[Mutation of EGFR signaling pathway and therapy for metastatic colorectal cancer].
For the patient in whom the Kras gene variation appears, cancer cell grow and continue to multiply even if blocked by EGFR inhibitor. A topping the offered figure effect of cetuximab is not accepted. The addition of cetuximab for treatment of metastatic colorectal cancer with Kras wild-type tumors is effective.
Nozawa
Keijirou
K
Dept. of Surgery, Teikyo University, Itabashi-ku, Tokyo, Japan.
Watanabe
Toshiaki
T
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000276:immunology / Q000627:therapeutic use; D000068818:Cetuximab; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D066246:ErbB Receptors / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D009154:Mutation; D009362:Neoplasm Metastasis; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D015398:Signal Transduction / Q000187:drug effects*; D018631:ras Proteins / Q000235:genetics*
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