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    KRAS KRAS proto-oncogene, GTPase [ Homo sapiens (human) ]

    Gene ID: 3845, updated on 20-Jun-2019

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Study in tumor cell lines shows that MEK1/2 inhibitors (MEKi) resistance driven by KRAS(G13D) amplification is not reversible; these cells do not exhibit growth defects upon MEKi withdrawal but undergo an ERK1/2-dependent epithelial-to-mesenchymal transition and exhibit resistance to commonly used chemotherapeutics.

    MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF<sup>V600E</sup> amplification whereas KRAS<sup>G13D</sup> amplification promotes EMT-chemoresistance.
    Sale MJ, Balmanno K, Saxena J, Ozono E, Wojdyla K, McIntyre RE, Gilley R, Woroniuk A, Howarth KD, Hughes G, Dry JR, Arends MJ, Caro P, Oxley D, Ashton S, Adams DJ, Saez-Rodriguez J, Smith PD, Cook SJ., Free PMC Article

    An actionable requirement for IKKalpha in KRAS-mutant lung adenocarcinoma.

    IκB Kinase α Is Required for Development and Progression of <i>KRAS</i>-Mutant Lung Adenocarcinoma.
    Vreka M, Lilis I, Papageorgopoulou M, Giotopoulou GA, Lianou M, Giopanou I, Kanellakis NI, Spella M, Agalioti T, Armenis V, Goldmann T, Marwitz S, Yull FE, Blackwell TS, Pasparakis M, Marazioti A, Stathopoulos GT., Free PMC Article

    KRAS mutation is associated with suppressed Th1/cytotoxic immunity in colorectal cancer, the extent of the effect being modulated by CMS subtype. These results add a novel immunobiological dimension to the biological heterogeneity of colorectal cancer.

    KRAS Mutation and Consensus Molecular Subtypes 2 and 3 Are Independently Associated with Reduced Immune Infiltration and Reactivity in Colorectal Cancer.
    Lal N, White BS, Goussous G, Pickles O, Mason MJ, Beggs AD, Taniere P, Willcox BE, Guinney J, Middleton GW., Free PMC Article

    Mutations in both the p53 tumor suppressor gene and K-ras oncogene are highly frequent in lung tumors from nonsmoking women in China. The predominance of G-->T transversions in both genes and the occurrence of p53 mutations within a specific GC rich region or at specific hotspot codons on the non-transcribed strand are consistent with exposure to smoky coal emissions.

    p53 and K-ras mutations in lung tissues and sputum samples of individuals exposed to smoky coal emissions in Xuan Wei County, China.
    Keohavong P, Lan Q, Gao W.

    two major subtypes of KRAS mutant cancers of the lung, pancreas, and large intestine, which reflect different KRAS effector engagement were identified.

    Differential Effector Engagement by Oncogenic KRAS.
    Yuan TL, Amzallag A, Bagni R, Yi M, Afghani S, Burgan W, Fer N, Strathern LA, Powell K, Smith B, Waters AM, Drubin D, Thomson T, Liao R, Greninger P, Stein GT, Murchie E, Cortez E, Egan RK, Procter L, Bess M, Cheng KT, Lee CS, Lee LC, Fellmann C, Stephens R, Luo J, Lowe SW, Benes CH, McCormick F., Free PMC Article

    MerTK mediates STAT3-KRAS/SRC-signaling axis for glioma stem cell maintenance

    MerTK mediates STAT3-KRAS/SRC-signaling axis for glioma stem cell maintenance.
    Eom H, Kaushik N, Yoo KC, Shim JK, Kwon M, Choi MY, Yoon T, Kang SG, Lee SJ.

    Data suggest that Kirsten Ras protein (KRAS) has prognostic value beyond mutation status in microsatellite stable (MSS) colorectal cancer (CRC).

    Alternative splicing expands the prognostic impact of KRAS in microsatellite stable primary colorectal cancer.
    Eilertsen IA, Sveen A, Strømme JM, Skotheim RI, Nesbakken A, Lothe RA.

    prolonged MAPK pathway inhibition could result in acquired resistance which is associated with increased malignant phenotype in KRAS mutant gastric cancer.

