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Annals of Oncology Advance Access published online on June 10, 2009
Annals of Oncology, doi:10.1093/annonc/mdn792
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© The Author 2009. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

review

HDAC inhibitor-based therapies and haematological malignancy

L. Stimson, V. Wood, O. Khan, S. Fotheringham and N. B. La Thangue*

Laboratory of Cancer Biology, Department of Clinical Pharmacology, University of Oxford, Oxford, UK

* Correspondence to: Prof. N. B. La Thangue; Laboratory of Cancer Biology, Department of Clinical Pharmacology, Old Road Campus Research Building, Old Road Campus, Oxford OX3 7DQ, UK. Tel: +44-1865-617090; Fax: +44-1865-617092; E-mail: nick.lathangue{at}ndcls.ox.ac.uk

Reversible acetylation mediated by histone deacetylase (HDAC) influences a broad repertoire of physiological processes, many of which are aberrantly controlled in tumour cells. Since HDAC inhibition prompts tumour cells to enter apoptosis, small-molecule HDAC inhibitors have been developed as a new class of mechanism-based anticancer agent, many of which have entered clinical trials. While the clinical picture is evolving and the precise utility of HDAC inhibitors remains to be determined, it is noteworthy that certain tumour types undergo a favourable response, in particular haematological malignancies. Vorinostat (suberoylanilide hydroxamic acid) has been approved for treating cutaneous T-cell lymphoma in patients with progressive, persistent or recurrent disease. Here, we discuss developments in our understanding of molecular events that underlie the anticancer effects of HDAC inhibitors and relate this information to the emerging clinical picture for the application of HDAC inhibitors in haematological malignancies.

cancer, clinical, haematological malignancy, HDAC, inhibitor, therapy

Received for publication October 2, 2008. Revision received December 18, 2008. Accepted for publication December 19, 2008.


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