Abstract

Lymphoid malignancies, mainly including lymphocytic leukemia and lymphoma, are a group of heterogeneous diseases. Although the clinical outcome of patients has been significantly improved with current immuno-chemotherapy, definitive biomarkers remain to be investigated, particularly those reflecting the malignant behavior of tumor cells and those helpful for developing optimal targeted therapy. Recently, genome-wide analysis reveals that altered genetic methylations play an important role in tumor progression through regulation of multiple cellular transduction pathways. This review describes the pathogenetic effect of the aberrant genetic methylation in lymphoid malignancies, with special emphasis on potential therapeutic strategies targeting key signaling networks.

Highlights

  • Lymphoid malignancies, mainly including lymphocytic leukemia and lymphoma, are a group of disorders that originate from neoplastic transformation of lymphocytes

  • Searching for biomarkers closely related to tumor progression is critical to better understand the disease pathogenesis and to develop subsequent targeted therapy

  • Aberrant promoter hypermethylation has been observed in cancer cells, which is responsible for the transcriptional silencing of tumor suppressor genes [1,2]

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Summary

Introduction

Mainly including lymphocytic leukemia and lymphoma, are a group of disorders that originate from neoplastic transformation of lymphocytes. Aberrant promoter hypermethylation has been observed in cancer cells, which is responsible for the transcriptional silencing of tumor suppressor genes [1,2]. 15 hypermethylated genes were recurrent in B-ALL patients irrespective of the cytogenetic subtypes, including genes involved in cell cycle arrest (MYOD1 and BTG4), cell development (FOXE3, TCF3, PAX5 and RAG1), differentiation (PTPRZ1, PPARG and IKZF1) and WNT pathway (sFRP-1) [10].

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