EGFR Exon 20 Insertion Mutations in Lung Adenocarcinomas: Prevalence, Molecular Heterogeneity, and Clinicopathologic Characteristics
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Marc Ladanyi | Natasha Rekhtman | B. Reva | M. Ladanyi | M. Kris | M. Arcila | C. Lau | K. Nafa | M. Zakowski | N. Rekhtman | J. Chaft | Mark G. Kris | Maria E. Arcila | Jamie E. Chaft | Maureen F. Zakowski | Khedoudja Nafa | Christopher Lau | Boris A. Reva
[1] 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.
[2] S. Gabriel,et al. EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy , 2004, Science.
[3] 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.
[4] Takayuki Kosaka,et al. Mutations of the Epidermal Growth Factor Receptor Gene in Lung Cancer , 2004, Cancer Research.
[5] Shih-Feng Tsai,et al. High Frequency of Epidermal Growth Factor Receptor Mutations with Complex Patterns in Non–Small Cell Lung Cancers Related to Gefitinib Responsiveness in Taiwan , 2004, Clinical Cancer Research.
[6] M. Ostland,et al. Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[7] M. Ladanyi,et al. Rapid polymerase chain reaction-based detection of epidermal growth factor receptor gene mutations in lung adenocarcinomas. , 2005, The Journal of molecular diagnostics : JMD.
[8] 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.
[9] William C Hahn,et al. Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants , 2005, PLoS medicine.
[10] 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.
[11] T. Chou,et al. Mutation in the Tyrosine Kinase Domain of Epidermal Growth Factor Receptor Is a Predictive and Prognostic Factor for Gefitinib Treatment in Patients with Non–Small Cell Lung Cancer , 2005, Clinical Cancer Research.
[12] M. Nishimura,et al. Non-responsiveness to gefitinib in a patient with lung adenocarcinoma having rare EGFR mutations S768I and V769L. , 2006, Lung cancer.
[13] M. Meyerson,et al. Allele-dependent variation in the relative cellular potency of distinct EGFR inhibitors , 2007, Cancer biology & therapy.
[14] H. Sasaki,et al. EGFR exon 20 insertion mutation in Japanese lung cancer. , 2007, Lung cancer.
[15] P. Jänne,et al. Prospective study of gefitinib in epidermal growth factor receptor fluorescence in situ hybridization-positive/phospho-Akt-positive or never smoker patients with advanced non-small-cell lung cancer: the ONCOBELL trial. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[16] Alona Muzikansky,et al. Response to treatment and survival of patients with non-small cell lung cancer undergoing somatic EGFR mutation testing. , 2007, The oncologist.
[17] M. Meyerson,et al. PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib. , 2007, Cancer research.
[18] Alona Muzikansky,et al. First-line gefitinib in patients with advanced non-small-cell lung cancer harboring somatic EGFR mutations. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[19] M. Meyerson,et al. BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models , 2008, Oncogene.
[20] Yih-Leong Chang,et al. Lung Cancer with Epidermal Growth Factor Receptor Exon 20 Mutations Is Associated with Poor Gefitinib Treatment Response , 2008, Clinical Cancer Research.
[21] 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.
[22] Susan Quinn,et al. Neratinib, an irreversible pan-ErbB receptor tyrosine kinase inhibitor: results of a phase II trial in patients with advanced non-small-cell lung cancer. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[23] I. Petersen,et al. EGFR mutation detection in NSCLC—assessment of diagnostic application and recommendations of the German Panel for Mutation Testing in NSCLC , 2010, Virchows Archiv.
[24] M. Ladanyi,et al. EGFR Exon 19 Insertions: A New Family of Sensitizing EGFR Mutations in Lung Adenocarcinoma , 2011, Clinical Cancer Research.
[25] C. Sander,et al. Predicting the functional impact of protein mutations: application to cancer genomics , 2011, Nucleic acids research.
[26] A. Iafrate,et al. A platform for rapid detection of multiple oncogenic mutations with relevance to targeted therapy in non-small-cell lung cancer. , 2011, The Journal of molecular diagnostics : JMD.
[27] P. Jänne,et al. Phase I Dose-Escalation Study of the Pan-HER Inhibitor, PF299804, in Patients with Advanced Malignant Solid Tumors , 2011, Clinical Cancer Research.
[28] M. Ladanyi,et al. Detection of KRAS and BRAF mutations in colorectal carcinoma roles for high-sensitivity locked nucleic acid-PCR sequencing and broad-spectrum mass spectrometry genotyping. , 2011, The Journal of molecular diagnostics : JMD.
[29] G. Giaccone,et al. Characterization of epidermal growth factor receptor mutations in non-small-cell lung cancer patients of African-American ancestry , 2011, Oncogene.
[30] M. Ladanyi,et al. Reflex testing of resected stage I through III lung adenocarcinomas for EGFR and KRAS mutation: report on initial experience and clinical utility at a single center. , 2011, The Journal of thoracic and cardiovascular surgery.
[31] Masahiro Tsuboi,et al. International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society International Multidisciplinary Classification of Lung Adenocarcinoma , 2011, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.
[32] M. Ladanyi,et al. Coexistence of PIK3CA and Other Oncogene Mutations in Lung Adenocarcinoma–Rationale for Comprehensive Mutation Profiling , 2011, Molecular Cancer Therapeutics.
[33] M. Ladanyi,et al. Clarifying the Spectrum of Driver Oncogene Mutations in Biomarker-Verified Squamous Carcinoma of Lung: Lack of EGFR/KRAS and Presence of PIK3CA/AKT1 Mutations , 2012, Clinical Cancer Research.
[34] M. Ladanyi,et al. Prevalence, Clinicopathologic Associations, and Molecular Spectrum of ERBB2 (HER2) Tyrosine Kinase Mutations in Lung Adenocarcinomas , 2012, Clinical Cancer Research.
[35] G. Mulligan,et al. Tissue microarray analysis reveals protein expression patterns and potential biomarkers of clinical benefit to bortezomib in relapsed/refractory non‐Hodgkin lymphoma , 2012, British journal of haematology.
[36] M. Ladanyi,et al. Screening for Germline EGFR T790M Mutations Through Lung Cancer Genotyping , 2012, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.
[37] S. Kobayashi,et al. EGFR exon 20 insertion mutations in non-small-cell lung cancer: preclinical data and clinical implications. , 2012, The Lancet. Oncology.
[38] William Pao,et al. Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1 , 2012, Proceedings of the National Academy of Sciences.