ATM loss in CLL (del(11q) or somatic mutation): historically poor-prognostic with chemoim...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-ATM-LOSS-CLL |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-CLL |
| Sources | SRC-CIVIC SRC-ESMO-CLL-2024 SRC-NCCN-BCELL-2025 |
Actionability Facts
| Biomarker | BIO-HRR-PANEL |
|---|---|
| Variant | ATM loss (11q deletion or somatic mutation) |
| Disease | DIS-CLL |
| ESCAT tier | IIA |
| Recommended combinations | acalabrutinib (preferred for cardiac safety), zanubrutinib, ibrutinib, venetoclax + obinutuzumab (fixed-duration) |
| Contraindicated monotherapy | FCR (fludarabine-cyclophosphamide-rituximab) in ATM-deficient CLL — inferior outcomes |
| Evidence summary | ATM loss in CLL (del(11q) or somatic mutation): historically poor-prognostic with chemoimmunotherapy (FCR), but BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib) and venetoclax+obinutuzumab abrogate this risk. Avoid FCR in ATM-deficient CLL. ESCAT IIA (treatment-modifying) / OncoKB Level 3A. |
Notes
Note: TP53 disruption (del(17p) or TP53 mutation) is the dominant adverse prognostic — ATM is secondary. Test del(11q) by FISH and ATM by NGS in all CLL pre-treatment.
Used By
No reverse references found in the YAML corpus.