作者: Omie Mills , Nelly A. Nasir , Jonathan R. Strosberg , Larry K. Kvols , Domenico Coppola
DOI: 10.1007/978-90-481-3725-1_17
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摘要: Evidence is rapidly accumulating to allow construction of a working hypothesis the pathogenesis PENs. Many studies have contributed significantly our current understanding PEN tumorigenesis and progression. We learned, mainly through study β-cell regulation, that neogenesis transdifferentiation, replication, hypertrophy, apoptosis work together control endocrine cell mass. However, pluripotent stem cells thought play role in transdifferentiation aree yet be discovered. Studies found many same mechanisms operate during pancreatic development embryo, also regulate mass adults. One could imagine how deregulation these processes lead oncogenesis. All are steered by regulators such as glucose, c-Myc, P13K-AKT/PKB, PDX-1, Ngn-3, others. members complex molecular pathways been implicated Genetic syndromes, which include PENs one their components, for identification genes associated with genesis PENs, including MEN1 gene, vHL NF-1 TSC1 TSC2 genes. Advanced testing, currently making it more feasible pursue newer lines genetic unravel an increasing number chromosomal aberrations Multiple alterations, involving migratory, cycle, angiogenic functions, promote development, growth, invasion, metastases. As result studies, phase III trials novel therapies targeting mTOR, VEGF other targets progress. Focused investigation various mediators/mechanisms will contribute diagnostic, therapeutic, preventive stratagies, well facilitate prognostic predictive markers, while continuing advance