t(11;14) IGH/CCND1 is the defining genetic lesion of MCL — drives cyclin D1 overexpressio...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-CCND1-T1114-MCL |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-MCL |
| Sources | SRC-CIVIC SRC-ESMO-MCL-2024 SRC-NCCN-BCELL-2025 |
Actionability Facts
| Biomarker | BIO-T11-14-IGH-CCND1 |
|---|---|
| Variant | t(11;14)(q13;q32) IGH/CCND1 |
| Disease | DIS-MCL |
| ESCAT tier | IA |
| Recommended combinations | acalabrutinib + bendamustine + rituximab (1L), BR or R-CHOP/R-DHAP + autoSCT (1L fit, TP53-WT), venetoclax + ibrutinib (R/R), brexu-cel (R/R 2L+) |
| Evidence summary | t(11;14) IGH/CCND1 is the defining genetic lesion of MCL — drives cyclin D1 overexpression. BTKi (acalabrutinib + rituximab — TRIANGLE, Dreyling Lancet 2024; ECHO — Wang NEJM 2024) is the new 1L standard regardless of fitness for TP53-mut; high-dose AraC + autoSCT historically (LyMa, MCL Younger). Venetoclax (CCND1 → BCL2-mediated anti-apoptosis rationale) active R/R. |
Notes
ESCAT IA. Disease-defining; doesn't 'select' BTKi but the DIS-MCL algorithm is BTKi-centric.
Used By
No reverse references found in the YAML corpus.