C.R. FERREIRA*, J.P. CARVALHOy, F.A. SOARESz, S.A.C. SIQUEIRA§ & F.M. CARVALHO*
Departments of *Pathology and Obstetrics and Gynecologic, University of Sao Paulo Medical School,
Sao Paulo, Brazil; Department of Pathology, Hospital do Cancer A.C. Camargo, Sao Paulo, Brazil; and
§Division of Surgical Pathology, University of Sao Paulo Medical School, Sao Paulo, Brazil

International Journal of Gynecological Cancer 2008, 18, 59–65

Link to abstract

The goal of the study was to prove that mucinous ovarian tumors associated with PMP are secondary to primary tumors of appendiceal origin. This hypothesis excludes PMP that originates from mature ovarian teratomas which could be considered the only case in which the ovary is the primary site of the tumor. An ovarian teratoma is a tumor of the ovaries that contain tissues of organs such as the lungs, brain, or intestines. The immunophenotype of ovarian teratomas suggest that they are derived from a gastrointestinal-type mucinous epithelial component.

Knowing that most ovarian mucinous tumors associated with PMP present with borderline histology type, the investigators in this study argue that mucinous primary tumors should be classified as benign or malignant, while mucinous secondary tumors should be classified as borderline. By using various histochemical methods, the investigators tested for the presence of certain proteins and other markers like CK20, CK7, MUC5AC, MUC2, MUC1, and MUC6. Borderline tumors with or without PMP revealed no significant difference in expression of any of these markers. However, non-PMP associated mucinous tumors in comparison with PMP associated tumor revealed significant difference in the expression of CK20 and MUC2. This difference persisted in comparing borderline tumors with the benign/malignant tumors. This finding supports the claim that borderline mucinous ovarian tumors are secondary, and the claim that borderline mucinous intestinal tumors are also secondary.

MUC2 is a glycoprotein that is specific to PMP. It was present in all of the PMP tumor cell samples and also in borderline cancers. 100% of all borderline and PMP cancer cells expressed MUC2. The authors suggest mucus re accumulation can be inhibited by targeting the molecule MIC2. This could prove to be an effective way of controlling the disease.

In conclusion, the study supports the notion that tumors associated with PMP differ from primary intestinal-type mucinous ovarian tumors with respect to MUC2 and CK20expression. These differences are directly related to borderline histology. Their immunohistochemical results suggest not only that PMP is likely a secondary disease derived from gastrointestinal tract epithelium, especially the appendix, but also that it is also caused by an accumulation of MUC2-type mucin.