Sethi Vrishketan, Giri Bhuwan, Saluja Ashok, Dudeja Vikas
Department of Surgery and Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, 1120 NW 14th Street, 4th Floor, Miami, FL, 33156, USA.
Dig Dis Sci. 2017 Jul;62(7):1778-1786. doi: 10.1007/s10620-017-4603-1. Epub 2017 May 12.
With the current epidemic of diagnosed pancreatic cystic neoplasms on the rise, a substantial amount of work has been done to unravel their biology, thus leading to implications on clinical decision making. Recent genetic profiling of resected human specimens has identified alterations in signaling pathways involving KRAS and GNAS signaling as early events in the pathogenesis of intraductal pancreatic mucinous neoplasms. Progressively, mutations in genes such as TP53, SMAD4, RNF43, and others are thought to characterize invasive and advanced lesions. The role of inflammation in fueling the growth and transformation of these cysts has also begun to be studied with greater interest. A number of promising clinical studies have attempted to integrate these genetic insights into classifying these cysts and treating patients. We have reviewed existing literature on similar lines besides commenting on some useful animal models that recapitulate molecular and phenotypic progression of these cysts.
随着当前确诊的胰腺囊性肿瘤的流行趋势上升,人们已经开展了大量工作来揭示其生物学特性,从而对临床决策产生影响。最近对切除的人体标本进行的基因分析已经确定,涉及KRAS和GNAS信号传导的信号通路改变是导管内胰腺黏液性肿瘤发病机制中的早期事件。逐渐地,诸如TP53、SMAD4、RNF43等基因的突变被认为是侵袭性和晚期病变的特征。炎症在促进这些囊肿生长和转变中的作用也开始受到更多关注。一些有前景的临床研究试图将这些基因见解整合到这些囊肿的分类和患者治疗中。除了对一些重现这些囊肿分子和表型进展的有用动物模型进行评论外,我们还按照类似思路回顾了现有文献。