Expression Pattern and Possible Clinical Significance of CD81 In Myeloid Leukemia

CD81, a cell surface protein belonging to the tetraspanin family, is overexpressed in 60-90% of acute myeloid leukemia (AML) patients and correlates with aggressive disease manifestations. Clinically, CD81-positive AML demonstrates elevated total leucocytic counts, increased lactate dehydrogenase (LDH) levels, higher bone marrow blast percentages, and a predominance in M1-M5 French-American-British (FAB) subtypes. Critically, this marker predicts adverse outcomes: reduced complete remission rates (12% vs. 24% in CD81-negative cohorts), higher relapse incidence (38% vs. 12%), and inferior overall, event-free, and relapse-free survival. Multivariate analyses confirm CD81 as an independent prognostic indicator, even within cytogenetically normal AML or NPM1-mutated subgroups. Current AML risk stratification depends heavily on cytogenetic and molecular profiling (e.g., NPM1, FLT3-ITD). Nevertheless, 40-50% of patients lack identifiable high-risk genetic lesions, complicating clinical prognostication. Although flow cytometry enables rapid detection of CD81 surface expression, this biomarker remains underutilized in risk models despite its adverse impact mirroring established high-risk features. Mechanistically, CD81s involvement in metastasis and stem cell quiescence positions it as both a prognostic tool and a candidate therapeutic target. Notably, CD81 expression remains uncharacterized in chronic myeloid leukemia (CML). Given CMLs distinct BCR::ABL1-driven pathogenesis and clinical trajectory from chronic phase to blast crisis, evaluating CD81s role may reveal novel biological insights or therapeutic vulnerabilities during disease progression.