Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-46231
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.
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.
73 downloads since deposited on 18 Feb 2011
14 downloads since 12 months
|Referees:||Fink D, Fedier A|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Clinic for Gynecology|
|Dewey Decimal Classification:||610 Medicine & health|
|Deposited On:||18 Feb 2011 15:43|
|Last Modified:||19 Oct 2013 09:23|
|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|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page