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Recent data suggest that SEL1L may play an important role in pancreatic carcinoma, similar to breast cancer, where the expression of SEL1L has been associated with a reduction in both proliferative activity in vitro and clinical tumor aggressiveness. To investigate this possibility, we examined the expression of Sel1L in a series of primary pancreatic carcinomas by immunohistochemistry and characterized the effects of Sel1L overexpression both in vitro and in vivo. In 74 pancreatic cancers analysed, 36% lacked Sel1L expression, although there was no significant correlation between the expression of Sel1L and any clinicopathologic parameter, including survival. However, immunohistochemical reactivity for Sel1L and Dpc4/Smad4 was concordant in 69% of cases (chi(2) test P&<0.004). Overexpression of SEL1L in stably transfected pancreatic cancer cells caused both a decrease in clonogenicity and anchorage-independent growth as well as a significant increase in the levels of activin A and SMAD4. When implanted in nude mice, Suit-2-SEL1L-overexpressing clones displayed a considerably reduced rate of tumor growth. Thus, it can be hypothesized that Sel1L plays an important function in the growth and aggressiveness of pancreatic carcinoma. Moreover, our data provide evidence that SEL1L has an impact on the expression of genes involved in regulation of cellular growth, possibly through the TGF-beta signaling pathway.

A case of extrauterine Müllerian adenosarcoma of the peritoneum in a 20-year-old woman is reported. The tumor was widely based on the abdominopelvic wall and there were no unusual features in the genital organs. The cut surface of the tumor showed a marked gelatinous appearance. The tumor was composed of an admixture of benign Müllerian-type epithelium and sarcomatous stroma. The predominant element of the sarcomatous area was rhabdomyosarcoma, which showed a close resemblance to well-differentiated embryonal rhabdomyosarcoma. In another sarcomatous area, fibroblastic cells without myoblastic properties diffusely proliferated in a marked myxoid background with some collagen bundles. Both the mitotic count and Ki-67 proliferative index of these cells were lower than those of rhabdomyoblastic cells. On follow up, the patient was disease free for 1 year postoperatively, without any subsequent treatment. The present case indicates that extrauterine adenosarcoma can also show histological heterogeneity as do uterine adenosarcomas. The remarkable myxoid change of this tumor seemed to be more largely due to a fibromyxoid element than a rhabdomyosarcomatous element, and the coexistence of the former may be related to the less aggressive behavior of this tumor.