Faculty Bibliography

PURPOSE: Cystadenofibromas are benign ovarian neoplasms. Their most typical features on sonography (US) are unilocular cysts with small, shadowing hyperechoic, solid papillae without internal vascularity. In the past, they were virtually always surgically removed to exclude malignancy. This study was undertaken to review the sonographic appearances of benign cystadenomas. METHODS: We retrospectively reviewed the transvaginal US studies of 32 cases of pathologically proven ovarian cystadenofibromas. RESULTS: Twenty-two of the tumors presented as unilocular cystic structures with one or more solid, hyperechoic, shadowing, mural nodules with no discernible blood flow projecting from the inner cyst wall. Ten lesions were multiloculated with multiple small solid areas, with scant or no blood vessels. CONCLUSIONS: Cystadenofibromas do not always have a classic appearance on transvaginal US and color Doppler imaging. In our series, however, the majority (69%) presented as unilocular cysts with one or more small solid, avascular projections from the inner cyst wall. These features had 100% reliability for a diagnosis of benign cystadenofibroma in this small series. Further study is necessary to confirm the reliability of this finding for benign cystadenofibroma, thus possibly avoiding or minimizing any surgical exploration. (c) 2014 Wiley Periodicals, Inc. J Clin Ultrasound, 2014.

OBJECTIVE: To determine, by evaluation of histological slides, images and descriptions of early (second-trimester) placenta accreta (EPA) and placental implantation in cases of Cesarean scar pregnancy (CSP), whether these are pathologically indistinguishable and whether they both represent different stages in the disease continuum leading to morbidly adherent placenta in the third trimester. METHODS: The database of a previously published review of CSP and EPA was used to identify articles with histopathological descriptions and electronic images for pathological review. When possible, microscopic slides and/or paraffin blocks were obtained from the original researchers. We also included from our own institutions cases of CSP and EPA for which pathology specimens were available. Two pathologists examined all the material independently and, blinded to each other's findings, provided a pathological diagnosis based on microscopic appearance. Interobserver agreement in diagnosis was determined. RESULTS: Forty articles were identified, which included 31 cases of CSP and 13 cases of EPA containing histopathological descriptions and/or images of the pathology. We additionally included six cases of CSP and eight cases of EPA from our own institutions, giving a total of 58 cases available for histological evaluation (37 CSP and 21 EPA) containing clear definitions of morbidly adherent placenta. In the 29 cases for which images/slides were available for histopathological evaluation, both pathologists attested to the various degrees of myometrial and/or scar tissue invasion by placental villi with scant or no intervening decidua, consistent with the classic definition of morbidly adherent placenta. Based on the reviewed material, cases with a diagnosis of EPA and those with a diagnosis of CSP showed identical histopathological features. Interobserver correlation was high (kappa = 0.93). CONCLUSIONS: EPA and placental implantation in CSP are histopathologically indistinguishable and may represent different stages in the disease continuum leading to morbidly adherent placenta in the third trimester

Soft tissue sarcomas are a heterogeneous group of tumors associated with poor clinical outcome. Although a subset of soft tissue sarcomas is characterized by simple karyotypes and recurrent chromosomal translocations, the mechanisms driving cytogenetically complex sarcomas are largely unknown. Clinical evidence led us to partially inactivate Pten and Tp53 in the smooth muscle lineage of mice, which developed high-grade undifferentiated pleomorphic sarcomas, leiomyosarcomas, and carcinosarcomas that widely recapitulate the human disease, including the aberrant karyotype and metastatic behavior. Pten was found haploinsufficient, whereas the wild-type allele of Tp53 invariably gained point mutations. Gene expression profiles showed up-regulated Notch signaling in Pten(Delta/+)Tp53(Delta/+) tumors compared with Pten(+/+)Tp53(Delta/+) tumors. Consistently, Pten silencing exacerbated the clonogenic and invasive potential of Tp53-deficient bone marrow-derived mouse mesenchymal stem cells and tumor cells and activated the Notch pathway. Moreover, the increased oncogenic behavior of Pten(Delta/+)Tp53(Delta/+) and shPten-transduced Pten(+/+)Tp53(Delta/+) tumor cells was counteracted by treatment with a gamma-secretase inhibitor, suggesting that the aggressiveness of those tumors can be attributed, at least in part, to enhanced Notch signaling. This study demonstrates a cooperative role for Pten and Tp53 suppression in complex karyotype sarcomas while establishing Notch as an important functional player in the cross talk of these pathways during tumor progression. Our results highlight the importance of molecularly subclassifying patients with high-grade sarcoma for targeted treatments.

Two cases of adrenocortical heterotopia are reported. One is in a full-term placenta. The other is adjacent to the ovarian hilum of an adult. Both are incidental findings. Despite sharing similar histological and immunological features, they show different growth patterns. The literature is reviewed and adrenocortical heterotopias of different locations are compared. New hypotheses of its histogenesis are discussed.