T/myeloid mixed-phenotype acute leukemia not otherwise specified (MPAL NOS) is an uncommon and aggressive leukemia without well-established treatment guidelines, particularly when relapsed. Venetoclax plus a hypomethylating agent offers a promising option in this situation since studies support its use in both acute myeloid and, albeit with fewer data to date, acute T-cell-lymphoblastic leukemias. We report the successful eradication of T/myeloid MPAL NOS relapsed after allogeneic stem cell transplant with venetoclax plus decitabine. A consolidative allogeneic stem cell transplant from a second donor was subsequently performed, and the patient remained without evidence of disease more than one year later. Further investigation is indicated to evaluate venetoclax combined with hypomethylating agents and/or other therapies for the management of T/myeloid MPAL NOS.
Autologous hematopoietic cell transplantation following induction therapy is standard of care for most patients with newly diagnosed multiple myeloma. 1 Though active coronavirus disease-2019 (COVID-19) infection is typically a contraindication to aggressive therapy, little is known about the safety of autologous hematopoietic cell transplantation (HCT) after apparent resolution of acute symptoms and undetectable pathogen by nasopharyngeal PCR. We report here a case of newly diagnosed multiple myeloma who developed acute COVID-19 infection following induction and chemomobilization, experienced protracted viral detection, then underwent autologous HCT with minimal early toxicity. His post-transplant course and later convalescence were complicated by a number of clinical problems. A 72-year-old man was diagnosed with multiple myeloma, lambda light chain subtype, Revised-International Staging System-2 (R-ISS-2), after presenting with fatigue and weight loss, and was found to have anemia, thrombocytopenia, renal insufficiency, proteinuria, hypercalcemia, and multiple lytic bone lesions. Marrow showed 45% abnormal plasma cells that were lambda light chain restricted and serum lambda free light chain was elevated to 15.450 gm/L. Fluorescence in situ hybridization (FISH) analysis showed gain of CKS1B at 1q21.3, monosomy 13, and loss of IgH at 14q32. He received a course of plasmapheresis along with 4 cycles of cyclophosphamide-bortezomib-dexamethasone (CyBorD) therapy with complete response as assessed by normalization of serum free light chains and marrow plasma cell percentage. Considering the high-risk profile of R-ISS-2, markedly elevated light chains, and amplification of 1q on FISH, 2 along
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