ANTI-EGFR ANTIBODY TREATMENT IN KRAS G13D MUTATION-TYPE COLORECTAL CANCERS: CASE REPORTS

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Abstract

Anti-EGFR antibody is effective for Kras wild-type colorectal cancers (CRCs), but not effective for the Kras mutation-type. Recently, some reports have shown that it is effective for Kras G13D mutation-type CRCs. Herein, we reported two cases of Kras G13D mutation-type CRCs treated by anti-EGFR antibody with sufficient explanation and informed consent. Case 1: a 66-year-old female patient underwent left colectomy for descending colon cancer in January 2009. The clinical stage was IIIb. Although adjuvant chemotherapy was given, metastasis to para-aortic lymph nodes occurred in January 2010. After four cycles of xelox + bevacizumab and 17 cycles of FOLFIRI, the recurrent tumors showed progression in July 2011. The primary tumor had Kras G13D mutation, therefore, 6 cycles of Cetuximab administration was conducted. The serum level of CEA was decreased (from 45.5 to 18.9), and no deterioration of para-aortic lymph node metastasis was seen. However, new lesions of lymph node metastasis and hydronephrosis occurred, and chemotherapy was stopped. Case 2: A 62-year-old female patient underwent transverse colectomy and total hysterectomy + with bilateral salpingo-oophorectomy for transverse colon cancer and ovarian metastases in March 2009.Clinical stage was IV. Eight cycles of FOLFOX followed by four cycles of 5FU/LV and capecitabine monotherapy were given as adjuvant chemotherapy. In August 2010, peritoneal dissemination and lung metastasis were detected. After 14 cycles of FOLFOX + Bevacizumab, the recurrent tumors showed progression. The primary tumor had Kras G13D mutation; therefore, four cycles of panitumumab administration was conducted. Although the serum levels of tumor markers were decreased (CEA: from 328.2 to 267.2, CA19-9: from 55.2 to 28.8), the lung metastasis showed progression, and chemotherapy was stopped. Although the evidence level is still limited, anti-EGFR antibody treatment may be an option in Kras G13D mutation-type CRCs.

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