# Case Report: From multiple myeloma to plasmablastic lymphoma – a diagnostic dilemma in unraveling a rare transformation

**Authors:** Mohamad Shraim, Ahmad Salameh, Akram Karama, Mohaned Abu Lihya

PMC · DOI: 10.3389/fonc.2026.1778123 · Frontiers in Oncology · 2026-03-10

## TL;DR

A rare case of multiple myeloma transforming into plasmablastic lymphoma is reported, highlighting diagnostic challenges and treatment response.

## Contribution

This is the 10th reported case of multiple myeloma transforming into plasmablastic lymphoma, emphasizing diagnostic and therapeutic implications.

## Key findings

- The patient's kappa-restricted myeloma transformed into lambda-restricted plasmablastic lymphoma, indicating clonal evolution.
- DA-EPOCH chemotherapy led to significant disease regression in this rare transformation case.
- Diagnostic differentiation between PBL and PBM requires careful clinical and pathological evaluation.

## Abstract

Plasmablastic lymphoma (PBL) is a rare and aggressive subtype of diffuse large B-cell lymphoma. Its transformation from multiple myeloma (MM) is an exceptionally rare event, with only nine cases reported in the literature. Differentiating PBL from plasmablastic myeloma (PBM) is a significant diagnostic challenge due to overlapping morphological and immunophenotypic features, yet it is critical for determining the appropriate treatment regimen.

We report the case of a woman in her 50s with a seven-year history of kappa-restricted MM who presented with a right leg mass. Biopsy confirmed a lambda-restricted plasmacytoma, indicating an extramedullary relapse. Two months after initiating therapy for myeloma relapse, she developed right inguinal lymphadenopathy. A lymph node biopsy revealed lambda-restricted plasmablasts positive for CD138, CD56, C-MYC, and Ki67 (100%), and negative for CD79a and EBER. In the absence of systemic MM-related end-organ damage and the presence of nodal disease, a diagnosis of PBL was favored over PBM.

The patient was subsequently treated with DA-EPOCH chemotherapy (dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin), leading to significant regression of disease on interim PET scan. This case represents the 10th reported transformation of MM to PBL and highlights the diagnostic dilemma posed by these entities. It underscores the importance of clinical context, the potential for clonal evolution (evidenced by a light-chain switch), and the efficacy of lymphoma-specific chemotherapy in this setting.

## Linked entities

- **Proteins:** SDC1 (syndecan 1), NCAM1 (neural cell adhesion molecule 1), MYC (MYC proto-oncogene, bHLH transcription factor), CD79A (CD79a molecule)
- **Chemicals:** etoposide (PubChem CID 36462), prednisone (PubChem CID 5865), vincristine (PubChem CID 5978), cyclophosphamide (PubChem CID 2907), doxorubicin (PubChem CID 31703)
- **Diseases:** multiple myeloma (MONDO:0009693), plasmablastic lymphoma (MONDO:0017347)

## Full-text entities

- **Genes:** NCAM1 (neural cell adhesion molecule 1) [NCBI Gene 4684] {aka CD56, MSK39, NCAM}, MYC (MYC proto-oncogene, bHLH transcription factor) [NCBI Gene 4609] {aka MRTL, MYCC, bHLHe39, c-Myc}, CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, SDC1 (syndecan 1) [NCBI Gene 6382] {aka CD138, SDC, SYND1, syndecan}
- **Diseases:** lymphoma (MESH:D008223), lymphadenopathy (MESH:D008206), PBL (MESH:D000069293), plasmacytoma (MESH:D010954), diffuse large B-cell lymphoma (MESH:D016403), nodal disease (MESH:D004194), end-organ damage (MESH:C564816), MM (MESH:D009101)
- **Chemicals:** EPOCH (MESH:C079446), DA (MESH:C025953), etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13008669/full.md

## References

13 references — full list in the complete paper: https://tomesphere.com/paper/PMC13008669/full.md

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Source: https://tomesphere.com/paper/PMC13008669