Literature DB >> 18789222

[Histone deacetylases: a new class of efficient anti-tumor drugs].

Denis Mottet1, Vincent Castronovo.   

Abstract

Circa twenty-five years ago, cancer research was dominated by the concept that the origin of cancer was genetic. Thousands of genetic alterations have indeed been identified involving more than hundred different genes in cancer development. Today, the model has evolved: it has been demonstrated that malignancies can be initiated not only through genetic alterations but also through epigenetic deregulations. By altering the expression of gene involved in cell regulation, epigenetic alterations, such as histone acetylation, play a key role in the initiation and progression of neoplasm. It has been shown that an imbalance between the acelylated and deacetylated status of chromatin is significantly involved in the acquisition of a malignant phenotype. Thus, the modulation of the histone acetylation level by histone deacetylase (HDAC) inhibitors could lead to a genetic re-programmation in cancer cells that would favor apoptosis and prevent proliferation. The potential therapeutic value of several HDAC inhibitors for cancer patients has been evaluated in clinical assays with very promising outcome. Indeed, the first inhibitors available for patients has been recently approved for cancer patients tracing the way for a new class of promising anti-cancer therapy modalities.

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Year:  2008        PMID: 18789222     DOI: 10.1051/medsci/20082489742

Source DB:  PubMed          Journal:  Med Sci (Paris)        ISSN: 0767-0974            Impact factor:   0.818


  1 in total

1.  HDAC5 promotes colorectal cancer cell proliferation by up-regulating DLL4 expression.

Authors:  Ping He; Jiexiong Liang; Tiansong Shao; Yang Guo; Yingchen Hou; Yang Li
Journal:  Int J Clin Exp Med       Date:  2015-04-15
  1 in total

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