Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer

By J. Morton, P. Timpson, S. Karim, Rachel A. Ridgway, D. Athineos, B. Doyle, N. Jamieson, K. Oien, A. Lowy, V. Brunton and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2010

653 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e221e2016c1161ab9912135c696674a942876f70

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In Molecular Biology

1. S. Piccolo
2. M. Cordenonsi
3. Rebecca S. Y. Wong
4. Antonio Rosato
5. S. Dupont
6. J. Erler
7. K. Guan

In Oncology

1. S. Piccolo
2. Rebecca S. Y. Wong
3. J. Erler
4. M. Cordenonsi

Citations in the corpus

• Metabolic control of YAP and TAZ by the mevalonate pathway (2014, background): “On the contrary, presence of mutant p53 leads to a marked increase in the incidence of highly metastatic carcinomas in various mouse models (Doyle et al., 2010; Lang et al., 2004; Morton et al., 2010; Olive et al., 2004).”
• Apoptosis in cancer: from pathogenesis to treatment (2011, background): “One example is the downregulation of p53, a tumour suppressor gene, which results in reduced apoptosis and enhanced tumour growth and development [1] and inactivation of p53, regardless of the mechanism, has been linked to many human cancers [2-4].”
• 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): “This may help to explain our previous observations that mutant p53, but not loss-of-function p53, leads to PDAC metastasis in this mouse model (Morton et al , 2010b).”