Research ArticleGastric cancer

Methylation Subtypes and Large-Scale Epigenetic Alterations in Gastric Cancer

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Science Translational Medicine  17 Oct 2012:
Vol. 4, Issue 156, pp. 156ra140
DOI: 10.1126/scitranslmed.3004504

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The Silent Treatment of Gastric Cancer

A new study by Zouridis and colleagues refutes the old adage that “silence is golden”—at least in the realm of gene methylation and epigenetic silencing in cancer. To decipher the effects of “silence” on gastric cancer, the authors analyzed gene methylation patterns in 240 gastric tumors and compared them to those of 94 matched samples of adjacent normal tissue.

Gastric cancer is one of the most common types of cancer worldwide—and one of the most deadly, with few effective treatment options available. As a possible source of therapeutic targets, scientists are searching for genetic and epigenetic alteration patterns characteristic of these tumors. Here, the authors extensively characterized methylation patterns in human gastric cancers, which revealed tumor-specific arrangements of hyper- and hypomethylation. Zouridis and colleagues also identified a subset of cancers that fell into the CpG island methylator phenotype (CIMP) subgroup, which is associated with more extensive methylation and lower chances of survival in younger patients. As a possible pharmaceutical intervention, the authors tested the effects of the demethylating drug 5-aza-2′-deoxycytidine in CIMP tumor cell lines and found that their proliferation was significantly decreased when compared with non-CIMP cell lines.

A broader analysis of gene regions that undergo modifications in cancers likely will identify new therapeutic targets and corresponding treatments. But for patients with high-risk gastric cancers that fall into the CIMP subgroup, silenced DNA is golden because it serves as a target for currently available drugs.

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