Deciphering the cancer imprintome | Zendy

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Deciphering the cancer imprintome

Author(s) -

David Monk

Publication year - 2010

Publication title -

briefings in functional genomics

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.22

H-Index - 67

eISSN - 2041-2647

pISSN - 2041-2649

DOI - 10.1093/bfgp/elq013

Subject(s) - epigenetics , biology , genomic imprinting , cancer epigenetics , dna methylation , carcinogenesis , genetics , histone , epigenomics , epigenetic regulation of neurogenesis , cancer , gene , computational biology , gene expression , histone methyltransferase

Genetic events alone cannot explain the entire process of carcinogenesis. It is estimated that there are more epigenetic alterations in cancer than DNA mutations, and disiphering driver and secondary events is essential to understand early processes of tumorigenesis. Epigenetic modifications control gene activity, governing whether a gene is transcribed or silent. In cancer, global patterns of two epigenetic marks, histone modifications and DNA methylation, are known to be extensively deregulated. Tumour cells are also characterized by loss-of-imprinting, a key epigenetic developmental mechanism. Genomic imprinting is the parent-of-origin, monoallelic expression of genes and is controlled by differentially DNA-methylated regions and allelic-histone modifications. With specific emphasis on imprinted loci this review will discuss alterations in DNA methylation and histone modifications in cancer. The recent advances in technology that might facilitate the identification and characterization of the epigenetic profiles of cancer will also be described.

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