Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation

[1]  K. O'Byrne,et al.  Molecular and clinical predictors of outcome for cetuximab in non-small cell lung cancer (NSCLC): Data from the FLEX study. , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[2]  A. Gemma,et al.  First-line gefitinib versus first-line chemotherapy by carboplatin (CBDCA) plus paclitaxel (TXL) in non-small cell lung cancer (NSCLC) patients (pts) with EGFR mutations: A phase III study (002) by North East Japan Gefitinib Study Group. , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  F. Cappuzzo,et al.  Genetic abnormalities of the EGFR pathway in African American Patients with non-small-cell lung cancer. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[4]  J. Downward Cancer: A tumour gene's fatal flaws , 2009, Nature.

[5]  Calum MacAulay,et al.  Oncogene Mutations, Copy Number Gains and Mutant Allele Specific Imbalance (MASI) Frequently Occur Together in Tumor Cells , 2009, PloS one.

[6]  D. Feldser,et al.  Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma , 2009, Nature.

[7]  William Pao,et al.  Lung Cancer in Never Smokers: Molecular Profiles and Therapeutic Implications , 2009, Clinical Cancer Research.

[8]  Y. Yatabe,et al.  9002 A phase III, first-line trial of gefitinib versus cisplatin plusdocetaxel for patients with advanced or recurrent non-small cell lungcancer (NSCLC) harboring activating mutation of the epidermal growthfactor receptor (EGFR) gene: a preliminary results of WJTOG 3405 , 2009 .

[9]  Ben S. Wittner,et al.  Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1 , 2009, Nature.

[10]  Gregory J Riely,et al.  Impact of Epidermal Growth Factor Receptor and KRAS Mutations on Clinical Outcomes in Previously Untreated Non–Small Cell Lung Cancer Patients: Results of an Online Tumor Registry of Clinical Trials , 2009, Clinical Cancer Research.

[11]  D. Hwang,et al.  Gastrosplenic fistula from Hodgkin's lymphoma. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[12]  Koichi Yamazaki,et al.  Combined Survival Analysis of Prospective Clinical Trials of Gefitinib for Non–Small Cell Lung Cancer with EGFR Mutations , 2009, Clinical Cancer Research.

[13]  Patricia Greninger,et al.  A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. , 2009, Cancer cell.

[14]  Laura Tolosi,et al.  Predicting drug susceptibility of non-small cell lung cancers based on genetic lesions. , 2009, The Journal of clinical investigation.

[15]  Michael J. Emanuele,et al.  A Genome-wide RNAi Screen Identifies Multiple Synthetic Lethal Interactions with the Ras Oncogene , 2009, Cell.

[16]  W. Sellers,et al.  PI3K pathway activation mediates resistance to MEK inhibitors in KRAS mutant cancers. , 2009, Cancer research.

[17]  Sridhar Ramaswamy,et al.  Synthetic Lethal Interaction between Oncogenic KRAS Dependency and STK33 Suppression in Human Cancer Cells , 2009, Cell.

[18]  Takeshi Imamura,et al.  Role of Ras Signaling in the Induction of Snail by Transforming Growth Factor-β* , 2009, Journal of Biological Chemistry.

[19]  Takayuki Kosaka,et al.  Prognostic Implication of EGFR, KRAS, and TP53 Gene Mutations in a Large Cohort of Japanese Patients with Surgically Treated Lung Adenocarcinoma , 2009, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[20]  Y. Ohe,et al.  EGFR mutations predict survival benefit from gefitinib in patients with advanced lung adenocarcinoma: a historical comparison of patients treated before and after gefitinib approval in Japan. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[21]  Ralph Weissleder,et al.  Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers , 2008, Nature Medicine.

[22]  Edward S. Kim,et al.  Gefitinib versus docetaxel in previously treated non-small-cell lung cancer (INTEREST): a randomised phase III trial , 2008, The Lancet.

[23]  Allan Balmain,et al.  Kras regulatory elements and exon 4A determine mutation specificity in lung cancer , 2008, Nature Genetics.

