Quantifying the Effects of Structured Reporting on Report Turnaround Times and Proofreading Workload in Neuroradiology.

RATIONALE AND OBJECTIVES: To assess the effects of a change from free text reporting to structured reporting on resident reports, the proofreading workload and report turnaround times in the neuroradiology daily routine. MATERIALS AND METHODS: Our neuroradiology section introduced structured reporting templates in July 2019. Reports dictated by residents during dayshifts from January 2019 to March 2020 were retrospectively assessed using quantitative parameters from report comparison. Through automatic analysis of text-string differences between report states (i.e. draft, preliminary and final report), Jaccard similarities and edit distances of reports following read-out sessions as well as after report sign-off were calculated. Furthermore, turnaround times until preliminary and final report availability to clinicians were investigated. Parameters were visualized as trending line graphs and statistically compared between reporting standards. RESULTS: Three thousand five hundred thirty-eight reports were included into analysis. Mean Jaccard similarity of resident drafts and staff-reviewed final reports increased from 0.53 ± 0.37 to 0.79 ± 0.22 after the introduction of structured reporting (p < .001). Both mean overall edits on draft reports by residents following read-out sessions (0.30 ± 0.45 vs. 0.09 ± 0.29; p < .001) and by staff radiologists during report sign-off (0.17 ± 0.28 vs. 0.12 ± 0.23, p < .001) decreased. With structured reporting, mean turnaround time until preliminary report availability to clinicians decreased by 20.7 minutes (246.9 ± 207.0 vs. 226.2 ± 224.9; p < .001). Similarly, final reports were available 35.0 minutes faster on average (558.05 ± 15.1 vs. 523.0 ± 497.3; p = .002). CONCLUSION: Structured reporting is beneficial in the neuroradiology daily routine, as resident drafts require fewer edits in the report review process. This reduction in proofreading workload is likely responsible for lower report turnaround times.

Surface molecule CD229 as a novel target for the diagnosis and treatment of multiple myeloma.

BACKGROUND: To date, multiple myeloma remains an incurable malignancy due to the persistence of minimal residual disease in the bone marrow. In this setting, monoclonal antibodies against myeloma-specific cell surface antigens represent a promising therapeutic approach, which is however hampered by a lack of appropriate target structures expressed across all pathogenic myeloma cell populations. We, therefore, investigated functionally relevant immunoreceptors specifically associated with myeloma cells as well as their clonogenic precursors. DESIGN AND METHODS: Potential target proteins were identified using antibody arrays against phosphorylated immunoreceptors with lysates from myeloma cell lines. CD229 expression was confirmed in primary myeloma cells by reverse transcriptase polymerase chain reaction, western blot, fluorescence-activated cell sorting, and immunohistochemistry. Apoptosis, clonogenic growth, and sensitivity to chemotherapy were determined following short-interfering RNA-mediated downregulation of CD229. Antibody-dependent cellular and complement-dependent cytotoxicity were analyzed using a monoclonal antibody against CD229 to demonstrate the antigen's immunotherapeutic potential. RESULTS: Our screening assay identified CD229 as the most strongly over-expressed/phosphorylated immunoreceptor in myeloma cell lines. Over-expression was further demonstrated in the CD138-negative population, which has been suggested to represent myeloma precursors, as well as on primary tumor cells from myeloma patients. Accordingly, CD229 staining of patients' bone marrow samples enabled the identification of myeloma cells by flow cytometry and immunohistochemistry. Down-regulation of CD229 led to a decreased number of viable myeloma cells and clonal myeloma colonies, and enhanced the anti-tumor activity of conventional chemotherapeutics. Targeting CD229 with a monoclonal antibody resulted in complement- and cell-mediated lysis of myeloma cells. CONCLUSIONS: Our results demonstrate that the immunoreceptor CD229 is specifically over-expressed on myeloma cells including their clonogenic precursors and contributes to their malignant phenotype. Monoclonal antibodies against this protein may represent a promising diagnostic and immunotherapeutic instrument in this disease.

Cancer-testis antigens MAGE-C1/CT7 and MAGE-A3 promote the survival of multiple myeloma cells.

BACKGROUND: Multiple myeloma is a life-threatening disease and despite the introduction of stem cell transplantation and novel agents such as thalidomide, lenalidomide, and bortezomib most patients will relapse and develop chemoresistant disease. Therefore, alternative therapeutic modes for myeloma are needed and cancer-testis antigens such as MAGE-C1/CT7 and MAGE-A3 have been suggested to represent a class of tumor-specific proteins particularly suited for targeted immunotherapies. Surprisingly, the biological role of cancer-testis genes in myeloma remains poorly understood. DESIGN AND METHODS: We performed the first investigation of the function of two cancer-testis antigens most commonly expressed in myeloma, MAGE-C1/CT7 and MAGE-A3, using an RNA interference-based gene silencing model in myeloma cell lines. Functional assays were used to determine changes in proliferation, cell adhesion, chemosensitivity, colony formation, and apoptosis resulting from gene-specific silencing. RESULTS: We show that the investigated genes are not involved in regulating cell proliferation or adhesion; however, they play an important role in promoting the survival of myeloma cells. Accordingly, knock-down of MAGE-C1/CT7 and MAGE-A3 led to the induction of apoptosis in the malignant plasma cells and, importantly, both genes were also essential for the survival of clonogenic myeloma precursors. Finally, silencing of cancer-testis genes further improved the response of myeloma cells to conventional therapies. CONCLUSIONS: Cancer-testis antigens such as MAGE-C1/CT7 and MAGE-A3 play an important role in promoting the survival of myeloma cells and clonogenic precursors by reducing the rate of spontaneous and chemotherapy-induced apoptosis and might, therefore, represent attractive targets for novel myeloma-specific therapies.