Effect of preoperative FOLFOX chemotherapy on CCL20/CCR6 expression in colorectal liver metastases
| Autor: | Rubie, Claudia, Frick, Vilma Oliveira, Ghadjar, Pirus, Wagner, Mathias, Justinger, Christoph, Graeber, Stefan, Sperling, Jens, Kollmar, Otto, Schilling, Martin K |
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| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Adult
Male Receptors CCR6 Chemokine CCL20 Organoplatinum Compounds Liver Neoplasms Leucovorin chemical and pharmacologic phenomena hemic and immune systems Middle Aged digestive system diseases Ki-67 Antigen Antineoplastic Combined Chemotherapy Protocols Preoperative Period Biomarkers Tumor Humans Original Article Fluorouracil Colorectal Neoplasms Aged Cell Proliferation |
| Popis: | To evaluate the influence of preoperative FOLFOX chemotherapy on CCL20/CCR6 expression in liver metastases of stage IV colorectal cancer (CRC) patients.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).Of the 53 patients who received FOLFOX, time to liver surgery was ≤ 1 mo in 14 patients, ≤ 1 year in 22 patients and1 year in 17 patients, respectively. In addition, we investigated the proliferation rate of CRC cells in liver metastases in the different patient groups. Both CCL20 and CCR6 mRNA and protein expression levels were significantly increased in patients who received preoperative FOLFOX chemotherapy ≤ 12 mo before liver surgery (P0.001) in comparison to patients who did not undergo FOLFOX treatment. Further, proliferation of CRLM cells as measured by Ki-67 was increased in patients who underwent FOLFOX treatment. CCL20 and CCR6 expression levels were significantly increased in CRLM patients who had undergone preoperative FOLFOX chemotherapy.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. |
| Databáze: | OpenAIRE |
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