Elusive liver factor that causes pancreatic α cell hyperplasia: A review of literature  

作　　者：Run Yu Yun Zheng Matthew B Lucas Yun-Guang Tong 

机构地区：[1]Carcinoid and Neuroendocrine Tumor Center,Cedars-Sinai Medical Center [2]Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine [3]Princeton University [4]Department of Medicine, Cedars-Sinai Medical Center, UCLA School of Medicine [5]Department of Pathology,Xinxiang Medical University

出　　处：《World Journal of Gastrointestinal Pathophysiology》2015年第4期131-139,共9页世界胃肠病理生理学杂志（英文版）（电子版）

基　　金：Supported by National Cancer Institute of the National Institutes of Health,No.R00CA138914(YT);National Natural Science Foundation,No.81372216(YT)

摘　　要：Tumors and cancers of the gastrointestinal tract and pancreas are commonly derived from precursor lesions so that understanding the physiological, cellular, and molecular mechanisms underlying the pathogenesis of precursor lesions is critical for the prevention and treatment of those neoplasms. Pancreatic neuroendocrine tumors(PNETs) can also be derived from precursor lesions. Pancreatic α cell hyperplasia(ACH), a specific and overwhelming increase in the number of α cells, is a precursor lesion leading to PNET pathogenesis. One of the 3 subtypes of ACH, reactive ACH is caused by glucagon signaling disruption and invariably evolves into PNETs. In this article, the existing work on the mechanisms underlying reactive ACH pathogenesis is reviewed. It is clear that the liver secretes a humoral factor regulating α cell numbers but the identity of the liver factor remains elusive. Potential approaches to identify the liver factor are discussed.Tumors and cancers of the gastrointestinal tract and pancreas are commonly derived from precursor lesions so that understanding the physiological, cellular, and molecular mechanisms underlying the pathogenesis of precursor lesions is critical for the prevention and treatment of those neoplasms. Pancreatic neuroendocrine tumors(PNETs) can also be derived from precursor lesions. Pancreatic α cell hyperplasia(ACH), a specific and overwhelming increase in the number of α cells, is a precursor lesion leading to PNET pathogenesis. One of the 3 subtypes of ACH, reactive ACH is caused by glucagon signaling disruption and invariably evolves into PNETs. In this article, the existing work on the mechanisms underlying reactive ACH pathogenesis is reviewed. It is clear that the liver secretes a humoral factor regulating α cell numbers but the identity of the liver factor remains elusive. Potential approaches to identify the liver factor are discussed.

关 键 词：PANCREATIC α CELL HYPERPLASIA HUMORAL FACTOR Pancr 

分 类 号：R735.9[医药卫生—肿瘤]