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Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

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Decoding Waldenström Macroglobulinemia Through Genomics, Epigenomics and Cellular Interactions.

Tereza Růžičková^1,2, Michal Kaščák^3,4, Zuzana Chyra^3,4

¹Babak Myeloma Group, Department of Pathophysiology, Faculty of Medicine, Masaryk University, 625 00 Brno, Czech Republic.

International Journal of Molecular Sciences

|June 26, 2026

Summary

This summary is machine-generated.

Waldenström macroglobulinemia is a rare cancer. Key mutations like MYD88 and CXCR4 drive its complexity, leading to new targeted therapies such as Bruton's tyrosine kinase inhibitors.

Keywords:

CXCR4 L252P L265P MYD88 TP53 Waldenström macroglobulinemia microRNA signaling pathways

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Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Waldenström macroglobulinemia (WM) is a rare lymphoplasmacytic malignancy.
Characterized by bone marrow infiltration and monoclonal immunoglobulin M production.
WM exhibits biological complexity due to genetic alterations, signaling pathways, and the bone marrow microenvironment.

Purpose of the Study:

To review the molecular pathogenesis of Waldenström macroglobulinemia.
To discuss the impact of genetic mutations on disease understanding and treatment.
To explore current and emerging therapeutic strategies for WM.

Main Methods:

Review of genetic studies, including MYD88 and CXCR4 mutations.
Analysis of cytogenetic, epigenetic, and microRNA data.
Evaluation of clinical outcomes with targeted therapies.

Main Results:

MYD88 and CXCR4 mutations are central to WM pathogenesis and evolution.
Advances in molecular understanding have improved therapeutic strategies.
Bruton's tyrosine kinase inhibitors show promise, but treatment resistance is a challenge.

Conclusions:

Molecular insights have refined the understanding of WM.
Targeted therapies, including BTK inhibitors, offer personalized treatment options.
Integrating molecular and microenvironmental data will improve risk stratification and treatment efficacy.