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Filter by:The goal of this randomized, controlled clinical trial is to test a new concept for communication skills training (on-site supportive communication training (on-site SCT) in cancer care. The study aims to determine the impact of on-site SCT on patients' rating of oncologists' communication abilities. Oncologists participating in the study will be randomly allocated to the intervention or control group. In the intervention group each doctor will have a total of three intervention days at intervals of 3-4 weeks. On an intervention day, a psychologist will sit in and observe doctor-patient consultations. After the first consultations, 30 minutes are allocated for feedback to the doctor by the psychologist. After the last consultation of the day, 60 minutes are allocated for thorough feedback and establishment of learning goals to focus on until the next intervention day. Doctor's in the control group will conduct communication as usual. Researchers will compare the control and intervention groups to see if patients' rating of doctors' interpersonal and communication skills increase when the doctors have participated in on-site SCT. The 15-item Communication Assessment Tool (CAT) will be used. It will also be investigated whether on-site SCT increases the doctors' rating of themselves in relation to communication efficacy and job satisfaction and decrease their experience of burnout.
The PI3K, protein kinase B (AKT), and mTOR signaling network promotes cell growth, survival, metabolism, and motility, but becomes a critical oncogenic driver under aberrant conditions that control the tumor microenvironment and angiogenesis. The PI3K-AKT-mTOR axis is the most frequently deregulated signaling pathway in primary osteosarcoma and other bone tumors. PI3Ka has high rates of 25-50% activating mutations associated with tumor formation in osteosarcoma. Other causes of pathway hyperactivation include loss of function of the tumor suppressor PTEN, gain-of-function mutations in AKT and PDK1, or upregulation of receptor tyrosine kinases. TQB3525 is an orally bioavailable, potent, dual catalytic site inhibitor of PI3Ka and PI3Kd. Tumor growth inhibition has been demonstrated in multiple xenograft osteosarcoma models with PI3K-mutant, PTEN-null cell lines. The investigators try to investigate TQB3525 in primary osteosarcoma and other bone tumors for its safety, tolerability, dose-limiting toxicities (DLT), MTD and antitumor efficacy.