title: Kras, Pten, NF-κB, and inflammation: dangerous liaisons.
abstract: Ying and colleagues identify a novel function of Pten as a haploinsufficient tumor suppressor in human pancreatic cancer development. Genomic, genetic, and biochemical data reveal that Pten loss and Kras mutation cooperate to accelerate pancreatic cancer development by altering PI3K regulation to enhance NF-κB activation and upregulate downstream cytokine genes; this provides a protumorigenic and metastatic microenvironment.
authors.affiliation: Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA. pjchiao@mdanderson.org
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Chiao
authors.forename: Jianhua
authors.initials: J
authors.lastname: Ling
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics*; D000818:Animals; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics*; D016207:Cytokines / Q000235:genetics*; D006801:Humans; D016328:NF-kappa B / Q000235:genetics*; D051059:PTEN Phosphohydrolase / Q000235:genetics*; D010190:Pancreatic Neoplasms / Q000235:genetics*
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human; C487757:Pten protein, mouse