The mTOR pathway is frequently activated in pancreatic ductal adenocarcinoma and chronic pancreatitis.

摘要: INTRODUCTION Mammalian target of rapamycin (mTOR) is a serine/threonine kinase critical to cell growth and proliferation through its effects on protein translation. Activation the phosphatidylinositol 3-kinase/Akt/mTOR pathway has been described in various tumor types. Earlier studies have demonstrated loss phosphatase tensin homolog deleted chromosome 10 (PTEN) function some pancreatic ductal adenocarcinomas (PDAs). We performed immunohistochemistry for PTEN p-RPS6 (major downstream mTOR effector) group PDAs. An assessment chronic pancreatitis (CP) normal pancreas (NL) was parallel. MATERIALS AND METHODS Tissue microarrays were constructed from 49 PDA, 27 CP, 12 NL. Cases scored as follows: (intact: ≥ 5% staining lost: < 5%) (0, 1+: modest intensity cells 2+: strong cells). RESULTS Forty-one percent PDAs PTEN, 75% immunoreactivity (1+ 22 2+ 3). uniformly intact NL CP. Although only noted 1 control (8%), 1+ positivity observed 62% CONCLUSIONS activation, evidenced by immunoreactivity, frequent PDA. expression also highlighting importance this both neoplastic inflammatory processes. Given evidence activation existence specific anti-mTOR therapeutics, represents logical directed biologic therapy.