Activin and inhibin, estrogens and NFκB, play roles in ovarian tumourigenesis is there crosstalk?

Ovarian cancer may be the most frequently lethal gynaecological malignancy but the heterogeneous nature of the disease and the advanced stage at which it is usually diagnosed, have contributed to the paucity of information relating to its aetiology and pathogenesis. Members of the TGF-β superfamily, estrogen and NFκB have all been implicated in the development and progression of cancers from a wide range of tissues. In the ovary, TGF-β superfamily members and estrogen play key roles in maintaining normal function. To date, little is known about the capacity of NFκB to influence normal ovarian function except that it is ubiquitously expressed. In this review we will highlight the roles that inhibin/activin, estrogen and NFκB, have been attributed within carcinogenesis and examine the potential for crosstalk between these pathways in ovarian cancer pathogenesis.

► Ovarian cancer is usually identified at a late stage when prognosis is poor.
► Ovarian cancer pathogenesis is poorly understood.
► Inhibin and activin, estrogen and NFκB play roles in cancer development.
► Crosstalk between inhibin/activin, estrogen and NFκB signalling pathways may facilitate ovarian tumourigenesis.