The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
RAF Suppression Synergizes with MEK Inhibition in KRAS Mutant Cancer Cells
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In the citing paper
“Ongoing clinical studies involving strategies targeting MEK alongside feedback or alternative survival pathways have thus far revealed activity in only subsets of patients”
From A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution (2017) · cites this paper as Lamba et al., 2014
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Pooled RNA interference (RNAi) sensitizer screens are in principle suitable for the challenge, but historically they have only been performed with drugs targeting a single KRAS effector node in a single cell line”
From A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution (2017) · cites this paper as Lamba et al., 2014
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“approaches combining MEK inhibitors with inhibitors of ERK feedback reactivation, including the receptor tyrosine kinases (RTKs) ERBB3, IGF1R, and FGFR1”
From A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution (2017) · cites this paper as Lamba et al., 2014
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Our screens identified previously described MEKi sensitizers, including those that function through the PI3K/AKT/mTOR pathway (AKT1, AKT2, RICTOR, MTOR, and IGF1R), through suppression of ERK pathway feedback reactivation (or incomplete pathway inhibition) (BRAF, RAF1, MAPK1, MAPK3, KRAS, and FGFR1), and through the YAP1 pathway”
From A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution (2017) · cites this paper as Lamba et al., 2014
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“a fact which is likely attributed to the intrinsic molecular, genetic, and clinical heterogeneity of KRAS mutant tumors”
From A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution (2017) · cites this paper as Lamba et al., 2014
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Citations
Cites
K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
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Panitumumab–FOLFOX4 Treatment and RAS Mutations in Colorectal Cancer
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“Mutations in the gene encoding the guanosine triphosphatase protein KRAS, the principal of the three isoforms of RAS, are present in approximately 20% of all cancers and are associated with poor prognosis and resistance to therapy (Prior et al., 2012; Pylayeva-Gupta et al., 2011).”
RAS oncogenes: the first 30 years
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“The architecture of the EGFR-RAS-MEKsignaling pathway is evolutionarily ancient and increased in complexity during evolution (Malumbres and Barbacid, 2003; Yarden and Pines, 2012).”
Ras history: The saga continues
Cox, A. D., & Der, C. J. (2010) · Small GTPases · doi:10.4161/sgtp.1.1.12178 · Cited by 706
MEK Inhibition Leads to PI3K/AKT Activation by Relieving a Negative Feedback on ERBB Receptors
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Cited by
Sorted by citations
Targeting KRAS mutant cancers with a covalent G12C-specific inhibitor
Janes, M. R., Zhang, J., Li, L.-S., Hansen, R., Peters, U., Guo, X., Chen, Y., Babbar, A., Firdaus, S. J., Darjania, L., et al. (2018) · Cell · doi:10.1016/j.cell.2018.01.006 · Cited by 1,172
MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road
Caunt, C. J., Sale, M. J., Smith, P. D., & Cook, S. J. (2015) · Nature Reviews Cancer · doi:10.1038/nrc4000 · Cited by 606
The EGFR-specific antibody cetuximab combined with chemotherapy triggers immunogenic cell death
Pozzi, C., Cuomo, A., Spadoni, I., Magni, E., Silvola, A., Conte, A., Sigismund, S., Ravenda, P. S., Bonaldi, T., Zampino, M. G., et al. (2016) · Nature Medicine · doi:10.1038/nm.4078 · Cited by 292
KRAS G12C NSCLC Models Are Sensitive to Direct Targeting of KRAS in Combination with PI3K Inhibition
Misale, S., Fatherree, J. P., Cortez, E., Li, C., Bilton, S., Timonina, D., Myers, D. T., Lee, D., Gomez-Caraballo, M., Greenberg, M., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-0368 · Cited by 259
Targeting KRAS(G12C): From Inhibitory Mechanism to Modulation of Antitumor Effects in Patients
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Development of combination therapies to maximize the impact of KRAS-G12C inhibitors in lung cancer
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MEK inhibitors activate Wnt signalling and induce stem cell plasticity in colorectal cancer
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RAS: Striking at the Core of the Oncogenic Circuitry
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“Previously, RNA interference (RNAi) screening with shRNA library to knockdown targeted genes has been widely used [18, 19].”
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Metadata
- Authors
- Lamba, S., Russo, M., Sun, C., Lazzari, L., Cancelliere, C., Grernrum, W., Lieftink, C., Bernards, R., Di Nicolantonio, F., & Bardelli, A.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2014-09
- Volume
- 8
- Issue
- 5
- Pages
- 1475-1483
- ISSN
- 2211-1247
- Cited by
- 110
- References
- 11
- Language
- en
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