Molecular Pathogenesis and Targeted Therapy of Pancreatic Cancer
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Accumulation of multiple genetic and/or epigenetic abnormalities is required for generation and progression of cancers, and the survival of cancer cells might depend on addiction to these abnormalities. Because disruption of such dependency on the abnormal molecules should cause the cancer cell death, so-called oncogene addiction is the rationale for molecular targeted therapy. Pancreatic cancer, especially pancreatic ductal adenocarcinoma, is one of the most lethal malignancies in humans, and remains a challenging problem in targeted therapy compared to other malignancies such as pancreatic neuroendocrine tumor. This review summarizes the molecular pathogenesis of pancreatic cancer on the basis of the recent studies of driver mutations including chromatin remodeling factors, and promising concepts “cancer stemness” and “stromal niche” for the strategy of novel targeted therapy.
KeywordsPancreatic Cancer Gemcitabine Cancer Stem Cell Cetuximab Erlotinib
I sincerely appreciate the opportunity to write this review article, by the recommendation of the Japanese Society of Gastroenterological Surgery (JSGS) and the Society of Surgical Oncology. I thank all of my colleagues and collaborators at Tokyo Medical and Dental University, Osaka University, Kyushu University, Tokushima University, and Brown Medical School. This work was supported by Grant-in-Aid for Scientific Research on Innovative Areas, Scientific Research (A), Project of Development of Innovative Research on Cancer Therapeutics from Ministry of Education, Culture, Sports, Science and Technology of Japan, and Health and Labour Sciences Research Grant from Ministry of Health Labour and Welfare of Japan. I was a recipient of JSGS Award Science for the year 2013.
Conflict of interest
The author declares no conflict of interest.
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