Therefore, cancer cells which divide much more rapidly than most other cells in the body will be more severely affected by decitabine just because they replicate more. In cancer cells, and more specifically in haematological malignancies, it seems that DNA hypermethylation is really critical for their development. Methylation of CpG islands upstream of tumor suppressor genes in order to silence them seems to be critical for these type of cancers. Thus at optimal doses, decitabine blocks this type of methylation and has an anti-neoplastic effect. Research
Atherosclerosis
A number of investigators have shown a relationship between atherosclerosis and disturbed blood flow. This upregulates DNA methyltransferase expression, which leads to genome-wide DNA methylation alterations and global gene expression changes. These studies have revealed several mechanosensitive genes, such as HoxA5, Klf3, and Klf4, whose promoters were hypermethylated by disturbed blood flow, but rescued by DNA methyltransferases inhibitors such as 5-aza-2-deoxycytidine. It has been found that use of this DNA methyltranferase inhibitor prevents atherosclerosis lesion formation and reduces the production of inflammatory cytokines by macrophages. References
Further reading
Moon C, Kim SH (June 2009). "Use of epigenetic modification to induce FOXP3 expression in naïve T cells". Transplant. Proc. 41 (5): 1848–1854. doi:10.1016/j.transproceed.2009.02.101. PMID 19545742. External links
"Decitabine". Drug Information Portal. U.S. National Library of Medicine.
HIV elimination
Graft-versus-host disease has been implicated in eliminating several cases of HIV, including The Berlin Patient and 6 others in Spain. See also
Graft-versus-tumor effect
Immunosuppression
Transplant rejection

References
Further reading
Ferrara JLM, Deeg HJ, Burakoff SJ. Graft-Vs.-Host Disease: Immunology, Pathophysiology, and Treatment. Marcel Dekker, 1990 ISBN 0-8247-9728-0
Polsdorfer, JR Gale Encyclopedia of Medicine: Graft-vs.-host disease


== External links ==