MUC1 and MUC2 in pancreatic neoplasia
- 1John Dingell Veterans Administration Medical Center, 4646 John Road, Detroit, MI 48201, USA
- 2Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
- 3Harper University Hospital, 3990 John R, Detroit, MI 48201, USA
- Correspondence to: Dr N V Adsay Harper University Hospital, Wayne State University Medical School, Department of Pathology, 3990 John R, Detroit, MI 48201, USA; adsayvmed.wayne.edu
- Accepted 22 September 2003
Abstract
MUCs are glycoproteins with various roles in homeostasis and carcinogenesis. Among other actions, MUC1 may inhibit cell–cell and cell–stroma interactions and function as a signal transducer, participating in cancer progression. In contrast, MUC2 is normally found only in goblet cells, where it contributes to the protective barrier function of these cells. Recently, a tumour suppressor role has been demonstrated for MUC2, and both MUC1 and MUC2 appear to have important roles in pancreatic neoplasia. MUC1 appears to be a marker of aggressive phenotype and may facilitate the vascular spread of carcinoma cells. In contrast, MUC2 is rarely detectable in aggressive pancreatic tumours, but is commonly expressed in intraductal papillary mucinous neoplasms (IPMNs), which are rare, indolent tumours, in intestinal IPMNs, and in indolent colloid carcinomas. MUC2 appears to be not only a marker of this indolent pathway, but also partly responsible for its less aggressive nature. Thus, in pancreatic neoplasia, MUC1 and MUC2 have potential diagnostic and prognostic value as markers of aggressive and indolent phenotypes, respectively, and have potential as therapeutic targets.
- EGFR, epidermal growth factor receptor
- IPMN, intraductal papillary mucinous neoplasia
- MAPK, mitogen activated protein kinase
- PanIN, pancreatic intraepithelial neoplasia
- TCF, T cell factor
