Faculty Opinions recommendation of Differential effects of oncogenic K-Ras and N-Ras on proliferation, differentiation and tumor progression in the colon.
By C. Der. 2008
595 citations recorded by the source corpus.
Subfields: Oncology
View Paper: https://www.semanticscholar.org/paper/57fd4456735a522b670da981a71f4d82dc0dff38
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Oncology
- Jianming Zhang
- K. Rossman
- G. A. Hobbs
- Anurag Singh
- Nathanael S. Gray
- C. Der
- N. Bardeesy
- J. Settleman
Citations in the corpus
- A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. (2009, background): “K-ras mutations occur most frequently in adenocarcinomas of the lung, pancreas, and colon, and mutational activation of K-Ras in these tissues is sufficient to initiate neoplasia in mice (Aguirre et al., 2003; Haigis et al., 2008; Johnson et al., 2001).”
- Early detection of cancer (2022, unknown): “For example,mouse models allowing exploration of early tumorigenesis and that more closely recapitulate human disease (including immunocompetent and conditional expression models) now exist for nonmelanoma squamous cell carcinoma (32), pancreatic adenocarcinoma (33), colon cancer (34), and lung aden”
- MEK1 mutations confer resistance to MEK and B-RAF inhibition (2009, background): “Preclinical studies suggest that some NRAS-mutant melanomas may also exhibit sensitivity to RAF or MEK inhibition (4, 29), whereas KRAS mutations have conferred only marginal sensitivity (30).”
- A comprehensive survey of Ras mutations in cancer (2012, unknown): “Ras) promoted widespread colonic epithelial hyperplasia as well as neoplasia when combined with the adenomatous polyposis coli mutations commonly seen in colon cancer (59).”
- RAS isoforms and mutations in cancer at a glance (2016, background): “In one study, the Kras G12D mutation but not the Nras G12D mutation promoted colon cancer development in Apc-deficient mice, supporting the ability of KRAS but not NRAS to initiate the formation of colon cancer (Haigis et al., 2008).”
- Targeting the cancer kinome through polypharmacology (2010, unknown): “Mutations in KRAS do not, in general, sensitize tumour cells to inhibitors of Raf or Mek 43,46 .”