Hematology

HMA+venetoclax matches intensive chemotherapy in AML with chromosome 5/7 abnormalities; allo-SCT remains pivotal

In AML with -7 and/or -5/del5q, remission rates were similar with intensive chemotherapy and HMA+venetoclax (43% vs 52%, p=0.2). Adjusted analyses showed no overall survival difference between intensive chemotherapy and HMA+venetoclax (HR 1.02, p=0.9202). Adverse survival was linked instead to older age, prior myeloid disease, monosomal or complex karyotypes, and KRAS mutations. Among patients aged 60–75, overall survival remained similar between strategies, supporting equipoise in older adults. Allo-SCT significantly improved overall survival regardless of frontline therapy and was the strongest predictor of long-term survival (HR 0.36). These data support HMA+venetoclax as a reasonable bridge to allo-SCT in chromosome 5/7–aberrant AML, especially in older or comorbid patients. 1

Treosulfan–fludarabine conditioning improves survival and chronic GVHD versus reduced-intensity busulfan–fludarabine in AML alloHCT

In 352 AML patients undergoing alloHCT, treosulfan–fludarabine produced higher 24‑month event-free survival than busulfan–fludarabine (65% vs 53%, p=0.01). Overall survival also favored treosulfan (73% vs 65%), with EFS gains across AML risk categories. Benefits were pronounced in patients with comorbidity index >2, where EFS reached 62% vs 42% (p=0.02). Treosulfan reduced both relapse and non-relapse mortality and lowered extensive chronic GVHD at 24 months (15.1% vs 28.1%, p=0.01). GVHD-free, relapse-free survival improved with treosulfan (53% vs 40%, p=0.02), and the safety profile was more favorable overall. 2

ctDNA dynamics strongly predict outcomes in classical Hodgkin lymphoma

This individual-participant meta-analysis pooled 10 studies and 1,158 Hodgkin lymphoma patients to assess ctDNA prognostic value. High baseline ctDNA was associated with inferior progression-free survival (HR 2.74; 95% CrI 1.30–5.75) and shorter 5‑year restricted mean survival time. Interim ctDNA positivity conferred markedly worse PFS (HR 5.99; 3.46–10.13) with substantial survival time loss. End-of-treatment ctDNA positivity showed the strongest association with progression risk (HR 13.4; 3.97–41.87). Elevated baseline and post-treatment ctDNA also predicted worse overall survival, with HRs around 2.5–4.7. Implementation will require assay standardization, validated thresholds, and demonstration of ctDNA’s independent value alongside existing prognostic tools. 3