ABSTRACT
This report presented an overview of the patient selection, technical considerations and clinical evidence for robotic mitral valve surgery. A review of comparative outcomes to medical therapy, sternotomy approach, and the MitraClip device suggested that robotic mitral valve surgery is safe and effective in specialized centres. Potential benefits include a reliable and durable repair, with reduced perioperative morbidity and improved quality of life. Future studies should aim to delineate mid- and long-term clinical and echocardiographic outcomes following robotic mitral valve repair compared to the conventional sternotomy approach.
ABSTRACT
AIMS: Sex cord stromal tumours (SCSTs) of the ovary encompass several histological tumour subtypes that are defined by characteristic histological features. Some can show morphological overlap with other subtypes of SCSTs, as well as with non-SCSTs. The E-cadherin/catenin complex constitutes the adherens junction, which is well developed in epithelial tissue, but the constituent molecules are also expressed in several non-epithelial tumours. The aim of this study was to determine whether the expression patterns of E-cadherin and catenins in ovarian SCSTs can be of diagnostic utility. METHODS AND RESULTS: We studied the expression of E-cadherin, α-, ß- and γ-catenin in 55 tumours using immunohistochemistry. We found that all tumour subtypes showed nuclear expression of E-cadherin, while only microcystic stromal tumours (MCSTs) displayed a distinct profile, with nuclear localization of all three catenins in almost all cases. CONCLUSIONS: We conclude that the E-cadherin expression profile in SCSTs can assist in distinguishing between SCSTs and non-SCSTs in which there is no nuclear expression of E-cadherin. The nuclear localization of catenins may be of potential use in distinguishing MCST from other subtypes of SCST.
Subject(s)
Biomarkers, Tumor/metabolism , Cadherins/metabolism , Ovarian Neoplasms/metabolism , Sex Cord-Gonadal Stromal Tumors/metabolism , Antigens, CD , Desmoplakins/metabolism , Female , Humans , Immunohistochemistry , Middle Aged , Ovarian Neoplasms/pathology , Ovary/metabolism , Sex Cord-Gonadal Stromal Tumors/pathology , alpha Catenin/metabolism , beta Catenin/metabolism , gamma CateninABSTRACT
Amplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. We used a MYC target gene signature that predicts poor neuroblastoma prognosis to identify the histone chaperone FACT (facilitates chromatin transcription) as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small-molecule curaxin compound CBL0137 markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with standard chemotherapy by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN-amplified neuroblastoma cells and suggesting a treatment strategy for MYCN-driven neuroblastoma.
