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Genome‐Wide Analysis of Epigenetics in Cancer
Author(s) -
LEE MAXWELL P.
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2003.tb05965.x
Subject(s) - epigenetics , biology , genome , human genome , gene , genetics , dna methylation , computational biology , chromatin , cpg site , gene expression
A bstract : Human cancers are caused by multiple mechanisms. Research in the last 30 years has firmly established the roles of a group of genes including oncogenes, tumor suppressor genes, and DNA repair genes in human cancers. The activation and inactivation of these cancer genes can be caused by genetic mutations or epigenetic alterations. The epigenetic changes in cancers include methylation of CpG islands, loss of imprinting, and chromatin modification. The completion of the genome sequences of many organisms including the human has transformed the traditional approach to molecular biology research into an era of functional genome research. Traditional research usually involves the study of one or a few genes (proteins) in a particular biological process in normal physiology or disease. Functional genome research takes advantage of newly available genome sequences and high‐throughput genome technologies to study genes and/or proteins to inform the perspective of entire biological processes. I will focus on recent progress in the identification of imprinted genes and methylation of CpG islands through genome‐wide analysis.