The metabolic marker tumour pyruvate kinase type M2 (tumour M2-PK) shows increased expression along the metaplasia-dysplasia-adenocarcinoma sequence in Barrett's oesophagus
The metabolic marker tumour pyruvate kinase type M2 (tumour M2-PK) shows increased expression along the metaplasia-dysplasia-adenocarcinoma sequence in Barrett's oesophagus
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DOI：
10.1136/jcp.2004.018150
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发表时间：
2004-11-01
影响因子：
3.4
通讯作者：
Jankowski, JAZ
中科院分区：
文献类型：
--
作者：
Koss, K;Harrison, RF;Jankowski, JAZ
背景：增殖和肿瘤细胞表达糖酵解同工酶--丙酮酸激酶型M2(M2-PK)。在肿瘤细胞中，M2-PK通常以二聚体形式存在(肿瘤M2-PK)，导致糖酵解的磷代谢产物积聚，使细胞侵袭低氧和低葡萄糖浓度的区域。目的：研究肿瘤M2-PK在Barrett食管化生-异型增生-腺癌序列中的表达，并评估其在食道癌预后中的作用。材料/方法：190例食管炎性反流性食管炎，37例Barrett‘s食管炎，21例高度不典型增生，112例腺癌和3例对照肿瘤。结果：所有病例均有M2-PK的表达，且胞浆表达随癌前病变-异型增生-腺癌的发展而增加。结论：肿瘤M2-PK不是Barrett腺癌的特异性标记物，但可作为化生、异型增生-腺癌序列中转化和高增殖克隆的重要标记物。
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.