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Acute Leukemias

Immunoglobulin gamma heavy chain gene with somatic hypermutation is frequently expressed in acute myeloid leukemia

Abstract

Expression of immunoglobulin (Ig), a marker characteristic of B cells, has been reported in epithelial cells and has been suggested to have a role in their survival and growth. We assessed the frequency and level of Ig gamma heavy chain (IgG) expression in acute myeloid leukemia (AML), and found that IgG was expressed at a high frequency and level in AML cell lines and primary myeloblasts, but not in monocytes or neutrophils from patients with non-hematopoietic neoplasms or healthy controls. AML-derived IgG had the same molecular weight as B cell-derived IgG and was secreted. We further detected IgG VHDJH transcripts in AML cell lines and sorted primary myeloblasts, confirming that IgG expression was indeed produced by AML cells. AML-derived IgG gene rearrangements showed evidence of somatic hypermutation of the variable (V) gene segments, and restricted (AML cell lines) or biased (primary myeloblasts) V usage. Anti-human IgG reduced cell viability and induced apoptosis in AML cell lines. Although the function of the AML-derived IgG is unclear, our findings suggest that AML-derived IgG may be a novel AML-related gene that contributes to leukemogenesis and AML progression. AML-derived IgG may serve as a useful molecular marker for monitoring minimal residual disease or designing target therapy.

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Acknowledgements

This work was supported by a research fund awarded to C Cameron Yin from The University of Texas MD Anderson Cancer Center (#18079170) and a research fund awarded to Xiaoyan Qiu from National Natural Science Foundation of China (#30973389). We thank Amelia Scholtz and Kathryn Carnes from Scientific Publication at The University of Texas MD Anderson Cancer Center for editorial review of the manuscript.

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Correspondence to X Qiu or C C Yin.

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Qiu, X., Sun, X., He, Z. et al. Immunoglobulin gamma heavy chain gene with somatic hypermutation is frequently expressed in acute myeloid leukemia. Leukemia 27, 92–99 (2013). https://doi.org/10.1038/leu.2012.184

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