ABSTRACT
Introduction: Sonographer-led-discharge was proposed in a maternity unit to provide a holistic service, cut waiting times, ease staffing pressures and increase job satisfaction. This study explored sonographers' experiences and perspectives of this new extended role and other areas of non-obstetric role extension. Understanding these will inform future practice and the success of the proposed obstetric sonographer-led-discharge and career structure. Methods: A mixed methodology, cross-sectional study was performed, with a purposive, non-probability sample using an online data collection tool. The data were analysed using descriptive statistics and thematic analysis. Results: In total, 93 sonographers participated in the study. Of these, 25% of sonographers currently practising obstetric ultrasound said they would not undertake the proposed obstetric sonographer-led-discharge role extension although 90% of the participants said role extension provides job satisfaction. Several themes emerged from the data, including job satisfaction, benefits to the hospital, improved patient pathway, time, personal factors, litigation and intra- and interprofessional resistance. A total of 54% of staff currently performing a role extension have experienced either inter- or intraprofessional conflict and only 48.5% said their workload was manageable. Conclusions: The data collected suggested that, with training and support, the proposed obstetric sonographer-led-discharge role is an appropriate role extension for sonographers. These findings support the premise of the proposed sonographic career structure, although the inter- and intraprofessional resistance identified in the study could form a significant barrier if it is not appropriately considered and managed.
ABSTRACT
BACKGROUND: Many urothelial carcinomas (UC) contain activating PIK3CA mutations. In telomerase-immortalized normal urothelial cells (TERT-NHUC), ectopic expression of mutant PIK3CA induces PI3K pathway activation, cell proliferation and cell migration. However, it is not clear whether advanced UC tumors are PIK3CA-dependent and whether PI3K pathway inhibition is a good therapeutic option in such cases. METHODS: We used retrovirus-mediated delivery of shRNA to knock down mutant PIK3CA in UC cell lines and assessed effects on pathway activation, cell proliferation, migration and tumorigenicity. The effect of the class I PI3K inhibitor GDC-0941 was assessed in a panel of UC cell lines with a range of known molecular alterations in the PI3K pathway. RESULTS: Specific knockdown of PIK3CA inhibited proliferation, migration, anchorage-independent growth and in vivo tumor growth of cells with PIK3CA mutations. Sensitivity to GDC-0941 was dependent on hotspot PIK3CA mutation status. Cells with rare PIK3CA mutations and co-occurring TSC1 or PTEN mutations were less sensitive. Furthermore, downstream PI3K pathway alterations in TSC1 or PTEN or co-occurring AKT1 and RAS gene mutations were associated with GDC-0941 resistance. CONCLUSIONS: Mutant PIK3CA is a potent oncogenic driver in many UC cell lines and may represent a valuable therapeutic target in advanced bladder cancer.
