The metabolic marker tumour pyruvate kinase type M2 (tumour M2-PK) shows increased expression along the metaplasia–dysplasia–adenocarcinoma sequence in Barrett’s oesophagus
- 1Department of Gastroenterology, University Hospital Birmingham, Edgbaston, Birmingham B15 2TH, UK
- 2Digestive Diseases Centre, University Department of Genetics and Molecular Medicine, Level 4, Windsor Building, Leicester Royal Infirmary, Leicester LE1 5WW, UK
- 3Department of Pathology, The Medical School, University Hospital Birmingham, Edgbaston, Birmingham B15 2TT, UK
- 4Department of Thoracic Surgery, Birmingham Heartlands Hospital, Birmingham, B9 5SS, UK
- Correspondence to: Dr K Koss Digestive Diseases Centre, University Department of Genetics and Molecular Medicine, Level 4, Windsor Building, Leicester Royal Infirmary, Leicester LE1 5WW, UK; konradkossyahoo.com
- Accepted 1 June 2004
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.
