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Enhancing the antitumor activity of ErbB blockade with histone deacetylase (HDAC) inhibition

dc.contributor.authorChinnaiyan, Prakashen_US
dc.contributor.authorVarambally, Sooryanarayanaen_US
dc.contributor.authorTomlins, Scott A.en_US
dc.contributor.authorRay, Somaen_US
dc.contributor.authorHuang, Shyhminen_US
dc.contributor.authorChinnaiyan, Arul M.en_US
dc.contributor.authorHarari, Paul M.en_US
dc.date.accessioned2012-12-11T17:37:19Z
dc.date.available2012-12-11T17:37:19Z
dc.date.issued2006-02-15en_US
dc.identifier.citationChinnaiyan, Prakash; Varambally, Sooryanarayana; Tomlins, Scott A.; Ray, Soma; Huang, Shyhmin; Chinnaiyan, Arul M.; Harari, Paul M. (2006). "Enhancing the antitumor activity of ErbB blockade with histone deacetylase (HDAC) inhibition." International Journal of Cancer 118(4): 1041-1050. <http://hdl.handle.net/2027.42/94461>en_US
dc.identifier.issn0020-7136en_US
dc.identifier.issn1097-0215en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/94461
dc.description.abstractMolecular inhibition of the ErbB signaling pathway represents a promising cancer treatment strategy. Preclinical studies suggest that enhancement of antitumor activity can be achieved by maximizing ErbB signaling inhibition. Using cDNA microarrays, we identified histone deacetylase (HDAC) inhibitors as having strong potential to enhance the effects of anti‐ErbB agents. Studies using a 20,000 element (20K) cDNA microarray demonstrate decreased transcript expression of ErbB1 (epidermal growth factor receptor) and ErbB2 in DU145 (prostate) and ErbB2 in SKBr3 (breast) cancer cell lines. Additional changes in the DU145 gene expression profile with potential interaction to ErbB signaling include down‐regulation of caveolin‐1 and hypoxia inducible factor 1‐α (HIF1‐α), and up‐regulation of gelsolin, p19(INK4D) and Nur77. Findings were validated using real time RT‐PCR and Western blot analysis. Enhanced proliferative inhibition, apoptosis induction and signaling inhibition were demonstrated when combining HDAC inhibition with ErbB blockade. These results suggest that used cooperatively, anti‐ErbB agents and HDAC inhibitors may offer a promising strategy of dual targeted therapy. Additionally, microarray data suggest that the beneficial interaction of these agents may not derive solely from modulation of ErbB expression, but may result from effects on other oncogenic processes including angiogenesis, invasion and cell cycle kinetics. © 2005 Wiley‐Liss, Inc.en_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherEGFRen_US
dc.subject.otherSAHAen_US
dc.subject.otherErbBen_US
dc.subject.otherHDAC Inhibitoren_US
dc.titleEnhancing the antitumor activity of ErbB blockade with histone deacetylase (HDAC) inhibitionen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelOncology and Hematologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.contributor.affiliationotherDepartment of Human Oncology, University of Wisconsin Comprehensive Cancer Center, 600 Highland Avenue, Madison, WI 53792‐0600, USAen_US
dc.contributor.affiliationotherDepartment of Human Oncology, University of Wisconsin, Madison, WI, USAen_US
dc.identifier.pmid16152586en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/94461/1/21465_ftp.pdf
dc.identifier.doi10.1002/ijc.21465en_US
dc.identifier.sourceInternational Journal of Canceren_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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