MYC Amplification in Epithelioid Angiosarcoma of the Urinary Bladder and Prostate Following Prostate Radiotherapy: A Case Report with a Novel Molecular Alteration.

Epithelioid angiosarcoma is a rare variant of angiosarcoma. Radiation-associated epithelioid angiosarcoma of the urinary bladder and prostate is an exceedingly rare tumor and there are only 8 cases of epithelioid angiosarcoma of the urinary bladder and prostate associated with previous radiotherapy in the literature. To the best of our knowledge, MYC gene amplification has not been previously reported in epithelioid angiosarcoma of the urinary bladder and prostate following radiotherapy, although it is observed in radiation-associated angiosarcoma of other anatomic sites. Here we report the first case of epithelioid angiosarcoma of the urinary bladder and prostate with MYC gene amplification detected by fluorescence in situ hybridization (FISH) analysis in a 70-year-old male patient 10 years after receiving radiation and hormonal therapy for prostate cancer.

Complete Depletion of Daratumumab Interference in Serum Samples from Plasma Cell Myeloma Patients Improves the Detection of Endogenous M-Proteins in a Preliminary Study.

BACKGROUND: Therapeutic humanized IgG1 kappa monoclonal antibody (t-mAb), daratumumab (DARA) is a Food and Drug Administration approved drug for the treatment of relapsed/refractory plasma cell myeloma (PCM). DARA appears on serum protein electrophoresis (SPEP) and on serum immunofixation (sIFE) as an IgG kappa monoclonal immunoglobulin protein (M-protein), complicating the assessment of the patients' response to therapy. A more ominous threat to patient safety can occur with the misinterpretation of the presence of a small t-mAb spike as being the residual product of the patient's neoplastic clone, presented either as oligoclonality or new clonality, which could result in incorrect interpretation of failure to achieve remission. METHODS: In this report, we describe a novel and cost-effective technique based on biotinylated recombinant CD38 and streptavidin-coated magnetic beads to capture and remove residual DARA present in PCM patient serum samples. The treated samples are then run like regular samples on SPEP and sIFE. We validated this simple technique in DARA-spiked PCM samples and patient samples on DARA treatment. RESULTS: Our simple capture technique completely extracted DARA in all of the tested serum specimens and allowed the assessment of residual M-protein without DARA interference. The results were reproducible and highly specific for DARA, and did not have any impact on endogenous M-protein migration and quantification by SPEP and sIFE. The cost of this technique is much lower and it can be performed in-house with a very short turnaround time compared to the currently available alternative methods. There is a great need for such reflex technologies to avoid interpretation errors. CONCLUSIONS: This method is an effective way to eliminate DARA interference in SPEP and sIFE, and can be easily implemented in any clinical laboratory without any patent restriction. This simple technique can be adopted for other t-mAbs using their respective ligands and will help to reduce additional doses of toxic treatment and further testing in patients on t-mAbs with a false positive M-protein spike.