In multiple myeloma, t(4;14) translocation places MMSET/FGFR3 under IgH control; ~30% of...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-FGFR3-MUTATION-MM |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-MM |
| Sources | SRC-CIVIC SRC-ESMO-MM-2023 SRC-NCCN-MM-2025 |
Actionability Facts
| Biomarker | BIO-FGFR3-MUTATION |
|---|---|
| Variant | FGFR3 activating (Y373C, K650E) with t(4;14) |
| Disease | DIS-MM |
| ESCAT tier | X |
| Contraindicated monotherapy | erdafitinib (no MM efficacy in trials), FGFR-TKI monotherapy in MM (insufficient evidence) |
| Evidence summary | In multiple myeloma, t(4;14) translocation places MMSET/FGFR3 under IgH control; ~30% of t(4;14) cases co-express FGFR3, with rare acquired activating point mutations (Y373C, K650E). Despite preclinical sensitivity, clinical trials of FGFR inhibitors (dovitinib, AZD4547) in MM showed limited efficacy; no FGFR-targeted therapy is approved in MM. Treatment is standard t(4;14) high-risk myeloma protocol (proteasome-inhibitor-based). |
Notes
ESCAT X — biological rationale present but no actionable clinical evidence. t(4;14) status defines high-risk MM and influences proteasome-inhibitor-based regimen choice (KRd, IsaKRd, daratumumab combos), but FGFR3 itself is not a treatment target in MM.
Used By
No reverse references found in the YAML corpus.