Literature DB >> 19515748

HDAC inhibitor-based therapies and haematological malignancy.

L Stimson1, V Wood, O Khan, S Fotheringham, N B La Thangue.   

Abstract

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.

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Year:  2009        PMID: 19515748     DOI: 10.1093/annonc/mdn792

Source DB:  PubMed          Journal:  Ann Oncol        ISSN: 0923-7534            Impact factor:   32.976


  50 in total

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2.  Combination of HDAC and topoisomerase inhibitors in small cell lung cancer.

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3.  Smoking induces epithelial-to-mesenchymal transition in non-small cell lung cancer through HDAC-mediated downregulation of E-cadherin.

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4.  HDAC isoenzyme expression is deregulated in chronic lymphocytic leukemia B-cells and has a complex prognostic significance.

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Journal:  Epigenetics       Date:  2012-10-29       Impact factor: 4.528

5.  Phase 2 study of panobinostat with or without rituximab in relapsed diffuse large B-cell lymphoma.

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Review 6.  The emerging role of lysine acetylation of non-nuclear proteins.

Authors:  Pierre Close; Catherine Creppe; Magali Gillard; Aurélie Ladang; Jean-Paul Chapelle; Laurent Nguyen; Alain Chariot
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7.  The novel deacetylase inhibitor AR-42 demonstrates pre-clinical activity in B-cell malignancies in vitro and in vivo.

Authors:  David M Lucas; Lapo Alinari; Derek A West; Melanie E Davis; Ryan B Edwards; Amy J Johnson; Kristie A Blum; Craig C Hofmeister; Michael A Freitas; Mark R Parthun; Dasheng Wang; Amy Lehman; Xiaoli Zhang; David Jarjoura; Samuel K Kulp; Carlo M Croce; Michael R Grever; Ching-Shih Chen; Robert A Baiocchi; John C Byrd
Journal:  PLoS One       Date:  2010-06-03       Impact factor: 3.240

8.  Inhibition of histone deacetylases.

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Journal:  Methods Mol Biol       Date:  2004

9.  Epstein-Barr virus-induced epigenetic alterations following transient infection.

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10.  A regulatory circuit that involves HR23B and HDAC6 governs the biological response to HDAC inhibitors.

Authors:  M New; H Olzscha; G Liu; O Khan; L Stimson; J McGouran; D Kerr; A Coutts; B Kessler; M Middleton; N B La Thangue
Journal:  Cell Death Differ       Date:  2013-05-24       Impact factor: 15.828

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