title: BRAF p.Val600Glu (V600E) somatic mutation is mainly associated with MSS phenotype in metastatic colorectal cancer.
abstract: BACKGROUND
  Oncogenic activation of EGF-signalling pathway is central to the progression of colorectal cancer. The use of mutations of the KRAS codons 12 and 13 as a selection biomarker for anti-endothelial growth factor receptor (EGFR) monoclonal antibody treatment is at present the first major step towards individualised treatment for patients with metastatic colorectal cancer. The impact of BRAF V600E mutation is not well documented.
  
  
  METHODS
  A total of 803 metastatic cancer samples from colorectal cancer patients were explored for KRAS exon 2 and BRAF exon 15 mutations. BRAF mutated samples were characterized for mismatch repair function.
  
  
  RESULTS
  Overall, 344 tumours were mutated, with 34 of them involving BRAF mutations (8 of microsatellite instability type). No specificity was found according to gender, age at diagnosis and tumour localisation.
  
  
  CONCLUSIONS
  A complete analysis of KRAS, BRAF and PIK3CA status may identify approximately 10-15% additional patients who are unlikely to respond an EGFR-targeted monoclonal antibody and who may benefit from prospective and specific new biomarker-driven studies.
authors.affiliation: Institut Paoli-Calmettes, Marseille, France.
authors.forename: Jinghua
authors.initials: J
authors.lastname: Qiu
authors.forename: Marion
authors.initials: M
authors.lastname: Compagnone
authors.forename: Sophy
authors.initials: S
authors.lastname: Laibe
authors.forename: Arnaud
authors.initials: A
authors.lastname: Lagarde
authors.forename: Anthony
authors.initials: A
authors.lastname: Goncalves
authors.forename: Olivier
authors.initials: O
authors.lastname: Turrini
authors.forename: Luc
authors.initials: L
authors.lastname: Xerri
authors.forename: Geneviève
authors.initials: G
authors.lastname: Monges
authors.forename: Sylviane
authors.initials: S
authors.lastname: Olschwang
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000556:secondary* / Q000628:therapy; D000293:Adolescent; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D002648:Child; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology* / Q000628:therapy; D066246:ErbB Receptors / Q000037:antagonists & inhibitors; D005260:Female; D018698:Glutamic Acid / Q000235:genetics; D006801:Humans; D008297:Male; D053842:Microsatellite Instability; D008875:Middle Aged; D009154:Mutation; D009362:Neoplasm Metastasis; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D014633:Valine / Q000235:genetics; D055815:Young Adult; D018631:ras Proteins / Q000235:genetics*
chemical_list: D000911:Antibodies, Monoclonal; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; D018698:Glutamic Acid; C512478:EGFR protein, human; D066246:ErbB Receptors; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins; D014633:Valine