# The Evolving Landscape of Anti-Clonal Therapy in Newly Diagnosed Systemic Light-Chain (AL) Amyloidosis: Evidence- and Time-Based Comparison with Multiple Myeloma

**Authors:** Rafael Ríos-Tamayo

PMC · DOI: 10.3390/life16020363 · Life · 2026-02-22

## TL;DR

This paper reviews how anti-clonal therapies developed for multiple myeloma are being adapted to treat systemic AL amyloidosis, a rare plasma cell disorder.

## Contribution

It provides a comparative analysis of the evolution of anti-clonal therapy in newly diagnosed AL amyloidosis versus multiple myeloma.

## Key findings

- Anti-clonal therapies originally developed for multiple myeloma are now being applied to AL amyloidosis with improved outcomes.
- Approximately 20% of newly diagnosed AL amyloidosis cases also meet criteria for multiple myeloma.
- Clinical trials remain the preferred treatment option for patients with AL amyloidosis.

## Abstract

Light-chain (AL) amyloidosis is a rare and incurable disease, classified under the category of plasma cell neoplasms and other diseases with paraproteins in the 5th Edition of the World Health Organization classification of lymphoid tumors. This entity shares some similarities with multiple myeloma (MM), remarkably a bone marrow infiltration of clonal plasma cells. Moreover, one out of five newly diagnosed cases of AL amyloidosis (NDAL) also fulfills the current diagnostic criteria for MM. A multidisciplinary therapy approach should be established, in which hematological therapy plays a crucial role. Anti-clonal therapy is the basis of hematological therapy, in addition to supportive therapy and emerging anti-fibrils therapy. In recent years, advances in the anti-clonal therapy for MM have progressively transferred to carefully selected patients with systemic AL amyloidosis, significantly improving outcomes in this rapidly changing field. This review aims to critically analyze the comparative evolution and evidence-based approach of anti-clonal therapy in NDAL vs. MM since the introduction of bortezomib. Participation in clinical trials remains the first option to consider in daily clinical practice.

## Linked entities

- **Diseases:** AL amyloidosis (MONDO:0019438), multiple myeloma (MONDO:0009693)

## Full-text entities

- **Genes:** GPRC5D (G protein-coupled receptor class C group 5 member D) [NCBI Gene 55507], TNFRSF17 (TNF receptor superfamily member 17) [NCBI Gene 608] {aka BCM, BCMA, CD269, TNFRSF13A}, CD38 (CD38 molecule) [NCBI Gene 952] {aka ADPRC 1, ADPRC1, cADPR1}, SLAMF7 (SLAM family member 7) [NCBI Gene 57823] {aka 19A, CD319, CRACC, CS1}
- **Diseases:** Plasma Cell Neoplasms and Other Diseases (MESH:D054219), MGs (MESH:D010265), toxicity (MESH:D064420), amyloidosis (MESH:D000686), AL (MESH:D000075363), clinical significance (MESH:D065309), non-Hodgkin lymphomas (MESH:D008228), amyloid (MESH:C000718787), cardiac involvement (MESH:D006331), WM (MESH:D008258), MG (MESH:D009157), plasma cell leukemia (MESH:D007952), injury to (MESH:D014947), PC disorders (MESH:D015324), MM (MESH:D009101), lymphoid tumors (MESH:D009369), organ failure (MESH:D009102), SMM (MESH:D000075122), cardiotoxicity (MESH:D066126)
- **Chemicals:** D (MESH:D003903), Melphalan (MESH:D008558), CAEL-101 (-), Isa (MESH:C000599209), Adriamycin (MESH:D004317), Elo (MESH:C546027), dexamethasone (MESH:D003907), lenalidomide (MESH:D000077269), bendamustine (MESH:D000069461), prednisone (MESH:D011241), daratumumab (MESH:C556306), ixazomib (MESH:C548400), A (MESH:D001151), doxycycline (MESH:D004318), T (MESH:D014316), birtamimab (MESH:C000609646), vincristine (MESH:D014750), C (MESH:D002244), monomethyl auristatin F (MESH:C513576), pomalidomide (MESH:C467566), pegylated liposomal doxorubicin (MESH:C506643), V (MESH:D014639), Bortezomib (MESH:D000069286), carfilzomib (MESH:C524865), thalidomide (MESH:D013792), belamab (MESH:C000631691), cyclophosphamide (MESH:D003520)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

112 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942640/full.md

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Source: https://tomesphere.com/paper/PMC12942640