CD79B in myelodysplastic syndromes and acute myeloid leukemia: an integrative computational and in vitro study

TL;DR

This study explores the role of CD79B in blood cancers like MDS and AML, finding it is often reduced and may affect cancer cell behavior and immune responses.

Contribution

The study is the first to investigate CD79B's role in MDS and AML through integrative computational and experimental approaches.

Findings

CD79B expression is consistently reduced in MDS and AML compared to normal controls.

Higher CD79B levels are linked to immune response and T-cell activation pathways.

Enforced CD79B expression in HL-60 cells increases apoptosis and alters cell-cycle distribution.

Abstract

CD79B is a key component of the B-cell receptor complex, but its relevance in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) remains unclear.

We screened immune-related genes in public MDS microarray datasets, prioritized CD79B, and validated its expression in an independent MDS cohort, an AML cohort, and peripheral blood samples from patients with MDS or AML transformed from MDS. Functional effects of CD79B overexpression were examined in HL-60 cells, and gene set enrichment and immune-infiltration analyses were used to explore CD79B-associated pathways.

CD79B expression was consistently reduced in MDS and AML compared with normal controls in public datasets and clinical samples. In HL-60 cells, enforced CD79B expression modestly altered cell-cycle distribution and increased apoptosis. Transcriptomic analyses linked higher CD79B expression to immune response and T-cell activation pathways and to global patterns of immune-cell infiltration.

These exploratory data suggest that CD79B downregulation is a recurrent feature of MDS and AML and that CD79B may influence leukemic cell behavior and immune microenvironmental signals. The findings generate hypotheses for future mechanistic studies and evaluation of CD79B as a potential biomarker in myeloid malignancies.

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