[24]  Brian H. Dunford-Shore,et al.  Somatic mutations affect key pathways in lung adenocarcinoma , 2008, Nature.

[25]  Kenji Eguchi,et al.  Phase III study, V-15-32, of gefitinib versus docetaxel in previously treated Japanese patients with non-small-cell lung cancer. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[26]  Issa J Dahabreh,et al.  Somatic Mutations of the Tyrosine Kinase Domain of Epidermal Growth Factor Receptor and Tyrosine Kinase Inhibitor Response to TKIs in Non-small Cell Lung Cancer: An Analytical Database , 2008, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[27]  Robert A. Weinberg,et al.  Ras oncogenes: split personalities , 2008, Nature Reviews Molecular Cell Biology.

[28]  Derek Y. Chiang,et al.  EML4-ALK Fusion Gene and Efficacy of an ALK Kinase Inhibitor in Lung Cancer , 2008, Clinical Cancer Research.

[29]  I. Wistuba,et al.  Phosphatidylinositol 3-Kinase Mediates Bronchioalveolar Stem Cell Expansion in Mouse Models of Oncogenic K-ras-Induced Lung Cancer , 2008, PloS one.

[30]  Sabine Tejpar,et al.  KRAS status and efficacy in the first-line treatment of patients with metastatic colorectal cancer (mCRC) treated with FOLFIRI with or without cetuximab: The CRYSTAL experience , 2008 .

[31]  M. Ladanyi,et al.  Frequency and Distinctive Spectrum of KRAS Mutations in Never Smokers with Lung Adenocarcinoma , 2008, Clinical Cancer Research.

[32]  W. Kolch,et al.  Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis. , 2008, Experimental cell research.

[33]  Derek Y. Chiang,et al.  Characterizing the cancer genome in lung adenocarcinoma , 2007, Nature.

[34]  Y. Yatabe,et al.  Mutations of the epidermal growth factor receptor gene and related genes as determinants of epidermal growth factor receptor tyrosine kinase inhibitors sensitivity in lung cancer , 2007, Cancer science.

[35]  Jude Kendall,et al.  Oncogenic cooperation and coamplification of developmental transcription factor genes in lung cancer , 2007, Proceedings of the National Academy of Sciences.

[36]  H. Aburatani,et al.  Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer , 2007, Nature.

[37]  T. Lynch,et al.  B3-03: A randomized multicenter phase III study of cetuximab (Erbitux®) in combination with Taxane/Carboplatin versus Taxane/Carboplatin alone as first-line treatment for patients with advanced/metastatic Non-small cell lung cancer (NSCLC) , 2007 .

[38]  Suzanne Schubbert,et al.  Hyperactive Ras in developmental disorders and cancer , 2007, Nature Reviews Cancer.

[39]  G. Stamp,et al.  Binding of Ras to Phosphoinositide 3-Kinase p110α Is Required for Ras- Driven Tumorigenesis in Mice , 2007, Cell.

[40]  J. Yates,et al.  PRAK Is Essential for ras-Induced Senescence and Tumor Suppression , 2007, Cell.

[41]  K. Matsuo,et al.  Risk factors differ for non‐small‐cell lung cancers with and without EGFR mutation: assessment of smoking and sex by a case‐control study in Japanese , 2007, Cancer science.

[42]  S. Gabriel,et al.  Epidermal Growth Factor Receptor Activation in Glioblastoma through Novel Missense Mutations in the Extracellular Domain , 2006, PLoS medicine.

[43]  M. White,et al.  RalB GTPase-Mediated Activation of the IκB Family Kinase TBK1 Couples Innate Immune Signaling to Tumor Cell Survival , 2006, Cell.

[44]  A. Balmain,et al.  A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice , 2006, Nature Genetics.

[45]  M. Meyerson,et al.  Non-small-cell lung cancer and Ba/F3 transformed cells harboring the ERBB2 G776insV_G/C mutation are sensitive to the dual-specific epidermal growth factor receptor and ERBB2 inhibitor HKI-272. , 2006, Cancer research.

