Epigenetics & Cancer Genomics

The field of cancer epigenetics is evolving rapidly on several fronts. Advances in our understanding of chromatin structure, histone modification, transcriptional activity and DNA methylation have resulted in an increasingly integrated view of epigenetics. In response to these insights, epigenetic therapy is expanding to include combinations of histone deacetylase inhibitors and DNA methyltransferase inhibitors. Zebularine, an orally administerable DNA methyltransferase inhibitor, has been a very promising recent addition to our arsenal of potentially useful drugs for epigenetic therapy. Epigenetics refers to alternate phenotypic states that are not based in differences in genotype, and are potentially reversible, but are generally stably maintained during cell division. The narrow interpretation of this concept is that of stable differential states of gene expression. 

The potential reversibility of epigenetic states offers exciting opportunities for novel cancer drugs that can reactivate epigenetically silenced tumor-suppressor genes. Epigenetic changes in cancer cells not only provide novel targets for drug therapy but also offer unique prospects for cancer diagnostics  The major interest in cancer epigenetics as a diagnostic tool is in localized epigenetic silencing. It is clear from this bird's-eye overview that the field of cancer epigeneticsis in flux. We can expect to see clinical implementation of both epigeneticcancer therapy and epigenetic cancer diagnostics in the next decade. Epigenetic control defects in cancer cells represent an emerging new area of investigation, where significant breakthroughs in the identification of the underlying molecular defects are anticipated in the next few years.

International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016, Birmingham, UK; Biotechnology World Convention, Aug 15-17, 2016, Sao Paulo, Brazil; International Conference on Synthetic Biology, Aug 18-19, 2016, London, UK, Annual Conference on Bio Science, Sept 12-13, 2016, Berlin, Germany; Noncoding RNAs in Health and Disease, February 21-24, 2016, Santa Fe, USA; Maintenance of Genome Stability March 7- 10, 2016, Panama, South America; Chromatin and Epigenetics, March 20-24, 2016 Whistler, Canada; Chromatin, Non-Coding RNAs and RNAP II Regulation in Development and Disease, March 29, 2016, Austin, USA; Chromatin Structure & Function, May 22-27, 2016, Les Diablerets, Switzerland

Epigenetic mechanisms act to change the accessibility of chromatin to transcriptional regulation locally and globally via modifications of the DNA and by modification or rearrangement of nucleosomes. Epigenetic gene regulation collaborates with genetic alterations in cancer development. This is evident from every aspect of tumour biology including cell growth and differentiation, cell cycle control, DNA repair, angiogenesis, migration, and evasion of host immunosurveillance. In contrast to genetic cancer causes, the possibility of reversing epigenetic codes may provide new targets for therapeutic intervention

Epigenetic programming is crucial in mammalian development, and stable inheritance of epigenetic settings is essential for the maintenance of tissue- and cell-type-specific functions. With the exception of controlled genomic rearrangements, such as those of the immunoglobulin and T-cell receptor genes in B and T cells, all other differentiation processes are initiated or maintained through epigenetic processes. Not surprisingly therefore, epigenetic gene regulation is characterized overall by a high degree of integrity and stability. 

  • Gene expression and epigenomics
  • Genes silencing
  • Cancer epigenetics
  • Cancer cells and genetic mutations
  • Cell based immunotherapy
  • Stem cell therapy for infectious diseases
  • Cell based immunosuppression in transplantation
  • Epigenetics of the antibody response
  • Epigenetic DNA repair and cancer

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