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National Cancer Center Research Institute, Japan
Title: Cloning Barrett's stem cells suggests paths to initiation of a precancerous lesion

Dr. Yusuke Yamamoto completed his Ph.D. in Molecular Physiology from Waseda University, Japan in 2008. He further pursued his postdoctoral studies under the supervision of Prof. Frank McKeon and A/Prof. Wa Xian at Genome Institute of Singapore. Presently, he is working as a Senior Staff Scientist at National Cancer Center Research Institute, Japan. He has been interested in how adult stem cells maintain their stemness throughout the lifespan as well as identifying cell-of-origin in esophageal adenocarcinomas and high grade serous ovarian carcinoma, which are the most aggressive type of cancers with poor prognosis. With his outstanding research work, he has published more than 40 papers in peer-reviewed journals, including Nature and Cell and holds one US patent on ‘Nanobio device of imitative anatomy structure’ in 2010 while another one, ‘Novel Diagnosis and Therapeutic Targets for Cervical Cancer’ is in the pipeline. He has presented his various research work in 15 national and international conferences and is a member of The Molecular Biology Society of Japan, Japanese Cancer Association and The Japanese Biochemical Society.


Stem cell populations of columnar epithelia collectively resist cloning in their immature states. By modifying the culture technique for human intestinal stem cells, we have cultured the stem cells from precancerous lesion known as Barretts esophagus which is intestinal metaplasia, emerged from a squamocolumnar junction and would eventually evolve to esophageal adenocarcinoma. Here we report the isolation and propagation of distinct, patient-matched stem cells of Barrett's, gastric and esophageal epithelia that yield divergent tumor types following in vitro transformation and xenografting. Exome-seq revealed a broad mutational spectrum unique to Barrett's stem cells that likely reflect the risk for oncogenesis. Remarkably, 25% of cases show no cancer-related genomic changes, suggesting that Barrett's initiates without driver mutations. Most cases, however, sustain patterns of deletions almost identical to adenocarcinoma. Notably, those suspected of low-grade dysplasia have p53 mutations or undergo amplifications of proto-oncogenes and receptor tyrosine kinases, implicating these events in lethal transitions. Our findings suggest paths for the initiation and progression of Barrett's esophagus and define a discrete stem cell underlying its regenerative growth whose eradication could prevent esophageal adenocarcinoma.

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