A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival.

By Anurag Singh, Patricia Greninger, Daniel R. Rhodes, L. Koopman, S. Violette, N. Bardeesy, J. Settleman. Cancer Cell, 2009

830 citations recorded by the source corpus.

Subfields: Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/0ff4142a8a6e84fd45d93c0b7df5e181471475d2

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Citations in the corpus

Targeting KRAS Mutant Cancers with a Covalent G12C-Specific Inhibitor. (2018, methodology): “Gene sets representing ERK signatures and curated KRAS dependency genes were obtained from previous reports (Bild et al., 2006; Chiaradonna et al., 2006; Dry et al., 2010; Kwong et al., 2015; Liberzon et al., 2015; Singh et al., 2009; Sweet-Cordero et al., 2005; Vallejo et al., 2017).”
Stromal elements act to restrain, rather than support, pancreatic ductal adenocarcinoma. (2014, background): “ShhPKCY tumors also exhibited a significant increase in Zeb1 and Slug expression, two markers of epithelialto-mesenchymal transition, consistent with the predominance of poorly differentiated and undifferentiated histology (Singh et al., 2009; Watanabe et al., 2009) (Figure S2B; p < 0.”
KRAS and YAP1 converge to regulate EMT and tumor survival (2014, background): “Singh et al. (2009) previously showed a correlation between KRAS dependency and epithelial morphology amongst KRAS-mutant cell lines and Cell.”
KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer (2018, background): “Finally, although one study suggested that only a subset of KRAS-mutant PDAC cell lines were addicted to mutant KRAS (Singh et al. 2009), a subsequent studydetermined that allKRAS-mutant PDAC cell lines showed significant growth impairment on acute or sustained KRAS suppression (Hayes et al. 2016).”
Subtypes of Pancreatic Ductal Adenocarcinoma and Their Differing Responses to Therapy (2011, background): “Others have found that cancer cell lines harboring mutant KRAS differ in their dependence on KRAS”
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer (2010, background): “…manipulating epithelial plasticity is reinforced by studies showing that depletion of Zeb1, either chemically or by RNA interference, in mesenchymal-like cells results in a partial epithelial metaplasia and either gain of K-Ras dependency or drug sensitivity (Singh et al., 2009; Li et al., 2009b).”
Co-occurring genomic alterations define major subsets of KRAS - mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities (2015, neutral): “Preclinical studies provide further support for this notion, and in fact markers designed to predict the varying degrees of KRAS dependence have been developed (8).”
The ZEB/miR‐200 feedback loop—a motor of cellular plasticity in development and cancer? (2010, background): “…that express zEB1 can overcome K-raS-dependent oncogene addiction owing to persisting survival signals after sh-mediated knockdown of oncogenic K-raS (Singh et al, 2009). the mir-200 side of the feedback loop favours apoptosis and sensitivity to toxic agents. re-expression of mir-200 family…”
Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State. (2016, methodology): “coli as truncated (1-169), hexahistidine-tagged forms as described by Ostrem and colleagues ( 6 ).”
Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer (2014, positive): “To gain insight into whether YAP1 might have a role in driving growth of human Kras-independent PDAC, we first compared its expression in previously established human Kras-dependent and Kras-independent PDAC cells (Singh et al., 2009; Collisson et al., 2011).”