Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse.

By N. Bardeesy, A. Aguirre, Gerald C. Chu, Kuang-Hung Cheng, L. Lopez, A. Hezel, Bin Feng, C. Brennan, Ralph Weissleder, Umar Mahmood and 4 more. Proceedings of the National Academy of Sciences of the United States of America, 2006

602 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d3d580ad469883d1609fdf66984dc6747596bbbe

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Citations in the corpus

Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy (2015, positive): “PC-1 could be split into two gene sets: a hazardous set of 321 transcripts, for which increased expression was associated with poor prognosis, and a protective set of 238 transcripts, for which increased expression was beneficial.”
Organoid Models of Human and Mouse Ductal Pancreatic Cancer (2014, result): “This contrasts with a previous report that Kras mutation and biallelic loss of p16/p19 promoted mPDA (Aguirre et al., 2003; Bardeesy et al., 2006) and may reflect differences in the genetic system or the initiating cellular compartment.”
Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer. (2006, background): “…locus (encoding both p16INK4A and p19ARF), or of p53, does not induce pancreatic neoplasia; however, concurrent KrasG12D expression and inactivation of Ink4a/Arf or p53 drives the development of advanced PDAC with short latency (Aguirre et al. 2003; Hingorani et al. 2005; Bardeesy et al. 2006).”
Pancreatic cancers require autophagy for tumor growth. (2011, positive): “Our studies employed a similar Kras-driven genetically engineered mouse model (GEMM) of PDAC (Hingorani et al. 2003; Bardeesy et al. 2006).”
EMT and dissemination precede pancreatic tumor formation (2012, methodology): “…by histologic analysis (‘‘PanIN’’ mice), PKCY animals were sacrificed at 8–10 weeks of age based on prior observations regarding tumor progression (Bardeesy et al., 2006); no PKCY mice (out of 18 examined) had evidence of carcinoma at this time point (see Extended Experimental Procedures for…”
Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer (2014, positive): “Activating mutations in KRAS are present in the majority of human PDAC cases, and genetically engineered mouse (GEM) models have substantiated critical roles of oncogenic Kras in driving tumor initiation and in enabling tumor progression along with deficiencies of P53, Ink4a/Arf, Smad4, and/or Pten ”
KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer (2018, background): “When coupled with mutational inactivation of Tp53 (Tp53R175H) (Hingorani et al. 2005), Cdkn2a (Aguirre et al. 2003; Bardeesy et al. 2006), or Smad4 (Kojima et al. 2007), PanIN formation was accelerated, progressing to rapid and high-frequency occurrence of metastatic PDAC.”
Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “…genomic alteration, and the comparison of specific models has pointed toward possible influences of genotype on genomic stability. p53 mutant tumors demonstrate a modest increase in copy number alterations in comparison with PDACs arising on an Ink4a/Arf mutant background (Bardeesy et al. 2006).”
Vitamin D Receptor-Mediated Stromal Reprogramming Suppresses Pancreatitis and Enhances Pancreatic Cancer Therapy (2014, positive): “The tumor cells for transplantation were derived from p48-Cre; Kras; p53 mice (Bardeesy et al., 2006) and express low levels of Vdr (Figures S5A and S5B).”