Genetics and biology of pancreatic ductal adenocarcinoma.

By A. Hezel, Alec C. Kimmelman, Ben Z Stanger, N. Bardeesy, R. DePinho. Genes & Development, 2006

1,455 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7e37ee1289b148a9123d427f6db73acdf94b04ef

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Citations in the corpus

• The dynamic nature of autophagy in cancer. (2011, unknown): “Pancreatic cancers almost universally possess activating Kras mutations (Hezel et al. 2006).”
• KRAS: feeding pancreatic cancer proliferation (2014, unknown): “Molecular profiling studies have reinforced the PanIN-to-PDAC progression by demonstrating that KRAS mutation is followed by subsequent inactivation of the tumor suppressor gene CDKN2A (or INK4A/ ARF, which encodes p14/Arf and p16/INK4A), followed by inactivation of two other tumor suppressor genes ”
• KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer (2018, background): “The PTEN lipid phosphatase and tumor suppressor negatively regulates the pathway by dephosphorylating PIP3 to PIP2 and is an important tumor suppressor in PDAC (Ying et al. 2016) and PTEN loss is found commonly in cancer.”
• Tissue-penetrating delivery of compounds and nanoparticles into tumors (2009, unknown): “The difference in the distribution of payloads linked to iRGD and other RGD peptides was even more pronounced when a genetically engineered model of de novo pancreatic ductal adenocarcinoma (PDAC; Hezel et al., 2006) with an extensive amount of interstitium was used as the target (Figure S4).”
• Pancreatic cancers require autophagy for tumor growth. (2011, unknown): “…adenocarcinoma (PDAC) has a well-defined spectrum of highly recurrent oncogenic lesions—such as activation of KRAS and loss/silencing/mutation of p53 , INK4A/ARF , and SMAD4 —this information has yet to be translated into effective therapies for the disease (for review, see Hezel et al. 2006).”
• EMT and dissemination precede pancreatic tumor formation (2012, methodology): “The model relies on the Pdx1-Cre transgenic strain (Gu et al., 2003) to generate pancreas-specific mutations in Kras and p53, genes that are mutated with high frequency in human pancreatic cancers (Hezel et al., 2006).”
• A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. (2009, background): “The observed relationship between K-Ras addiction, TGFb signaling, and epithelial differentiation is particularly interesting in the context of pancreatic adenocarcinomas, which undergo frequent homozygous deletion of the TGFb signaling component Smad4 ( 50% of cases) (Hezel et al., 2006).”