Genomic profiling enables personalized strategies to overcome drug resistance in multiple myeloma
Infections remain a major cause of morbidity and mortality in multiple myeloma (MM), driven by the interplay between disease‑induced immune dysfunction and treatment‑related immunosuppression.
Infections remain a major cause of morbidity and mortality in multiple myeloma (MM), driven by the interplay between disease‐induced immune dysfunction and treatment‐related immunosuppression. The introduction of proteasome inhibitors, immunomodulatory drugs, monoclonal antibodies, bispecific antibodies, and chimeric antigen receptor T (CAR‑T) cell therapy has markedly improved survival while simultaneously reshaping the infectious risk landscape. Different treatment strategies compromise immunity in distinct mechanisms. Conventional chemotherapy and some targeted agents primarily increase the risk of bacterial infections through neutropenia. Modern immunotherapies, however, produce profound and prolonged hypogammaglobulinemia alongside cellular immune deficits, predisposing patients to viral reactivation and opportunistic infections. BCMA‑targeting therapies (particularly bispecific antibodies and CAR‑T cells) cause sustained plasma cell depletion and durable humoral immune impairment, resulting in an infection pattern that can persist well beyond treatment completion. Effective prevention requires a risk‑stratified approach accounting for disease stage, treatment regimen, cumulative immunosuppression, and individual patient characteristics. source_claim_text_original": "In infections remain a major cause of morbidity and mortality in multiple myeloma (MM), driven by the interplay between disease‑induced immune dysfunction and treatment‑related immunosuppression."
Infections significantly impact progression and survival in MM by causing treatment delays, complications, and mortality.
Evidence level: Korai humán adat. Kis vagy feltáró emberi adat.
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