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Absence of H2AX gene mutations in B-cell leukemias and lymphomas

Leukemia volume 19, page 464 (2005)Cite this article

TO THE EDITOR

H2AX is a core histone known to be involved in the cellular response to DNA double-strand breaks (DSBs); following DSBs, H2AX is rapidly phosphorylated (γ-H2AX)1 and is thought to play a role in recruiting DNA repair factors to the site of damage.2 In H2AX−/− mice, V(D)J recombination does not seem to be affected, although the numbers of T- and B-lymphocytes are reduced by 50%. However, class switch recombination appears to be impaired as evidenced by reduced switching to IgG.3 Recently, H2AX was proposed to be important in maintaining genomic stability, particularly in the context of p53 deficiency.4,5 Loss of a single H2AX allele compromises genomic integrity, via increased chromosomal aberrations, while on a p53-deficient background it enhances cancer susceptibility, promoting, among others, B-lineage lymphomas that tend to have mature features.4,5 Furthermore, H2AX−/− p53−/− mice have an increased number of translocations and develop various tumors including immature T- and B-cell lymphomas.4,5

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Acknowledgements

We thank Mattias Berglund, Ingrid Thörn, Mia Thorsélius, Ulf Thunberg and Gerard Tobin for providing DNA from different lymphoma and leukemia entities. This study was supported by grants from the Swedish Cancer Society and Lion's Cancer Research Foundation, Uppsala.

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  1. Rudbeck Laboratory, Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden

    S H Walsh & R Rosenquist

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  1. S H Walsh
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Correspondence to S H Walsh.

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Walsh, S., Rosenquist, R. Absence of H2AX gene mutations in B-cell leukemias and lymphomas. Leukemia 19, 464 (2005). https://doi.org/10.1038/sj.leu.2403651

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