[46]  J. Minna,et al.  Distinct Epidermal Growth Factor Receptor and KRAS Mutation Patterns in Non–Small Cell Lung Cancer Patients with Different Tobacco Exposure and Clinicopathologic Features , 2006, Clinical Cancer Research.

[47]  J. Minna,et al.  Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers. , 2006, Journal of the National Cancer Institute.

[48]  M. Barbacid,et al.  Tumour biology: Senescence in premalignant tumours , 2005, Nature.

[49]  C. Der,et al.  Signaling Interplay in Ras Superfamily Function , 2005, Current Biology.

[50]  Elisa Rossi,et al.  Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer. , 2005, Journal of the National Cancer Institute.

[51]  H. Lane,et al.  ERBB receptors and cancer: the complexity of targeted inhibitors , 2005, Nature Reviews Cancer.

[52]  Takayuki Kosaka,et al.  Mutations of the epidermal growth factor receptor gene predict prolonged survival after gefitinib treatment in patients with non-small-cell lung cancer with postoperative recurrence. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[53]  J. Minna,et al.  Somatic mutations of the HER2 kinase domain in lung adenocarcinomas. , 2005, Cancer research.

[54]  A. Pellicer,et al.  Inhibition of Ras oncogenic activity by Ras protooncogenes , 2005, International journal of cancer.

[55]  Takayuki Kosaka,et al.  Mutations of the Epidermal Growth Factor Receptor Gene in Lung Cancer , 2004, Cancer Research.

[56]  M Paesmans,et al.  The role of RAS oncogene in survival of patients with lung cancer: a systematic review of the literature with meta-analysis , 2004, British Journal of Cancer.

[57]  Channing J Der,et al.  Renewing the conspiracy theory debate: does Raf function alone to mediate Ras oncogenesis? , 2004, Trends in cell biology.

[58]  Daniel A. Haber,et al.  Gefitinib-Sensitizing EGFR Mutations in Lung Cancer Activate Anti-Apoptotic Pathways , 2004, Science.

[59]  S. Gabriel,et al.  EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy , 2004, Science.

[60]  Y. Yatabe,et al.  CK20 expression, CDX2 expression, K‐ras mutation, and goblet cell morphology in a subset of lung adenocarcinomas , 2004, The Journal of pathology.

[61]  Patricia L. Harris,et al.  Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. , 2004, The New England journal of medicine.

[62]  R. DePinho,et al.  Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defects. , 2004, Cancer cell.

[63]  David Cella,et al.  Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. , 2003, JAMA.

[64]  Masahiro Fukuoka,et al.  Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer (The IDEAL 1 Trial) [corrected]. , 2003, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[65]  Ming You,et al.  Wildtype Kras2 can inhibit lung carcinogenesis in mice , 2001, Nature Genetics.

[66]  C. Harris,et al.  p53 and K-ras mutations in lung cancers from former and never-smoking women. , 2001, Cancer research.

[67]  J. Luketich,et al.  Comparison of mutations in the p53 and K-ras genes in lung carcinomas from smoking and nonsmoking women. , 1999, Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology.

[68]  S. Lowe,et al.  Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a , 1997, Cell.

[69]  A. Marchetti,et al.  BRONCHIOLOALVEOLAR LUNG CARCINOMAS: K‐ras MUTATIONS ARE CONSTANT EVENTS IN THE MUCINOUS SUBTYPE , 1996, The Journal of pathology.

[70]  D. Lowy,et al.  Abnormal regulation of mammalian p21ras contributes to malignant tumor growth in von Recklinghausen (type 1) neurofibromatosis , 1992, Cell.

[71]  J. Minna,et al.  Mutations of ras genes distinguish a subset of non-small-cell lung cancer cell lines from small-cell lung cancer cell lines. , 1991, Oncogene.

[72]  S. Rodenhuis,et al.  Relationship between K-ras oncogene activation and smoking in adenocarcinoma of the human lung. , 1991, Journal of the National Cancer Institute.

[73]  C. Marshall,et al.  A polybasic domain or palmitoylation is required in addition to the CAAX motif to localize p21 ras to the plasma membrane , 1990, Cell.

