title: Cetuximab inhibits the growth of mucinous ovarian carcinoma tumor cells             lacking KRAS gene mutations.
abstract: The purpose of this study was to explore the possibility of targeted molecular             therapy with anti-epidermal growth factor receptor (anti-EGFR) antibody (cetuximab)             for the treatment of mucinous ovarian carcinoma. We analyzed EGFR protein expression             and KRAS gene mutations in 5 mucinous ovarian carcinoma cell lines RMUG-L, RMUG-S,             MN-1, OMC-1 and MCAS and evaluated the in vitro and in vivo effects of cetuximab             on each. EGFR expression was observed in all cell lines except for MN-1 cells,             and a KRAS gene mutation at codon 12 was detected only in the MCAS cell line.             Cetuximab inhibited RMUG-L and OMC-1 cell growth in vitro and completely blocked             RMUG-L tumor growth in vivo. On the other hand, cetuximab did not affect MCAS             cell growth in vitro and only partially reduced the MCAS tumor growth in vivo.             These results suggest the possibility of targeted molecular therapy with cetuximab             for mucinous ovarian carcinoma cells lacking a KRAS gene mutation.
authors.affiliation: Department of Obstetrics and Gynecology, Center for Molecular Medicine, School of Medicine, Jichi Medical University, Tochigi, Japan.
authors.forename: Naoto
authors.initials: N
authors.lastname: Sato
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Saga
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Mizukami
authors.forename: Dongdong
authors.initials: D
authors.lastname: Wang
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Fujiwara
authors.forename: Yuji
authors.initials: Y
authors.lastname: Takei
authors.forename: Shizuo
authors.initials: S
authors.lastname: Machida
authors.forename: Keiya
authors.initials: K
authors.lastname: Ozawa
authors.forename: Mitsuaki
authors.initials: M
authors.lastname: Suzuki
mesh_terms: D002288:Adenocarcinoma, Mucinous / Q000188:drug therapy / Q000235:genetics*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology*; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D001483:Base Sequence; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D000068818:Cetuximab; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000378:metabolism; D005091:Exons; D005260:Female; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009154:Mutation; D010051:Ovarian Neoplasms / Q000188:drug therapy / Q000235:genetics*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D023041:Xenograft Model Antitumor Assays; D018631:ras Proteins / Q000235:genetics*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins; D000068818:Cetuximab