, Volume 9, Issue 3, pp 328-341

The expression of several types of mucin is related to the biological behavior of pancreatic neoplasms

Purchase on Springer.com

$39.95 / €34.95 / £29.95*

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract.

Background/Purpose: Mucins are high molecular weight glycoproteins that have oligosaccharides attached to the apomucin protein backbone by O-glycosidic linkages. Here, we report the expression of MUC1 mucin (membrane-bound mucin), MUC2 mucin (intestinal-type secretory mucin), and MUC5AC mucin (gastric-type secretory mucin) in invasive ductal carcinomas (IDCs; n= 46) and intraductal papillary-mucinous neoplasms (IPMNs; n= 33) of the pancreas, and the relationship of this expression with malignant potential.

Methods: To clarify the precise expression pattern of mucins in IPMNs, we classified IPMNs into three histologic subtypes; IPMN-dark cell type (n= 19), IPMN-clear cell type (n= 10), and IPMN-compact cell type (n= 4).

Results: IDC, with a poor outcome, showed a pattern of MUC1(+), MUC2(−), and MUC5AC(+ or −). In contrast, IPMN-dark cell type tumors, with a fairly favorable outcome, showed a pattern of MUC1(−), MUC2(+), and MUC5AC(+), and IPMN-clear cell type tumors, with a favorable outcome, showed a pattern of MUC1(−), MUC2(−), and MUC5AC(+). On the other hand, IPMN-compact cell type tumors showed a pattern of MUC1(+), MUC2(−), and MUC5AC(+). In IPMN-dark cell type tumors with carcinomatous change showing invasive growth, the invasive areas acquired a characteristic of MUC1 expression that was usually seen in IDC, although their main noninvasive lesions showed no MUC1 expression. The IPMN-compact cell type tumors usually showed high cellular atypia and frequent MUC1 expression, even in the noninvasive areas.

Conclusions: Our study of the mucin expression pattern in IDC and IPMN shows that this pattern may be related to the biological behavior of pancreatic tumors and their malignant potential.

Received: May 11, 2001 / Accepted: September 26, 2001