Pancreatic cancer biology and genetics

By N. Bardeesy, R. DePinho. Nature Reviews. Cancer, 2002

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Tumor-stroma interactions in pancreatic ductal adenocarcinoma (2007, background): “nents, a phenomenon known as ‘desmoplasia’ that seems to promote tumor growth and invasion (67).”
Hedgehog signalling in cancer formation and maintenance (2003, background): “These findings are particularly important, as both SCLC and pancreatic adenocarcinoma are highly aggressive tumours with poor prognosi”
Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development (2011, background): “Genome-wide telomere attrition in somatic cells, for example, may generate naked DNA ends that act as a nidus for on-going genomic rearrangement (Bardeesy and DePinho, 2002; O’Hagan et al., 2002; Sahin and Depinho, 2010).”
Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “The cell-of-origin question is complicated by the developmental plasticity of the pancreas that enables transdifferentiation between cell lineages (Sharma et al. 1999; Meszoely et al. 2001; Bardeesy and DePinho 2002).”