Maitra Anirban, Hruban Ralph H
The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.
Cancer Cell. 2005 Sep;8(3):171-2. doi: 10.1016/j.ccr.2005.08.007.
PTEN (phosphatase and tensin homolog deleted on chromosome 10) is a negative regulator of the oncogenic PI3-K/Akt signaling pathway. Loss-of-function mutations of PTEN are seen in several human solid cancers. A murine model of conditional Pten inactivation in the pancreas is described that leads to acquisition of a profound metaplastic ductal phenotype accompanied by loss of differentiated acinar units. Evidence is presented for a centroacinar cell origin of the metaplastic "neoductules." These mice also develop invasive pancreatic adenocarcinomas at a low frequency, and provide a unique in vivo platform for exploring the role of PI3-K/Akt signaling in pancreatic neoplasia.
PTEN（第10号染色体缺失的磷酸酶及张力蛋白同源物）是致癌性PI3-K/Akt信号通路的负调节因子。PTEN的功能丧失性突变见于多种人类实体癌。本文描述了一种胰腺中条件性Pten失活的小鼠模型，该模型导致获得一种严重的化生导管表型，并伴有分化腺泡单位的丧失。有证据表明化生的“新导管”起源于中央腺泡细胞。这些小鼠也会以低频率发生侵袭性胰腺腺癌，并为探索PI3-K/Akt信号在胰腺肿瘤形成中的作用提供了一个独特的体内平台。
