Abstract
Abstract Background: Not much is known about different signalling pathways and its influence on metastasis in colon cancer. Phospho-ERK (pERK) is a downstream-target of K-Ras within the EGFR-Pathway. The goal of our investigations was the evaluation of the MAP-Kinase-cascade in regard to different ways of metastasis. Methods: 98 patients with adenocarcinom of the colon and a postoperative pT2/3-status, who underwent surgical resection between 2006 and 2008 at the University of Tübingen had been included within the study collective. 53 patients had no metastasis (control group), while 45 patients revealed primary metastasis: lymphogenetic metastasis (n=20), hepatic spread (n=20) and multiple metastasize (n=5). On a tissue-micro-Array pERK was stained by immunohistochemistry, the analysis was done semiquantitatively. Results: The graduation in immunohistochemistry was done as followed: negative staining (n=31), weak positive staining (n=36), moderate staining (n=20) and strong staining (n=11). 19 out of 31 negative patients (61%) revealed metastasis, while this had been 17 out of 36 weak positive (47%), 6 out of 20 (30%) moderate and 4 out of 11 (36%) strongly positive stained patients (p=0.229). No significant correlation was observed for lypmhogenetic (p=0.683) or multiple metastatic localization (p=0.666) and the pERK-expression. A significant correlation between the pERK-expression and the number of hepatic metastasis was observed (p=0.049). Additionally pERK-negative patients (31/98 = 32%) revealed a significant worse survival compared to those with positive pERK-staining (p=0.003). Conclusion: Our first results show, that a weak pERK-expression is correlated with a higher incidence in patients with liver metastasis. Patients without a pERK-expression revealed a worse survival compared to patients with pERK-expression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 455. doi:1538-7445.AM2012-455
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