    Prolonged MEK inhibition leads to acquired resistance and increased invasiveness in KRAS mutant gastric cancer.
    Choi KM, Cho E, Kim E, Shin JH, Kang M, Kim B, Han EH, Chung YH, Kim JY.

    Kras protein expression is controlled by a self-regulating feedforward mechanism mediated by eIF5A-PEAK1.Kras protein level is increased during pancreatic ductal adenocarcinoma progression with the highest levels of expression observed in metastatic cell populations.

    KRAS Oncoprotein Expression Is Regulated by a Self-Governing eIF5A-PEAK1 Feed-Forward Regulatory Loop.
    Fujimura K, Wang H, Watson F, Klemke RL., Free PMC Article

    A report of the possible use of abundance measures for K-Ras4A for predicting the survival of lung adenocarcinoma patients with KRAS mutations.

    Isoform specific gene expression analysis of KRAS in the prognosis of lung adenocarcinoma patients.
    Yang IS, Kim S., Free PMC Article

    KRAS-membrane interaction is tuned by multiple factors

    Quantitative biophysical analysis defines key components modulating recruitment of the GTPase KRAS to the plasma membrane.
    Lakshman B, Messing S, Schmid EM, Clogston JD, Gillette WK, Esposito D, Kessing B, Fletcher DA, Nissley DV, McCormick F, Stephen AG, Jean-Francois FL.,

    The results indicate that lung cancer patients carrying KRAS mutations are prone to multiple metastases in both lungs.

    Comparison of CT radiogenomic and clinical characteristics between EGFR and KRAS mutations in lung adenocarcinomas.
    Lv J, Zhang H, Ma J, Ma Y, Gao G, Song Z, Yang Y.

    Activation of KRas is associated with initiation and progression of glioma.

    Activation of KRas-ERK1/2 signaling drives the initiation and progression of glioma by suppressing the acetylation of histone H4 at lysine 16.
    Wei Y, Wang F, Sang B, Xu Z, Yang D.

    KRAS gene mutations do not affect downstream protein expression in colorectal cancer. KRAS protein is associated with poor tumor differentiation, older age, and a risk of tumor recurrence.

    Relationships among <i>KRAS</i> mutation status, expression of RAS pathway signaling molecules, and clinicopathological features and prognosis of patients with colorectal cancer.
    Wan XB, Wang AQ, Cao J, Dong ZC, Li N, Yang S, Sun MM, Li Z, Luo SX., Free PMC Article

    SHP2 inhibition is an unexpected vulnerability of KRAS-mutant non-small-cell lung cancer cells.

    SHP2 is required for growth of KRAS-mutant non-small-cell lung cancer in vivo.
    Mainardi S, Mulero-Sánchez A, Prahallad A, Germano G, Bosma A, Krimpenfort P, Lieftink C, Steinberg JD, de Wit N, Gonçalves-Ribeiro S, Nadal E, Bardelli A, Villanueva A, Bernards R.

    Letter: PIK3CA mutation, in particular, mutation of exon 9, has a significant positive association with KRAS mutation in colorectal cancer.

    Positive association of PIK3CA mutation with KRAS mutation but not BRAF mutation in colorectal cancer suggests co-selection is gene specific but not pathway specific.
    Susanti S, Fadhil W, Murtaza S, Hassall JC, Ebili HO, Oniscu A, Ilyas M.

    SHP2 has a critical function in promoting oncogenic RAS/MAPK pathway activation in cancers with RAS-GTP-dependent oncogenic BRAF, NF1 loss and nucleotide-cycling oncogenic KRAS.

    RAS nucleotide cycling underlies the SHP2 phosphatase dependence of mutant BRAF-, NF1- and RAS-driven cancers.
    Nichols RJ, Haderk F, Stahlhut C, Schulze CJ, Hemmati G, Wildes D, Tzitzilonis C, Mordec K, Marquez A, Romero J, Hsieh T, Zaman A, Olivas V, McCoach C, Blakely CM, Wang Z, Kiss G, Koltun ES, Gill AL, Singh M, Goldsmith MA, Smith JAM, Bivona TG., Free PMC Article

    No significant differences were found in the frequency of TP53 and K-ras mutations among patients in the 5 countries.