[74]  S. Rodenhuis,et al.  K-ras oncogene activation as a prognostic marker in adenocarcinoma of the lung. , 1990, The New England journal of medicine.

[75]  S. Hirohashi,et al.  Association of point mutation in c‐Ki‐ras oncogene in lung adenocarcinoma with particular reference to cytologic subtypes , 1990, Cancer.

[76]  P. Casey,et al.  p21ras is modified by a farnesyl isoprenoid. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[77]  J. L. Bos,et al.  ras oncogenes in human cancer: a review. , 1989, Cancer research.

[78]  J. Bos,et al.  The ras gene family and human carcinogenesis. , 1988, Mutation research.

[79]  F. McCormick,et al.  A cytoplasmic protein stimulates normal N-ras p21 GTPase, but does not affect oncogenic mutants. , 1987, Science.

[80]  S. Rodenhuis,et al.  Mutational activation of the K-ras oncogene. A possible pathogenetic factor in adenocarcinoma of the lung. , 1987, The New England journal of medicine.

[81]  D. Lowy,et al.  Harvey murine sarcoma virus p21 ras protein: biological and biochemical significance of the cysteine nearest the carboxy terminus. , 1984, The EMBO journal.

[82]  M. Barbacid,et al.  Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient. , 1984, Science.

[83]  Robert A. Weinberg,et al.  Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes , 1983, Nature.

[84]  H. Ruley Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture , 1983, Nature.

[85]  R. Newbold,et al.  Fibroblast immortality is a prerequisite for transformation by EJ c-Ha-ras oncogene , 1983, Nature.

[86]  C. Marshall,et al.  Identification of transforming gene in two human sarcoma cell lines as a new member of the ras gene family located on chromosome 1 , 1983, Nature.

[87]  M. Wigler,et al.  Three human transforming genes are related to the viral ras oncogenes. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[88]  Kenji Shimizu,et al.  Activation of the T24 bladder carcinoma transforming gene is linked to a single amino acid change , 1982, Nature.

[89]  Cori Bargmann,et al.  Mechanism of activation of a human oncogene , 1982, Nature.

[90]  Eugenio Santos,et al.  A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogene , 1982, Nature.

[91]  R. Weinberg,et al.  Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene , 1982, Nature.

[92]  C. Der,et al.  Transforming genes of human bladder and lung carcinoma cell lines are homologous to the ras genes of Harvey and Kirsten sarcoma viruses. , 1982, Proceedings of the National Academy of Sciences of the United States of America.

[93]  M. Wigler,et al.  Isolation and preliminary characterization of a human transforming gene from T24 bladder carcinoma cells , 1982, Nature.

[94]  M. Wigler,et al.  Human-tumor-derived cell lines contain common and different transforming genes , 1981, Cell.

[95]  R. Weinberg,et al.  Transforming genes of carcinomas and neuroblastomas introduced into mouse fibroblasts , 1981, Nature.

[96]  G. Cooper,et al.  Transforming activity of human tumor DNAs. , 1981, Proceedings of the National Academy of Sciences of the United States of America.

[97]  L. Tanoue,et al.  Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma , 2010 .

[98]  A. Joe,et al.  Oncogene addiction. , 2008, Cancer research.

[99]  G. Qiao,et al.  KRAS Mutations and Primary Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib , 2008 .

[100]  N. Hanna,et al.  EGF Receptor Gene Mutations Are Common in Lung Cancers From “Never Smokers” and Are Associated With Sensitivity of Tumors to Gefitinib and Erlotinib , 2006 .

[101]  Y. Ishikawa,et al.  High K-ras mutation rates in goblet-cell-type adenocarcinomas of the lungs , 2005, Journal of Cancer Research and Clinical Oncology.

[102]  J. Downward Targeting RAS signalling pathways in cancer therapy , 2003, Nature Reviews Cancer.

[103]  R. Dixon,et al.  Polyisoprenylation of Ras in vitro by a farnesyl-protein transferase. , 1990, Journal of Biological Chemistry.