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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog

Top mentioned proteins: EGFR, BRAF, HAD, CAN, PI3K
Papers using KRAS antibodies
Gene expression of the mismatch repair gene MSH2 in primary colorectal cancer
Erichsen Rune et al., In Clinical and Experimental Gastroenterology, 2010
... analyses, we used the commercially available DxS TheraScreen KRAS Mutation Kit (Qiagen, Copenhagen, Denmark) ...
CRAF inhibition induces apoptosis in melanoma cells with non-V600E BRAF mutations.
Najbauer Joseph, In PLoS ONE, 2008
... (Cell Signaling Technology, Beverly, MA); BRAF and NRAS (F-7; Santa Cruz Biotechnology, Santa Cruz, CA); KRAS (Novus Biologicals, Littleton, CO), PIK3CA (Millipore, ...
Papers on KRAS
Compound EGFR mutation is frequently detected with co-mutations of actionable genes and associated with poor clinical outcome in lung adenocarcinoma.
Chang et al., Seoul, South Korea. In Cancer Biol Ther, Feb 2016
Among the 115 missense mutations discovered in the tested genes, a few number of actionable mutations were detected irrelevant to the subtype of EGFR mutations, including ALK rearrangement, BCL2L11 intron 2 deletion, KRAS c.35G>A, PIK3CA c.1633G>A which are possible target of crizotinib, BH3 mimetics, MEK inhibitors, and PI3K-tyrosine kinase inhibitors, respectively.
Comparative Modeling, Molecular Docking, and Revealing of Potential Binding Pockets of RASSF2; a Candidate Cancer Gene.
Sehgal et al., Sāhīwāl, Pakistan. In Interdiscip Sci, Feb 2016
UNASSIGNED: RASSF2, potential tumor suppressor gene, acts as a KRAS-specific effectors protein and may promote apoptosis and cell cycle arrest.
Polycomb Repressive Complex 2 Is a Barrier to KRAS-Driven Inflammation and Epithelial-Mesenchymal Transition in Non-Small-Cell Lung Cancer.
van Lohuizen et al., Amsterdam, Netherlands. In Cancer Cell, Feb 2016
Here, we show that PRC2 is a critical regulator of KRAS-driven non-small cell lung cancer progression.
Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression.
Der et al., Chapel Hill, United States. In Cancer Cell, Feb 2016
We determined that direct pharmacologic inhibition of ERK suppressed the growth of a subset of KRAS-mutant pancreatic cancer cell lines and that concurrent phosphatidylinositol 3-kinase (PI3K) inhibition caused synergistic cell death.
MET Exon 14 Mutations in Non-Small-Cell Lung Cancer Are Associated With Advanced Age and Stage-Dependent MET Genomic Amplification and c-Met Overexpression.
Sholl et al., Boston, United States. In J Clin Oncol, Feb 2016
Clinical characteristics of MET exon 14 mutated NSCLCs were compared with those of NSCLCs with activating mutations in KRAS and EGFR.
The noncoding RNAs SNORD50A and SNORD50B bind K-Ras and are recurrently deleted in human cancer.
Khavari et al., Stanford, United States. In Nat Genet, Jan 2016
Loss of these snoRNAs also increased binding by farnesyltransferase to K-Ras and increased K-Ras prenylation, suggesting that KRAS mutation might synergize with SNORD50A and SNORD50B loss in cancer.
Targeting KRAS for diagnosis, prognosis, and treatment of pancreatic cancer: Hopes and realities.
Buscail et al., Toulouse, France. In Eur J Cancer, Jan 2016
UNASSIGNED: Mutation of the KRAS oncogene in pancreatic cancer is responsible for permanent activation of the P21 RAS protein and the cascade of signalling pathways.
Assessment of cytology based molecular analysis to guide targeted therapy in advanced non-small-cell lung cancer.
Ying et al., Beijing, China. In Oncotarget, Jan 2016
UNASSIGNED: To investigate the use of molecular testing on cytological specimens in selecting advanced non-small cell lung cancer (NSCLC) patients who are adequate for targeted treatment, a total of 137 NSCLC cases were analyzed by fluorescence in situ hybridization (FISH) for anaplastic lymphoma kinase (ALK) rearrangements, and Epidermal growth factor receptor (EGFR), kirsten rat sarcoma viral oncogene homolog (KRAS) mutations were evaluated by quantitative real-time PCR (qRT-PCR) platform combining amplification refractory mutation system (ARMS) primers and TaqMan probes.
High-Resolution CRISPR Screens Reveal Fitness Genes and Genotype-Specific Cancer Liabilities.
Moffat et al., Toronto, Canada. In Cell, Jan 2016
Moreover, we demonstrate that context-dependent fitness genes accurately recapitulate pathway-specific genetic vulnerabilities induced by known oncogenes and reveal cell-type-specific dependencies for specific receptor tyrosine kinases, even in oncogenic KRAS backgrounds.
Successful Treatment with Modified FOLFOX6 and Panitumumab in a Cecal Cancer Patient Undergoing Hemodialysis.
Hyodo et al., Tsukuba, Japan. In Intern Med, Dec 2015
Combination chemotherapy of mFOLFOX6 (5-fluorouracil, leucovorin, and oxaliplatin) plus panitumumab, a fully human monoclonal antibody against epidermal growth factor receptor (EGFR), is one of the standard treatments for metastatic colorectal cancer (mCRC) without KRAS mutation.
Profile of panitumumab as first-line treatment in patients with wild-type KRAS metastatic colorectal cancer.
Garrido-Laguna et al., Salt Lake City, United States. In Onco Targets Ther, Dec 2015
Targeted therapies against EGFR, vascular endothelial growth factor, and vascular endothelial growth factor receptor have expanded treatment options for patients with metastatic colorectal cancer (mCRC).
New genomic landscapes and therapeutic targets for biliary tract cancers.
Scarpa et al., Verona, Italy. In Front Biosci, Dec 2015
Comprehensive mutational profiling studies identified IDH1/2 and BAP1 as characteristic of intrahepatic cholangiocarcinomas, while extrahepatic cholangiocarcinomas and gallbladder carcinomas were characterized by frequent KRAS and TP53 alterations.
Impact of somatic mutations on patterns of metastasis in colorectal cancer.
Yaeger et al., New York City, United States. In J Gastrointest Oncol, Dec 2015
In this review, we describe our current understanding of associations between mutational activation of the KRAS, BRAF, PIK3CA, and NRAS oncogenes and clinical outcomes and metastatic patterns of mCRC.
[Regorafenib in patients with metastatic colorectal cancer: a review and an update].
Mansueto et al., In Recenti Prog Med, Dec 2015
In a phase III randomized, placebo-controlled study regorafenib, as compared to best supportive care, showed a statistically significant improvement in overall survival, irrespective of KRAS mutation status.
Exploiting the CRISPR/Cas9 PAM Constraint for Single-Nucleotide Resolution Interventions.
Bleris et al., Richardson, United States. In Plos One, Dec 2015
Specifically, we target the heterozygous G13A activating mutation of KRAS in colorectal cancer cells and we show reversal of drug resistance to a MEK small-molecule inhibitor.
An inducible kras(V12) transgenic zebrafish model for liver tumorigenesis and chemical drug screening.
Gong et al., Singapore, Singapore. In Dis Model Mech, 2012
Kras(V12) transgenic system offers a novel model for understanding hepatocarcinogenesis and a high-throughput screening platform for anti-cancer drugs.
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