Somatic mutations affect key pathways in lung adenocarcinoma

[1]  M. Meyerson,et al.  Mutations in the LKB1 tumour suppressor are frequently detected in tumours from Caucasian but not Asian lung cancer patients , 2008, British Journal of Cancer.

[2]  W. Gerald,et al.  Lung Adenocarcinoma: Modification of the 2004 WHO Mixed Subtype to Include the Major Histologic Subtype Suggests Correlations Between Papillary and Micropapillary Adenocarcinoma Subtypes, EGFR Mutations and Gene Expression Analysis , 2008, The American journal of surgical pathology.

[3]  Antonio Marchetti,et al.  Frequent mutations in the neurotrophic tyrosine receptor kinase gene family in large cell neuroendocrine carcinoma of the lung , 2008, Human mutation.

[4]  Daniel F. Gudbjartsson,et al.  A variant associated with nicotine dependence, lung cancer and peripheral arterial disease , 2008, Nature.

[5]  S. Heath,et al.  A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25 , 2008, Nature.

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

[7]  A. Sparks,et al.  The Genomic Landscapes of Human Breast and Colorectal Cancers , 2007, Science.

[8]  M. Mohammadi,et al.  A molecular brake in the kinase hinge region regulates the activity of receptor tyrosine kinases. , 2007, Molecular cell.

[9]  Tomoki Yokoyama,et al.  Nras and Kras mutation in Japanese lung cancer patients: Genotyping analysis using LightCycler. , 2007, Oncology reports.

[10]  Spyro Mousses,et al.  A transforming mutation in the pleckstrin homology domain of AKT1 in cancer , 2007, Nature.

[11]  D. Gutmann,et al.  Nucleophosmin mediates mammalian target of rapamycin-dependent actin cytoskeleton dynamics and proliferation in neurofibromin-deficient astrocytes. , 2007, Cancer research.

[12]  R. Wilson,et al.  Mutational Analysis of EGFR and Related Signaling Pathway Genes in Lung Adenocarcinomas Identifies a Novel Somatic Kinase Domain Mutation in FGFR4 , 2007, PloS one.

[13]  V. McKusick Mendelian Inheritance in Man and Its Online Version, OMIM , 2007, The American Journal of Human Genetics.

[14]  E. Birney,et al.  Patterns of somatic mutation in human cancer genomes , 2007, Nature.

[15]  Janakiraman Subramanian,et al.  Lung cancer in never smokers: a review. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[16]  G. Parmigiani,et al.  The Consensus Coding Sequences of Human Breast and Colorectal Cancers , 2006, Science.

[17]  J. Brahmer,et al.  Adjuvant treatment in non-small cell lung cancer: Where are we now? , 2006, Journal of the National Comprehensive Cancer Network : JNCCN.

[18]  Yun-Chul Hong,et al.  Genetic polymorphisms of ataxia telangiectasia mutated affect lung cancer risk. , 2006, Human molecular genetics.

[19]  M. Stratton,et al.  COSMIC 2005 , 2006, British Journal of Cancer.

[20]  Andrew D. Yates,et al.  Somatic mutations of the protein kinase gene family in human lung cancer. , 2005, Cancer research.

[21]  M. Meyerson,et al.  Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis. , 2005, Cancer research.

[22]  P. Hainaut,et al.  TP53 and KRAS mutation load and types in lung cancers in relation to tobacco smoke: distinct patterns in never, former, and current smokers. , 2005, Cancer research.

[23]  Elisabeth Brambilla,et al.  The 2004 World Health Organization classification of lung tumors. , 2005, Seminars in roentgenology.

[24]  J. Ferlay,et al.  Global Cancer Statistics, 2002 , 2005, CA: a cancer journal for clinicians.

[25]  M. Meyerson,et al.  EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. , 2005, The New England journal of medicine.

[26]  H. Varmus,et al.  Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain , 2005, PLoS medicine.

[27]  H. Varmus,et al.  KRAS Mutations and Primary Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib , 2005, PLoS medicine.

[28]  Andrew D. Yates,et al.  Athletics: Momentous sprint at the 2156 Olympics? , 2004, Nature.

[29]  R. Wilson,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. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[30]  David J. Chen,et al.  Role of DNA-PK in the cellular response to DNA double-strand breaks. , 2004, DNA repair.

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

[32]  K. Chin,et al.  Frequent Silencing of Low Density Lipoprotein Receptor-Related Protein 1B (LRP1B) Expression by Genetic and Epigenetic Mechanisms in Esophageal Squamous Cell Carcinoma , 2004, Cancer Research.

[33]  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.

[34]  M. Kurrer,et al.  APC mutations are infrequent but present in human lung cancer. , 2004, Cancer letters.

[35]  Nicole Benoit,et al.  p53 mutations and survival in stage I non-small-cell lung cancer: results of a prospective study. , 2003, Journal of the National Cancer Institute.

[36]  Christian A. Rees,et al.  Microarray analysis reveals a major direct role of DNA copy number alteration in the transcriptional program of human breast tumors , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[37]  David Sidransky,et al.  Inactivation of LKB1/STK11 is a common event in adenocarcinomas of the lung. , 2002, Cancer research.

[38]  A. Nicholson,et al.  Mutations of the BRAF gene in human cancer , 2002, Nature.

[39]  J. Minna,et al.  LRP-DIT, a putative endocytic receptor gene, is frequently inactivated in non-small cell lung cancer cell lines. , 2000, Cancer research.

[40]  T. Halazonetis,et al.  Chk2/hCds1 functions as a DNA damage checkpoint in G(1) by stabilizing p53. , 2000, Genes & development.

[41]  S. Hecht,et al.  Tobacco smoke carcinogens and lung cancer. , 1999, Journal of the National Cancer Institute.

[42]  R. Brezinschek,et al.  Mutation analysis of the PTEN/MMAC1 gene in lung cancer , 1998, Oncogene.

[43]  J. Barrett,et al.  Homozygous deletions at chromosome 9p21 and mutation analysis of p16 and p15 in microdissected primary non-small cell lung cancers. , 1995, Clinical cancer research : an official journal of the American Association for Cancer Research.

[44]  T. Sellers,et al.  Evidence for mendelian inheritance in the pathogenesis of lung cancer. , 1990, Journal of the National Cancer Institute.

[45]  P. O'Connell,et al.  A major segment of the neurofibromatosis type 1 gene: cDNA sequence, genomic structure, and point mutations , 1990, Cell.

[46]  J. Minna,et al.  p53: a frequent target for genetic abnormalities in lung cancer. , 1989, Science.

[47]  S. Rodenhuis,et al.  Incidence and possible clinical significance of K-ras oncogene activation in adenocarcinoma of the human lung. , 1988, Cancer research.

[48]  R. Weinberg,et al.  Deletions of a DNA sequence in retinoblastomas and mesenchymal tumors: organization of the sequence and its encoded protein. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[49]  Yang Wei-we,et al.  A Review on , 2008 .

[50]  T. Sellers,et al.  Environmental factors can confound identification of a major gene effect: Results from a segregation analysis of a simulated population of lung cancer families , 1998, Genetic epidemiology.

[51]  K. Münger,et al.  Oncoproteins encoded by the cancer-associated human papillomaviruses target the products of the retinoblastoma and p53 tumor suppressor genes. , 1991, Cold Spring Harbor symposia on quantitative biology.

[52]  N. Dobbs,et al.  Br. J. Cancer '." , 2022 .