The metabolic marker tumour pyruvate kinase type M2 (tumour M2-PK) shows increased expression along the metaplasia–dysplasia–adenocarcinoma sequence in Barrett's oesophagus. Issue 11 (27th October 2004)

• Record Type: Journal Article
• Authors: Koss, K; Harrison, R F; Gregory, J; Darnton, S J; Anderson, M R; Jankowski, J A Z
• Is Part Of: Journal of clinical pathology. Volume 57:Issue 11(2004)
• Page Start: 1156
• Page End: 1159
• Publication Date: 2004-10-27
• Subjects: M2-PK, pyruvate kinase type M2 -- PK, pyruvate kinase; Barrett's oesophagus -- dysplasia -- adenocarcinoma -- pyruvate kinase type M2 -- tumour M2-PK; Pathology -- Periodicals; Pathology, Molecular -- Periodicals; 616.0705
• DOI: 10.1136/jcp.2004.018150
• Languages: English
• ISSNs: 0021-9746

Abstract

Abstract : Background: Proliferating and tumour cells express the glycolytic isoenzyme, pyruvate kinase type M2 (M2-PK). In tumours cells, M2-PK usually exists in dimeric form (tumour M2-PK), causing the accumulation of glycolytic phosphometabolites, which allows cells to invade areas with low oxygen and glucose concentrations. Aims: To investigate the expression of tumour M2-PK during the metaplasia–dysplasia–adenocarcinoma sequence of Barrett's oesophagus, and to assess the prognostic usefulness of tumour M2-PK in oesophageal cancer. Materials/Methods: One hundred and ninety cases selected from the histopathology archives as follows: 17 reflux oesophagitis, 37 Barrett's oesophagus, 21 high grade dysplasia, 112 adenocarcinomas, and three control tumours. Sections were stained immunohistochemically with antibody to tumour M2-PK. Results: Tumour M2-PK was expressed in all cases, and increased cytoplasmic expression was seen with progression along the metaplasia–dysplasia–adenocarcinoma sequence. All cases of adenocarcinoma showed 100% staining so that tumour M2-PK was not a useful prognostic marker. Conclusions: Tumour M2-PK is not a specific marker of Barrett's adenocarcinoma, but may be important as a marker of transformed and highly proliferating clones during progression along the metaplasia–dysplasia–adenocarcinoma sequence.