P57 protein is implicated in some human imprinting disorders such as hydatiform mole and Beckwith-Wiedemann syndrome (BWS), both characterized by mesenchymal and vascular placental abnormalities. We investigated p57 immunohistochemical expression in placental vascular proliferative disorders of preterm and term placentas, including chorangiosis (n = 5), chorangiomatosis (n = 2), chorangiomas (n = 7), umbilical cord angioma (n = 1), and placental mesenchymal dysplasia (PMD) (n = 7). P57 was expressed in decidua, cytotrophoblast, intermediate trophoblast and stromal cells of normal terminal, intermediate and stem villi, umbilical cord, chorangiosis, chorangiomatosis, and chorangiomas. In contrast, there was a loss of p57 expression in stromal cells of dysplastic stem villi in all cases of PMD regardless of whether associated with BWS or not. P57 seems to be involved in the pathogenesis of a subset of placental vascular proliferative disorders in preterm and term placentas, such as PMD. The loss of p57 expression in PMD could be of diagnostic value in helping to distinguish this rare placental lesion from its mimickers.

Ovarian sex cord–stromal tumors (SCSTs) account for 8% of all primary ovarian neo-plasms. Accurate diagnosis is crucial since each subtype has a specific prognostic and treatment. Apart from fibrosarcomas, stromal tumors are benign while sex cord tumors may recur, sometimes with a significant time to relapse. Although the diagnosis based on morphology is straightforward, in some cases the distinction between stromal tumors and sex cord tumors may be tricky. Indeed, the immunophenotype is usually nonspecific between stromal tumors and sex cord tumors. Therefore, molecular pathology plays an important role in the diagnosis of such entities, with pathognomonic or recurrent alterations, such as FOXL2 variants in adult granulosa cell tumors. In addition, these neoplasms may be associated with genetic syndromes, such as Peutz–Jeghers syndrome for sex cord tumors with annular tubules, and DICER1 syndrome for Sertoli–Leydig cell tumors (SLCTs), for which the pathologist may be in the front line of syndromic suspicion. Molecular pathology of SCST is also relevant for patient prognosis and management. For instance, the DICER1 variant is associated with moderately to poorly differentiated SLCTS and a poorer prognosis. The present review summarizes the histomolecular criteria useful for the diagnosis of SCST, using recent molecular data from the literature.