Expression of cyclooxygenase-2 has no impact on survival in adenocarcinoma of the esophagogastric junction but is associated with favourable clinicopathologic features.
Histol Histopathol. 2016 Nov 17;:11843
Authors: Knief J, Reddemann K, Petrova E, Herhahn T, Wellner U, Thorns C
Abstract
Background COX-2 expression induces carcinogenesis and is thought to be an adverse prognostic factor in gastric carcinomas while the prognostic value of DNA mismatch repair (MMR) is still controversial. Concerning adenocarcinomas of the esophagogastric junction, no comprehensive data regarding either factors are available as of yet. Objective We assessed expression of COX-2, MLH1 and MSH2 in adenocarcinoma of the esophagogastric junction in relation to patients' survival and various clinicopathologic features. Design Immunohistochemical studies (using antibodies against COX-2, MLH1 and MSH2) were performed in a study population of 228 tumours. Follow-up data was available for all patients with a mean follow-up time of 42.8 months. Results 78 (34.2%) tumours were COX-2 negative, 148 (64.9%) showed COX-2 positivity. Assessment of COX-2 expression and clinicopathologic features revealed an inverse correlation with depth of tumour invasion and number of metastatic lymph nodes (p=0,021 and p=0,004, respectively). No correlation with other features could be demonstrated. 62 cases (27.2%) showed loss of DNA repair enzymes MLH1 and/or MSH2. MMR differed significantly between COX-2 positive and negative cases (p=0,028). Kaplan-Meier survival analyses revealed no impact on patients' survival for COX-2 expression or MMR status (p=0.837 and p=0.972, respectively).
CONCLUSIONS: Expression of COX-2 in adenocarcinomas of the esophagogastric junction seems to have no prognostic effect or impact on patients' survival but is associated with favourable clinicopathologic factors. MMR deficiency was more frequent in COX-2 negative tumours, but MMR status had no impact on survival and patients' outcome whatsoever.
PMID: 27854106 [PubMed - as supplied by publisher]
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