Literature DB >> 23351455

[Targeted epigenetic therapy of cancer. Achievements and perspectives].

Víctor Manuel Valdespino-Gómez1, Víctor Edmundo Valdespino-Castillo.   

Abstract

In this review, we provide an overview of the physiological and pathophysiological epigenetic changes of normal cells and cancer cells, and emphasize the achievements and the perspectives of cancer epigenetic therapy. Cancer epigenetic alterations correspond foremost to hypermethylation of tumor suppressor genes promotors, global DNA hypomethylation, and overexpression and activity of histone deacetylases. The purpose of epigenetic therapy is to revert the epigenetic alterations in cancer cells and obtain the "normal epigenome" restoration. Epigenetic targets in cancer therapy have focused on HDACs and DNMTs inhibition. The azacitidine and the decitabine, the vorinostat and the romidepsin were approved by US-FDA for treatment of myelodysplastic syndrome, and cutaneous T-cell lymphoma, respectively. Epigenetic and epigenomic changes in single or multiple genes have showed potential impact in cancer as early detection, prognosis and predictive marks. The epigenetic revolution has arrived for biology. The significant progress in epigenetic studies have allowed us, to understand new looks in the physiology and pathophysiology of embryonic development, cancer and other chronic diseases. Specific molecular epigenetic alterations in different cancer types, give us new strategies to design improved cancer therapy. The challenge for epigenetic investigators is design more specific epidrugs with lesser side effects.

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Year:  2012        PMID: 23351455

Source DB:  PubMed          Journal:  Cir Cir        ISSN: 0009-7411            Impact factor:   0.361


  2 in total

1.  Downregulation of HO-1 promoted apoptosis induced by decitabine via increasing p15INK4B promoter demethylation in myelodysplastic syndrome.

Authors:  D Ma; Q Fang; P Wang; R Gao; J Sun; Y Li; X Y Hu; J S Wang
Journal:  Gene Ther       Date:  2015-02-05       Impact factor: 5.250

2.  Targeting the SIN3A-PF1 interaction inhibits epithelial to mesenchymal transition and maintenance of a stem cell phenotype in triple negative breast cancer.

Authors:  Nidhi Bansal; Kevin Petrie; Rossitza Christova; Chi-Yeh Chung; Boris A Leibovitch; Louise Howell; Veronica Gil; Yordan Sbirkov; EunJee Lee; Joanna Wexler; Edgardo V Ariztia; Rajal Sharma; Jun Zhu; Emily Bernstein; Ming-Ming Zhou; Arthur Zelent; Eduardo Farias; Samuel Waxman
Journal:  Oncotarget       Date:  2015-10-27
  2 in total

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