Davor Galusic

Relapse remains the leading cause of treatment failure after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in acute myeloid leukemia (AML). Early identification of patients at increased post-transplant relapse risk is essential to enable intensified surveillance and pre-emptive therapeutic strategies. Wilms’ tumor 1 (WT1) is overexpressed in most AML cases and represents a broadly applicable molecular marker; however, its utility as a peripheral blood (PB) measurable residual disease (MRD) marker after allo-HSCT remains incompletely defined. In this prospective multicenter cohort study, 43 adults with AML in complete remission underwent allo-HSCT between 2021 and 2023. WT1 expression in PB was quantified using standardized real-time quantitative PCR before transplantation (WT1_pre) and at day +30 (WT1_30). Receiver operating characteristic analysis identified an optimal threshold for relapse prediction. A WT1 cutoff of ≥3 copies/10⁴ ABL discriminated relapse risk. WT1_30 demonstrated strong prognostic performance (AUC 0.79; p = 0.005), whereas WT1_pre showed more modest predictive value (AUC 0.69; p = 0.037). Patients with WT1_30 ≥ 3 had inferior 12-month progression-free survival compared with those with WT1_30 < 3 (52.9% vs. 90.9%, p = 0.0059) and a higher 12-month cumulative incidence of relapse (31% vs. 9%, p = 0.054). WT1_pre ≥ 3 was also associated with inferior progression-free and overall survival (both p = 0.0008). Relapsed patients had significantly higher WT1_30 levels than non-relapsed patients (median 5.0 vs. 2.0 copies/10⁴ ABL; p = 0.018). Peripheral blood WT1 expression, particularly at day +30, is associated with an increased relapse risk after allo-HSCT in AML and may support early post-transplant risk stratification. The identified cutoff should be considered exploratory and requires validation in larger independent cohorts.

Programmed death-ligand 1 (PD-L1) on tumor cells, including Hodgkin and Reed–Sternberg (HRS) cells in classical Hodgkin’s lymphoma (cHL), suppresses immune responses in the tumor immune microenvironment (TME). We analyzed PD-L1 expression in macrophages and HRS cells of 98 cHL cases and correlated the findings with clinicopathological features, overall survival (OS), and progression-free survival (PFS). Epstein–Barr virus (EBV) was detected by in situ hybridization for EBV-encoded RNA. Ten high-power fields were evaluated to count the total number of macrophages and PD-L1+ macrophages, and to calculate PD-L1 histoscore (H-score) in HRS cells. EBV-positive cHL was found in 22.5% of patients. The median H-score was 80 (range 0–300). Bulky disease was associated with a lower number of PD-L1+ macrophages, and extranodal disease with a higher number (p = 0.05). EBV-positive cHL showed a higher PD-L1 H-score in HRS cells and a greater number of PD-L1⁺ macrophages (p = 0.005); both of these features, along with the proportion of PD-L1⁺ macrophages, were associated with shorter PFS and OS (p < 0.001). High PD-L1 expression in HRS and macrophages may be linked to worse clinical outcomes.