Granulosa cell tumors (GCT) are unique sex-cord stromal tumors which
account for ∼8% of all ovarian malignancies. They exhibit morphological,
biochemical and hormonal features similar to proliferating granulosa
cells of the preovulatory follicle, including estrogen and inhibin
synthesis. A somatic missense mutation in the forkhead box L2 (FOXL2)
gene (C134W) is unique to adult GCT, and absent in other ovarian
cancers. FOXL2 is a transcription factor that plays a critical role in
ovarian function, in particular, proliferation and differentiation of
granulosa cells. The molecular mechanisms underlying the pathogenicity
of the mutant FOXL2 remain unresolved. Here we review the molecular
alterations known to be associated with mutant FOXL2 and the potential
signaling implications. Several studies suggest that dysregulated FOXL2
function may alter cell cycle progression and apoptosis. Further
insights into the molecular mechanism of GCT pathophysiology may
identify therapeutic targets for the treatment of these tumors.
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