Effects of on-site Supportive Communication Training (On-site SCT) on doctor-patient communication in oncology: Study protocol of a randomized, controlled mixed-methods trial.

BACKGROUND: The quality of communication in oncology significantly impacts patients' health outcomes, as poor communication increases the risk of unnecessary treatment, inadequate pain relief, higher anxiety levels, and acute hospitalizations. Additionally, ineffective communication skills training (CST) is associated with stress, low job satisfaction, and burnout among doctors working in oncology. While acknowledging the importance of effective communication, the specific features of successful CST remain uncertain. Role-play and recorded consultations with direct feedback appear promising for CST but may be time-consuming and face challenges in transferring acquired skills to clinical contexts. Our aim is to bridge this gap by proposing a novel approach: On-site Supportive Communication Training (On-site SCT). The concept integrates knowledge from previous studies but represents the first randomized controlled trial employing actual doctor-patient interactions during CST. METHODS: This randomized multicenter trial is conducted at three departments of oncology in Denmark. Doctors are randomized 1:1 to the intervention and control groups. The intervention group involves participation in three full days of On-site SCT facilitated by a trained psychologist. On-site SCT focuses on imparting communication techniques, establishing a reflective learning environment, and offering emotional support with a compassionate mindset. The primary endpoint is the change in percentage of items rated "excellent" by the patients in the validated 15-item questionnaire Communication Assessment Tool. The secondary endpoints are changes in doctors' ratings of self-efficacy in health communication, burnout, and job satisfaction measured by validated questionnaires. Qualitative interviews will be conducted with the doctors after the intervention to evaluate its relevance, feasibility, and working mechanisms. Doctors have been actively recruited during summer/autumn 2023. Baseline questionnaires from patients have been collected. Recruitment of new patients for evaluation questionnaires is scheduled for Q1-Q2 2024. DISCUSSION: This trial aims to quantify On-site SCT efficacy. If it significantly impacts patients/doctors, it can be a scalable CST concept for clinical practice. Additionally, qualitative interviews will reveal doctors' insight into the most comprehensible curriculum parts. TRIAL REGISTRATION: April 2023 - ClinicalTrials.gov (NCT05842083). April 2023 - The Research Ethics Committee at the University of Southern Denmark (23/19397).

Regulation of estrogen target genes and growth by selective estrogen-receptor modulators in endometrial cancer cells.

OBJECTIVE: Tamoxifen has mixed agonist/antagonist activities, leading to tissue-specific estrogen-like actions and endometrial cancer. The purpose of this study was to evaluate the effects of antiestrogens on the growth of estrogen receptor (ER)-positive ECC-1 endometrial cancer cells in vitro and in vivo. METHODS: We performed growth studies and luciferase assays using ERE-tK and AP-1 reporters. ERalpha protein expression was measured by Western blot after antiestrogen treatments. We investigated the actions of antiestrogens on the transcription of the pS2 gene in situ measured by Northern blot and the actions of antiestrogens on the VEGF protein secreted by ELISA. ERalpha, ERbeta, EGFR, and HER2/neu mRNAs were determined by RT-PCR. Last, ECC-1 tumors were developed by inoculation of cells into ovariectomized athymic mice and treated with estradiol (E2), tamoxifen, raloxifene, and a combination. RESULTS: E2 induced cell proliferation while antiestrogens did not. E2 and raloxifene down regulated ERalpha protein; in contrast, 4OHT did not. ICI182,780 completely degraded the receptor. ECC-1 cells express ERbeta at insignificant levels. Luciferase assays did not show any induction in ERE- nor AP-1-mediated transcription by antiestrogens. E2 caused a concentration-dependent increase in pS2 mRNA but antiestrogens did not. E2 increased VEGF expression in a dose-dependent manner and antiestrogens blocked E2 action. E2 down regulated HER2/neu while 4OHT and raloxifene did not change HER2/neu levels compared to control. In addition, EGFR mRNA was down regulated by E2 but raloxifene did not change it. Tamoxifen and raloxifene did not promote tumor growth in vivo. However, raloxifene (1.5 mg daily) only partially blocked E2-stimulated growth. CONCLUSION: Tamoxifen and raloxifene are antiproliferative agents and antiestrogens in ECC-1 endometrial cells in vitro and in vivo. The observation that selective estrogen-receptor modulators do not down regulate EGFR and HER2/neu mRNA may provide a potential role for these oncogenes in the development of raloxifene- or tamoxifen-stimulated endometrial cancer. The ECC-1 cell line could provide important new clues about the evolution of drug resistance to tamoxifen and raloxifene.