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Gastric cancer remains one of the leading neoplasms and currently ranks third in cancer mortality worldwide.1 Helicobacter pylori (H. pylori) infection, and the subsequent chronic inflammation that the organism induces, is a major risk factor for stomach cancer,2 along with smoking and a diet high in salt and nitrates (http://www.cancer.org/cancer/stomachcancer/detailedguide/stomach-cancer-risk-factors). Within the past several years, the focus on aetiology has shifted from epidemiology to understanding the genomic landscape that occurs during gastric transformation. Specifically, the gastric cancer genome analysis demonstrated that specific molecular signatures classify this cancer into at least four subtypes that can serve as the basis for patient stratification and precision therapies.3 ,4 Prior to whole genome analysis of gastric cancer, analysis of chromosomal abnormalities identified 17q12–21 as the site of DNA amplification in gastric cancer.5 Subsequently, El-Rifai and coworkers identified an expressed sequence tag (EST) that was one of the most frequently amplified genes at 17q12, and when sequenced corresponded to the 3′ untranslated region of the DARPP-32 (dopamine and cAMP-regulated phosphoprotein 32 000 Da) locus which encodes a phosphoprotein regulated by dopamine and cAMP.6–8 Overexpression of DARPP-32 in gastric cancer cell lines blocks fatty acid induced apoptosis, demonstrating its antiapoptotic effect.7
DARPP-32 also exists as a splice variant called t-DARPP. This truncated version of the DARPP-32 protein (168 residues) is missing …
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