Effect of preoperative FOLFOX chemotherapy on CCL20/CCR6 expression in colorectal liver metastases

作     者：Claudia Rubie Vilma Oliveira Frick Pirus Ghadjar Mathias Wagner Christoph Justinger Stefan Graeber Jens Sperling Otto Kollmar Martin K Schilling 

作者机构：Department of GeneralVisceralVascular and Paediatric SurgeryUniversity of the Saarland Department of Radiation OncologyInselspitalBern University Hospital and University of Bern Institute of PathologyUniversity of the Saarland Institute of Medical BiometricsEpidemiologyand Medical Informatics(IMBEI)University of the Saarland 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2011年第17卷第26期

页      面：3109-3116页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：肝脏 化疗 大肠癌 增殖率 M细胞 结直肠癌 蛋白表达 mRNA 

摘      要：AIM:To evaluate the influence of preoperative FOLFOX chemotherapy on CCL20/CCR6 expression in liver metastases of stage Ⅳ colorectal cancer(CRC) ***:Using Real Time-PCR,enzyme-linked immunosorbent assay,Western Blots and immunohistochemistry,we have analyzed the expression of CCL20,CCR6 and proliferation marker Ki-67 in colorectal liver metastasis(CRLM) specimens from stage Ⅳ CRC patients who received preoperative FOLFOX chemotherapy(n = 53) and in patients who did not receive FOLFOX chemotherapy prior to liver surgery(n = 29).RESULTS:Of the 53 patients who received FOLFOX,time to liver surgery was ≤ 1 mo in 14 patients,≤ 1 year in 22 patients and 1 year in 17 patients,*** addition,we investigated the proliferation rate of CRC cells in liver metastases in the different patient *** CCL20 and CCR6 mRNA and protein expression levels were significantly increased in patients who received preoperative FOLFOX chemotherapy ≤ 12 mo before liver surgery(P 0.001) in comparison to patients who did not undergo FOLFOX ***,proliferation of CRLM cells as measured by Ki-67 was increased in patients who underwent FOLFOX ***20 and CCR6 expression levels were significantly increased in CRLM patients who had undergone preoperative FOLFOX ***:This chemokine/receptor up-regulation could lead to increased proliferation/migration through an autocrine mechanism which might be used by surviving metastatic cells to escape cell death caused by FOLFOX.