HEREDITARY LEUKEMIA & MDS-AML

Hereditary Leukemia — familial predisposition to MDS and AML is more common than previously recognized, and identifying germline variants is critical for bone marrow transplant donor selection because related donors may carry the same predisposition.

Whole genome sequencing evaluates all hereditary leukemia and MDS predisposition genes — GATA2, DDX41, RUNX1, CEBPA, ETV6, ANKRD26, SAMD9, SAMD9L — ensuring that transplant donors are screened and families receive appropriate surveillance.

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About this condition

Leukemia — Hereditary & Familial MDS-AML

Hereditary predisposition to myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) is increasingly recognized as a distinct clinical entity. The WHO and ICC classifications now include 'myeloid neoplasms with germline predisposition' as a formal category. Key genes include GATA2 (haploinsufficiency causing immunodeficiency, lymphedema, and evolution to MDS/AML), DDX41 (the most common germline MDS/AML predisposition gene in adults, often with late onset), RUNX1 (familial platelet disorder with predisposition to AML), CEBPA (familial AML with high penetrance), ETV6 (thrombocytopenia with predisposition to ALL and MDS), and ANKRD26 (thrombocytopenia with MDS/AML risk).

The most critical clinical implication of hereditary MDS/AML diagnosis is bone marrow transplant (HSCT) donor selection. When a patient with MDS/AML requires HSCT, related donors are the preferred source — but if the MDS/AML has a germline cause, siblings have a 50% chance of carrying the same predisposition variant. Using a carrier sibling as a donor risks transplanting a marrow that will itself develop MDS/AML. Multiple cases of donor-derived MDS/AML have been reported when germline predisposition was not recognized. Current NCCN guidelines recommend germline testing of all MDS/AML patients before HSCT to guide donor selection.

GATA2 deficiency deserves special attention — it presents as a syndrome of immunodeficiency (MonoMAC — monocytopenia and mycobacterial infection, or DCML deficiency), lymphedema, and pulmonary alveolar proteinosis BEFORE progressing to MDS/AML. Recognition of the immunodeficiency phenotype enables proactive bone marrow monitoring and pre-emptive HSCT before acute leukemia develops. DDX41 is distinctive for its late onset — often presenting as MDS/AML in the 6th-7th decade, mimicking 'sporadic' MDS. Up to 5% of adult MDS/AML may have germline DDX41 variants.

DDX41 germline variants cause ~5% of adult MDS/AML — often presenting after age 60 and mimicking sporadic disease. Without germline testing, these cases are never identified as hereditary, and at-risk family members remain unscreened.

Gene locus
GATA2 (3q21.3), DDX41 (5q35.3), RUNX1 (21q22.12), CEBPA (19q13.11), ETV6 (12p13.2), ANKRD26 (10p12.1), SAMD9 (7q21.2)

Germline testing before HSCT is now standard — using a donor who carries the same leukemia predisposition risks donor-derived malignancy. WGS identifies all hereditary MDS/AML genes for safe transplant donor selection.

Donor-derived MDS/AML is preventable — germline testing before HSCT ensures related donors don't carry the same predisposition

Multiple published cases document MDS/AML developing in transplant recipients from germline variant-carrying sibling donors — sometimes years after successful engraftment. These devastating outcomes are preventable through pre-HSCT germline testing of the patient, followed by testing potential related donors. If the patient carries a germline MDS/AML predisposition variant, only non-carrier siblings or unrelated donors should be used. WGS of the patient identifies the germline variant; targeted testing of siblings confirms safe donors.

GATA2 deficiency presents as immunodeficiency before leukemia — early recognition enables pre-emptive HSCT

GATA2 haploinsufficiency produces progressive immunodeficiency (declining monocytes, B cells, NK cells, dendritic cells) that predisposes to severe mycobacterial infections, HPV-associated neoplasia, and pulmonary alveolar proteinosis — often years to decades before MDS/AML. Early GATA2 diagnosis through WGS enables bone marrow monitoring and pre-emptive HSCT while the patient is in a non-malignant state — avoiding HSCT in the setting of active leukemia, which has substantially worse outcomes.

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