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Promoter DNA methylation of CD10 in lymphoid malignancies

Leukemia volume 20, pages 1910–1912 (2006)Cite this article

The neutral endopeptidase 24.11, (NEP or CD10), is considered a regulator of B-cell growth and proliferation.2 The enzyme is a cell surface aminopeptidase capable of degrading a number of bioactive peptides with various functions that depend on the cell type or tissue of origin and is active in early bone marrow (BM) precursor B cells and lymph node germinal center (GC) B cells. In addition, CD10 is expressed in malignancies including precursor B cell acute lymphocytic leukemia (B-ALL), GC-related non-Hodgkin's lymphoma (NHL) such as Burkitt's lymphoma and follicular lymphoma (FL), and GC-related diffuse large B-cell lymphomas (DLBCL). It is not, however, expressed in terminally differentiated plasma cells of multiple myeloma (MM), in the pre-GC cells of mantle cell lymphoma (MCL), or in the pre- or post-GC cells of B-cell chronic lymphocytic leukemia (B-CLL). Thus, there is a biphasic pattern of CD10 cell surface protein expression that correlates with specific stages of development in both normal and neoplastic B cells and precursor B cells (Figure 1c).

The development of lymphoid malignancies involves the acquisition of a series of genetic and epigenetic alterations that give the cell a selective growth advantage. One cancer-related epigenetic alteration, gene promoter DNA methylation, occurs at cytosines within CG dinucleotides frequently clustered into cytosine-phosphate-guanosine (CpG) islands (reviewed by Laird3). When CpG sites within a promoter CpG island are predominately methylated, there is frequently little or no expression of the associated gene.4 Accumulating evidence indicates that abnormal DNA methylation of promoter and first exon CpG islands have profound effects on tumorigenesis. In fact, a number of individual genes have been reported as silenced in B-ALL and NHL with known roles in a variety of cellular processes suggesting that CpG island methylation is important in the genesis and clinical behavior of these malignancies.

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Acknowledgements

This work was supported by the National Cancer Institute grants CA100055 and CA097880 (CW Caldwell). KH Taylor and J Liu contributed equally to this work. We also appreciate the helpful editorial work of Ms Angel Surdin.

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  1. Department of Pathology and Anatomical Sciences, Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, MO, USA

    K H Taylor, J Liu, J Guo, H Shi & C W Caldwell

  2. Department of Statistics, Department of Health Management and Informatics, University of Missouri School of Medicine, Columbia, MO, USA

    J W Davis

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  1. K H Taylor
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Correspondence to C W Caldwell.

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Taylor, K., Liu, J., Guo, J. et al. Promoter DNA methylation of CD10 in lymphoid malignancies. Leukemia 20, 1910–1912 (2006). https://doi.org/10.1038/sj.leu.2404353

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