title: [KRAS Genetic Mutation Analysis Using the Clinical FFPE Samples of Colorectal Carcinomas: Comparative Study among 5 Methods].
abstract: Targeting of epidermal growth factor receptor (EGFR) with monoclonal antibodies such as cetuximab or panitumumab inhibits the activation of downstream signaling molecules of EGFR. Since EGFR inhibitor therapy has been approved for the treatment of colorectal carcinomas in patients with tumors lacking KRAS mutations, the detection of KRAS mutation is indispensable before starting therapy. Although several laboratory procedures have been developed to detect KRAS mutations, few comparative studies of the sensitivity of mutation detection have been performed for such procedures. Here, we compared the levels of detection in 5 commercial KRAS mutation detection methods using both standard DNA samples and formalin-fixed clinical samples obtained during surgery. Scorpion-ARMS assay has been reported as the most sensitive and we compared 4 other methods with Scorpion. Both PCR-rSSO assay and F-PHFA assay showed the highest concordance. As for the detection sensitivity, there were variations between clinical samples apparently due to sample quality or assay principles and methods. It is thus suggested that routine validation is required using samples prepared in each lab and the choice of assay may depend on various factors, such as lab environment, actual needs of physicians and patients, and the quality of the formalin-fixed specimens.
authors.forename: Kanae
authors.initials: K
authors.lastname: Okada
authors.forename: Naoko
authors.initials: N
authors.lastname: Asano
authors.forename: Yoko
authors.initials: Y
authors.lastname: Kajiura
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Shimoyama
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Tadashi
authors.initials: T
authors.lastname: Matsushita
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D000068818:Cetuximab / Q000627:therapeutic use; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000235:genetics*; D004247:DNA / Q000235:genetics; D004252:DNA Mutational Analysis / Q000379:methods*; D066246:ErbB Receptors; D006801:Humans; D058990:Molecular Targeted Therapy; D009154:Mutation; D000077544:Panitumumab; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics*; D011933:Reagent Kits, Diagnostic
chemical_list: D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents; C117307:KRAS protein, human; D011933:Reagent Kits, Diagnostic; D000077544:Panitumumab; D004247:DNA; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D000068818:Cetuximab