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Molecular biology of pancreatic cancer

World Journal of Gastroenterology 2011年第24期17卷 2897-2908页

作者： Miroslav Zavoral Petra Minarikova Filip Zavada cyril salek Marek Minarik Charles University 1st Medical FacultyInternal Clinic Institute of hematology and blood transfusion Center for Applied Genomics of Solid Tumors(CEGES) Genomac International

In spite of continuous research efforts directed at early detection and treatment of pancreatic cancer, the outlook for patients affected by the disease remains dismal. With most cases still being diagnosed at advanced stages, no improvement in survival prognosis is achieved with current diagnostic imaging approaches. In the absence of a dominant precancerous condition, several risk factors have been identified including family history, chronic pancreatitis, smoking, diabetes mellitus, as well as certain genetic disorders such as hereditary pancreatitis, cystic fibrosis, familial atypical multiple mole melanoma, and Peutz-Jeghers and Lynch syn- dromes. Most pancreatic carcinomas, however, remain sporadic. Current progress in experimental molecular techniques has enabled detailed understanding of the molecular processes of pancreatic cancer development. According to the latest information, malignant pancre- atic transformation involves multiple oncogenes and tumor-suppressor genes that are involved in a variety of signaling pathways. The most characteristic aberrations （somatic point mutations and allelic losses） affect onco- genes and tumor-suppressor genes within RAS, AK-I- and Wnt signaling, and have a key role in transcription and proliferation, as well as systems that regulate the cell cycle （SMAD/DPC, CDKN2A/p16） and apoptosis （TP53）. Understanding of the underlying molecular mechanisms should promote development of new methodology for early diagnosis and facilitate improvement in current approaches for pancreatic cancer treatment.

关键词： Pancreatic cancer Risk factors Molecularbiology Pancreatitis Diabetes

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