# Role of Radiotherapy in the Era of Novel Immune‐Based Treatment Strategies for Multiple Myeloma

**Authors:** Tom Schlusemann, Evgenii Shumilov, Gabriele Reinartz, David Rene Steike, Sebastian Lohmann, Stefan Gravemeyer, Matthias Stelljes, Georg Lenz, Hans Theodor Eich, Michael Oertel

PMC · DOI: 10.1002/hon.70186 · Hematological Oncology · 2026-03-15

## TL;DR

This paper reviews how radiotherapy is being used alongside new immune-based treatments for multiple myeloma.

## Contribution

It summarizes the evolving role of radiotherapy in combination with novel systemic therapies like CAR-T cells.

## Key findings

- Radiotherapy is used as bridging or salvage therapy alongside immune-based treatments.
- New systemic agents expand radiotherapy's role in managing oligoprogressive disease.
- Combined radiotherapy and systemic therapy approaches raise questions about efficacy and tolerability.

## Abstract

Radiotherapy (RT) constitutes an important treatment modality in multiple myeloma (MM), traditionally used for the management of symptomatic osteolytic and extramedullary lesions. Objectives of RT are symptom alleviation and prevention of complications such as neurological deficits and pathological fractures. Over the past decade, systemic therapy (ST) for MM has undergone substantial advancements, notably with the incorporation of monoclonal antibodies in frontline regimens, as well as the emergence of bispecific antibodies and chimeric antigen receptor T‐cells (CAR‐T) for relapsed and refractory disease. These therapeutic innovations have introduced new clinical challenges and expanded the indications for RT, including its role as bridging therapy prior to CAR‐T therapy, salvage therapy following CAR‐T failure, and in the management of oligoprogressive and/or extramedullary disease. The integration of novel systemic agents prompts critical questions regarding synergistic interactions, feasibility, efficacy, and tolerability of combined RT and ST approaches. Herein, we present a literature review summarizing current evidence stratified by systemic treatment modalities, and discuss the clinical implications within the contemporary therapeutic landscape of MM.

## Linked entities

- **Diseases:** multiple myeloma (MONDO:0009693)

## Full-text entities

- **Genes:** PDCD1 (programmed cell death 1) [NCBI Gene 5133] {aka ADMIO4, AIMTBS, CD279, PD-1, PD1, SLEB2}, MYOM2 (myomesin 2) [NCBI Gene 9172] {aka TTNAP}, SLAMF7 (SLAM family member 7) [NCBI Gene 57823] {aka 19A, CD319, CRACC, CS1}, CD38 (CD38 molecule) [NCBI Gene 952] {aka ADPRC 1, ADPRC1, cADPR1}, TNFRSF17 (TNF receptor superfamily member 17) [NCBI Gene 608] {aka BCM, BCMA, CD269, TNFRSF13A}, GPRC5D (G protein-coupled receptor class C group 5 member D) [NCBI Gene 55507], CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}
- **Diseases:** Tumor (MESH:D009369), malignant spinal cord compression (MESH:D013117), osseous and (MESH:C535395), osseous lesions (MESH:D000070896), cerebral (MESH:D002547), plasmacytomas (MESH:D010954), CR (MESH:D001766), epidural masses (MESH:C536030), Hodgkin lymphoma (MESH:D006689), plasma cell neoplasms (MESH:D054219), fracture (MESH:D050723), hematologic malignancies (MESH:D019337), large-B-cell lymphoma (MESH:D016393), dysphagia (MESH:D003680), thrombocytopenia (MESH:D013921), COVID-19 (MESH:D000086382), Lymphoma (MESH:D008223), fatigue (MESH:D005221), extramedullary plasmacytomas (MESH:C537514), neurological deficits (MESH:D009461), autoimmune fever (MESH:D005334), deaths (MESH:D003643), disease (MESH:D004194), KarMMa-3 (MESH:C537153), dermatitis (MESH:D003872), lesions (MESH:D009059), ICANS (MESH:C000722498), MM (MESH:D009101), EMD (MESH:D023981), hematologic toxicities (MESH:D006402), CRS (MESH:D000080424), abducens paresis (MESH:D010291), ST (MESH:D016609), headache (MESH:D006261), SD (MESH:D012735), alopecia (MESH:D000505), irradiated (MESH:D012793), neurotoxicity (MESH:D020258), bone pain (MESH:D010146), Toxicities (MESH:D064420), rib lesion (MESH:C537613), leukocytopenia (MESH:D007970)
- **Chemicals:** elotuzumab (MESH:C546027), bortezomib (MESH:D000069286), bendamustine (MESH:D000069461), pembrolizumab (MESH:C582435), melphalan (MESH:D008558), ixazomib (MESH:C548400), lenalidomide (MESH:D000077269), CAR T (-), thalidomide (MESH:D013792), doxorubicin (MESH:D004317), pomalidomide (MESH:C467566), Nivolumab (MESH:D000077594), Dexamethasone (MESH:D003907), vincristine (MESH:D014750), Daratumumab (MESH:C556306), isatuximab (MESH:C000599209), carfilzomib (MESH:C524865), cortisone (MESH:D003348)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** -HD7 — Homo sapiens (Human), Hybridoma (CVCL_B6E2), -3 — Mus musculus (Mouse), Hybridoma (CVCL_C6V6)

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12989191/full.md

## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC12989191/full.md

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Source: https://tomesphere.com/paper/PMC12989191