Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma

Article Abstract:

The cooperative interactions of two signature mutations in mice engineered to sustain pancreas-specific Cre-mediated activation of a mutant Kras allele (Kras (super G12D) and depletion of a conditional Ink4a/Arf tumor suppressor allele is assessed. The phenotypic impact of Kras (super G12D) alone was limited primarily to the development of focal premalignant ductal lesions, termed pancreatic intraepithelial neoplasias (PanINs), whereas the sole inactivation of Ink4a/Arf failed to produce any neoplastic lesions in the pancreas.

Diseases, Adenocarcinoma, Death of, Pancreatic duct

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Smad4 is dispensable for normal pancreas development yet critical in progression and tumour biology of pancreas cancer

Article Abstract:

Genetically engineered mice are used to determine the impact of SMAD4 deficiency on the development of the pancreas and on the initiation and/or progression of pancreatic ductal adenocarcinomas (PDAC). The results have provided genetic confirmation that SMAD4 is a PDAC tumor suppressor, functioning to block the progression of [KRAS.sup.G12D]-initiated neoplasms, whereas in a subset of advanced tumors, intact SMAD4 has facilitated epithelial-to-mesenchymal transition (EMT) and transforming growth factor-[beta]-dependent growth.

Science & research, Research, Cancer, Cancer genetics, Transforming growth factors, Structure, Report

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Genetics and biology of pancreatic ductal adenocarcinoma

Article Abstract:

Pancreatic ductal adenocarcinoma (PDAC) is found to be the fourth leading cause of cancer deaths and its fatal nature stems from its tendency to rapidly disseminate to the lymphatic system and distant organs. Genetic lesions on K-RAS oncogene and its signalling pathway, Raf-Mapk, nuclear factor [kappa]B and other genes may lead to cancer and pancreas is the main targeted organ.

Causes of, Risk factors, Carcinoma, Ductal, Ductal carcinoma

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