Breast cancer epigenetics:
editDNA methylation and histone modifications are the most commonly observed epigenetic factors that favour most cancer types. Histone modifications, miRNA expression to modify genetic matter, and DNA methylation are the most common forms of epigenetic alterations in chromatin. DNA methylation is the addition of a methyl group to the cytosine at CpG or CG dinucleotides. This is often seen in regions of DNA that have a higher frequency of CpG dinucleotides and in CpG islands. CpG islands are short DNA sequences which are usually non-methylated and favor transcription.[1] Methylation of CpG islands by DNA methyltransferases can repress transcription. DNMT1 helps to maintain methylation during replication. DNMT3A and 3B are involved in de-novo methylation.
As indicated, hypomethylation often causes overexpression of certain genes that favor tumorigenesis. Hypermethylation often favors gene silencing, mainly to silence tumor suppressor genes.[2]
- ^ Esteller, M (2011-11-16). "Epigenetics of breast cancer". Breast Cancer Research. 13 (S2). doi:10.1186/bcr3004. ISSN 1465-542X.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Chik, Flora; Szyf, Moshe (2010-10-27). "Effects of specific DNMT gene depletion on cancer cell transformation and breast cancer cell invasion; toward selective DNMT inhibitors". Carcinogenesis. 32 (2): 224–232. doi:10.1093/carcin/bgq221. ISSN 1460-2180.