Sunday, April 8, 2012

S'pore-based study identifies critical genes mutated in stomach cancer

SINGAPORE: An international team of scientists, led by researchers from Duke-NUS Graduate Medical School (Duke-NUS) in Singapore and the National Cancer Center Singapore (NCCS), has identified more than 600 genes that are mutated in stomach cancer, the second-most lethal cancer worldwide.

The study, which appears online on April 8, 2012 in Nature Genetics, paves the way for treatments tailored to the genetic make-up of individual stomach tumours.

Stomach cancer is the second leading cause of cancer death globally with more than 700,000 deaths each year, and is particularly common in East Asia.

Using state-of-the-art DNA sequencing technology, the research team analyzed tumour and normal tissue from stomach cancer patients, which led to the discovery of the novel gene mutations.

The study showed two of the 600 stomach cancer-associated genes identified, FAT4 and ARID1A, proved to be particularly interesting.

With more than 100,000 new cases of stomach cancer each year likely to be caused by mutations in FAT4 or ARID1A, drugs against these targets may lead to more effective treatment of stomach tumours and other cancers.

In addition to Duke-NUS and the National Cancer Center Singapore, the study also involved collaborators from the Cancer Science Institute of Singapore; Genome Institute of Singapore; National University of Singapore; Singapore General Hospital; Van Andel Research Institute, Michigan, USA; Northwestern University, Chicago, USA; Yonsei Cancer Center, Seoul, South Korea; Queen's University, Belfast, UK; and Welcome Trust Sanger Institute, Hinxton, UK.

Support for this study was provided by the National Medical Research Council (Ministry of Health, Singapore), as part of the Singapore Gastric Cancer Consortium.

Funding was also received from the Cancer Science Institute of Singapore, Duke-NUS Graduate Medical School, Genome Institute of Singapore (Agency for Science, Technology and Research), and the Lee Foundation.

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