EGFR status and KRAS/BRAF mutations in intestinal-type sinonasal adenocarcinomas

[1]  M. Hermsen,et al.  Gene amplification and protein overexpression of EGFR and ERBB2 in sinonasal squamous cell carcinoma , 2012, Cancer.

[2]  P. Delvenne,et al.  The human epidermal growth factor receptor (EGFR) gene in European patients with advanced colorectal cancer harbors infrequent mutations in its tyrosine kinase domain , 2011, BMC Medical Genetics.

[3]  XiaoNa Wei.  Mechanism of EGER-related cancer drug resistance , 2011, Anti-cancer drugs.

[4]  R. Palmqvist,et al.  Increased epidermal growth factor receptor expression at the invasive margin is a negative prognostic factor in colorectal cancer , 2011, International journal of cancer.

[5]  M. Fresno,et al.  Benign Lesions in Mucosa Adjacent to Intestinal-Type Sinonasal Adenocarcinoma , 2011, Pathology Research International.

[6]  M. Hermsen,et al.  Establishment and genetic characterization of an immortal tumor cell line derived from intestinal-type sinonasal adenocarcinoma , 2011, Cellular Oncology.

[7]  L. Terracciano,et al.  Combined analysis of specific KRAS mutation, BRAF and microsatellite instability identifies prognostic subgroups of sporadic and hereditary colorectal cancer , 2010, International journal of cancer.

[8]  L. Terracciano,et al.  Clinicopathological and protein characterization of BRAF‐ and K‐RAS‐mutated colorectal cancer and implications for prognosis , 2010, International journal of cancer.

[9]  Jie Gao,et al.  Relationship between EGFR expression, copy number and mutation in lung adenocarcinomas , 2010, BMC Cancer.

[10]  M. Diodoro,et al.  Epidermal growth factor receptor gene copy number in 101 advanced colorectal cancer patients treated with chemotherapy plus cetuximab , 2010, Journal of Translational Medicine.

[11]  Xin Lu,et al.  Metalloproteinases and osteoblast EGFR signaling in osteolytic bone metastasis of breast cancer , 2009, Cell cycle.

[12]  A. Franchi,et al.  Epidermal growth factor receptor expression and gene copy number in sinonasal intestinal type adenocarcinoma. , 2009, Oral oncology.

[13]  Sabine Tejpar,et al.  Implications for KRAS status and EGFR-targeted therapies in metastatic CRC , 2009, Nature Reviews Clinical Oncology.

[14]  F. Cappuzzo,et al.  Predictive value of EGFR and HER2 overexpression in advanced non-small-cell lung cancer , 2009, Oncogene.

[15]  M. Tsao,et al.  Overview of molecular testing in non-small-cell lung cancer: mutational analysis, gene copy number, protein expression and other biomarkers of EGFR for the prediction of response to tyrosine kinase inhibitors , 2009, Oncogene.

[16]  M. Hermsen,et al.  Genetic differences between primary larynx and pharynx carcinomas and their matched lymph node metastases by multiplex ligation-dependent probe amplification. , 2009, Oral oncology.

[17]  J. Pfeifer,et al.  Receptor tyrosine kinases in sinonasal undifferentiated carcinomas—Evaluation for EGFR, c‐KIT, and HER2/neu expression , 2009, Head & neck.

[18]  B. Ylstra,et al.  Genome‐wide analysis of genetic changes in intestinal‐type sinonasal adenocarcinoma , 2009, Head & neck.

[19]  Sjoerd J. Vosse,et al.  Across array comparative genomic hybridization: A strategy to reduce reference channel hybridizations , 2008, Genes, chromosomes & cancer.

[20]  A. Rosman,et al.  Prognostic implications of normal (<0.10 ng/ml) and borderline (0.10 to 1.49 ng/ml) troponin elevation levels in critically ill patients without acute coronary syndrome. , 2008, The American journal of cardiology.

[21]  S. Thibodeau,et al.  Salivary gland-type lung carcinomas: an EGFR immunohistochemical, molecular genetic, and mutational analysis study , 2008, Modern Pathology.

[22]  A. Lièvre,et al.  KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[23]  M. Hermsen,et al.  Genetic and clinical aspects of wood dust related intestinal-type sinonasal adenocarcinoma: a review , 2008, European Archives of Oto-Rhino-Laryngology.

[24]  U. Vogel,et al.  K-ras mutations in sinonasal cancers in relation to wood dust exposure , 2008, BMC Cancer.

[25]  Diane D. Liu,et al.  Epidermal growth factor receptor copy number alterations correlate with poor clinical outcome in patients with head and neck squamous cancer. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[26]  Felix Y. Feng,et al.  Integration of EGFR inhibitors with radiochemotherapy , 2006, Nature Reviews Cancer.

[27]  M. Pierotti,et al.  Phenotype–genotype correlation: Challenge of intestinal‐type adenocarcinoma of the nasal cavity and paranasal sinuses , 2006, Head & neck.

[28]  J. Rodrigo,et al.  Amplification of CCND1, EMS1, PIK3CA, and ERBB oncogenes in ethmoid sinus adenocarcinomas. , 2006, Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery.

[29]  F. Ciardiello,et al.  Prognostic Significance of Epidermal Growth Factor Receptor Expression in Colon Cancer Patients Undergoing Curative Surgery , 2006, Annals of Surgical Oncology.

[30]  M. Pacyna‐Gengelbach,et al.  Chromosomal imbalances in wood dust‐related adenocarcinomas of the inner nose and their associations with pathological parameters , 2005, The Journal of pathology.

[31]  R. Weber,et al.  Genetic analysis of sinonasal adenocarcinoma phenotypes: distinct alterations of histogenetic significance , 2005, Modern Pathology.

[32]  B. Perez-Ordonez,et al.  Expression of mismatch repair proteins, β catenin, and E cadherin in intestinal-type sinonasal adenocarcinoma , 2004, Journal of Clinical Pathology.

[33]  C. Suárez,et al.  Prognostic factors in sinonasal tumors involving the anterior skull base , 2004, Head & neck.

[34]  M. Hermsen,et al.  Comparative genomic hybridization in primary sinonasal adenocarcinomas. , 2003, Cancer.

[35]  O. Kleinsasser,et al.  Adenocarcinomas of the inner nose after exposure to wood dust , 1988, Archives of oto-rhino-laryngology.

[36]  M. Pierotti,et al.  TP53, p14ARF, p16INK4a and H‐ras gene molecular analysis in intestinal‐type adenocarcinoma of the nasal cavity and paranasal sinuses , 2003, International journal of cancer.

[37]  E. Berg,et al.  World Health Organization Classification of Tumours , 2002 .

[38]  N. Goldstein,et al.  Epidermal growth factor receptor immunohistochemical reactivity in patients with American Joint Committee on Cancer Stage IV colon adenocarcinoma , 2001, Cancer.

[39]  O. Domínguez,et al.  ras Gene mutations in ethmoid sinus adenocarcinoma , 1999, Cancer.

[40]  L. Hagmar,et al.  K-ras mutations in sinonasal adenocarcinomas in patients occupationally exposed to wood or leather dust. , 1998, Cancer letters.

[41]  S. Finkelstein,et al.  K-ras-2 and p53 genotyping of intestinal-type adenocarcinoma of the nasal cavity and paranasal sinuses. , 1996, Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc.

[42]  S. Mills,et al.  Sinonasal intestinal-type adenocarcinoma: immunohistochemical profile and comparison with colonic adenocarcinoma. , 1995, Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc.

[43]  Robert C. Wolpert,et al.  A Review of the , 1985 .