vorinostat (suberoylanilide hydroxamicacid), valproicacid,romidepsin (FK-228), and LBH589 comprise a relatively new class of potentanti canceragents. This study provides evidence for the potential of vorinostat to cause acquisition of multi drug resistance protein-independent resistance in HCT116 colon tumor cells. This acquired resistance is moderate(two-foldtothree-fold), is non-reversible, and correlates with the loss of responses typically seen with HDAC-inhibitors, that is the loss of acetylation of thehistones H2A, H2B, H3, and H4, the loss of the G2/M checkpoint activation, and the loss of caspase 3-dependent and caspase 7-dependent apoptosis. This acquired resistance also associates with cross-resistance to the hydroxamate-class(LBH589 and JNJ26481585)and to the aliphaticacid-class(valproicacid)HDAC inhibitors but not tothebenzamide-class(MGCD0103)and the cyclic peptide-class(romidepsin) HDAC inhibitors. The acquired HDAC inhibitor resistance described here.

Histonedeacetylase(HDAC)inhibitors such as vorinostat (suberoylanilide hydroxamicacid), valproicacid,romidepsin (FK-228), and LBH589 comprise a relatively new class of potentanti canceragents. This study provides evidence for the potential of vorinostat to cause acquisition of multi drug resistance protein-independent resistance in HCT116 colon tumor cells. This acquired resistance is moderate(two-foldtothree-fold), is non-reversible, and correlates with the loss of responses typically seen with HDAC-inhibitors, that is the loss of acetylation of thehistones H2A, H2B, H3, and H4, the loss of the G2/M checkpoint activation, and the loss of caspase 3-dependent and caspase 7-dependent apoptosis. This acquired resistance also associates with cross-resistance to the hydroxamate-class(LBH589 and JNJ26481585)and to the aliphaticacid-class(valproicacid)HDAC inhibitors but not tothebenzamide-class(MGCD0103)and the cyclic peptide-class(romidepsin) HDAC inhibitors. The acquired HDAC inhibitor resistance described here.

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Additional indexing

Item Type:Dissertation
Referees:Fink D, Fedier A
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Gynecology
Dewey Decimal Classification:610 Medicine & health
Language:German
Date:2010
Deposited On:18 Feb 2011 15:43
Last Modified:05 Apr 2016 14:48
Number of Pages:17
Additional Information:Acquired vorinostat resistance shows partial cross-resistance to "second-generation" HDAC inhibitors and correlates with loss of histone acetylation and apoptosis but not with altered HDAC and HAT activities / vorgelegt von Ioannis Dedes. - Zürich, 2009
Related URLs:http://opac.nebis.ch/F/?local_base=NEBIS&con_lng=GER&func=find-b&find_code=SYS&request=006217249
Permanent URL: https://doi.org/10.5167/uzh-46231

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