    Tumor Protein p53 and K-ras Gene Mutations in Peruvian Patients with Gallbladder Cancer
    Vidaurre T, Casavilca S, Montenegro P, Gomez H, Calderón M, Navarro J, Aramburu J, Poquioma E, Tsuchiya Y, Asai T, Ajioka Y, Sato A, Ikoma T, Nakamura K., Free PMC Article

    introducing a rapid and sensitive microarray-based assay for the multiplex detection of minority mutations of oncogenes (KRAS, NRAS and BRAF) with relevant diagnostics implications in tissue biopsies and plasma samples in metastatic colorectal cancer patients

    Analysis of KRAS, NRAS and BRAF mutational profile by combination of in-tube hybridization and universal tag-microarray in tumor tissue and plasma of colorectal cancer patients.
    Damin F, Galbiati S, Soriani N, Burgio V, Ronzoni M, Ferrari M, Chiari M., Free PMC Article

    Mutant Kras-induced upregulation of CD24 enhances prostate cancer stemness and bone metastasis

    Mutant Kras-induced upregulation of CD24 enhances prostate cancer stemness and bone metastasis.
    Weng CC, Ding PY, Liu YH, Hawse JR, Subramaniam M, Wu CC, Lin YC, Chen CY, Hung WC, Cheng KH.

    These data underscore a critical sex-specific role for epithelial Stat3 signaling in K-ras mutant Lung adenocarcinomas.

    Sex specific function of epithelial STAT3 signaling in pathogenesis of K-ras mutant lung cancer.
    Caetano MS, Hassane M, Van HT, Bugarin E, Cumpian AM, McDowell CL, Cavazos CG, Zhang H, Deng S, Diao L, Wang J, Evans SE, Behrens C, Wistuba II, Fuqua SAW, Lin H, Stabile LP, Watowich SS, Kadara H, Moghaddam SJ., Free PMC Article

    EGFR and KRAS mutation status was associated with the expression of AKT, p-AKT, DR5, and DcR1 in non-small cell lung cancer

    Association of EGFR and KRAS mutations with expression of p-AKT, DR5 and DcR1 in non-small cell lung cancer.
    Zhao XD, Deng HB, Lu CL, Bao YX, Lu X, Deng LL.

    Pancreatic juice from PDAC patients is rich in KRAS mutations often not seen in the primary tumor and possibly reflecting precancerous lesions in other regions of the pancreas. The inclusion of TP53 mutation detection and additional markers must therefore be considered for fully exploiting the clinical potential of pancreatic juice samples in early cancer detection

    Mutation analysis by deep sequencing of pancreatic juice from patients with pancreatic ductal adenocarcinoma.
    Choi MH, Mejlænder-Andersen E, Manueldas S, El Jellas K, Steine SJ, Tjensvoll K, Sætran HA, Knappskog S, Hoem D, Nordgård O, Hovland R, Molven A., Free PMC Article

    Gain-of-function mutations in KRAS, FGFR1, and TRPV4 are present in 72% of giant cell lesions of the jaw (GCLJ). TRPV4 mutations induce sustained activation of ERK1/2, indicating that their effects converge with that of KRAS and FGFR1 mutations on the activation of the MAPK pathway in GCLJ.

    TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw.
    Gomes CC, Gayden T, Bajic A, Harraz OF, Pratt J, Nikbakht H, Bareke E, Diniz MG, Castro WH, St-Onge P, Sinnett D, Han H, Rivera B, Mikael LG, De Jay N, Kleinman CL, Valera ET, Bassenden AV, Berghuis AM, Majewski J, Nelson MT, Gomez RS, Jabado N., Free PMC Article

    This study demonstrated that no significant difference of KRAS status between colon cancer and rectal cancer. KRAS mutation was much more frequent in right-sided colon cancer (RCC) compared with left-sided colon cancer (LCC) and LCC patients with KRAS mutation has a poor prognosis compared with KRAS wild type, but RCC patients did not show the similar effect.

    Impact of primary colorectal Cancer location on the KRAS status and its prognostic value.
    Xie MZ, Li JL, Cai ZM, Li KZ, Hu BL., Free PMC Article

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