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. 2003 Aug 8;114(3):359-70.
doi: 10.1016/s0092-8674(03)00566-x.

Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors

Craig H Bassing  1 , Heikyung Suh, David O Ferguson, Katrin F Chua, John Manis, Mark Eckersdorff, Megan Gleason, Rodrick Bronson, Charles Lee, Frederick W Alt
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Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors

Craig H Bassing et al. Cell. .
Free article

V体育ios版 - Abstract

We employed gene targeting to study H2AX, a histone variant phosphorylated in chromatin surrounding DNA double-strand breaks. Mice deficient for both H2AX and p53 (H(delta/delta)P(-/-)) rapidly developed immature T and B lymphomas and solid tumors VSports手机版. Moreover, H2AX haploinsufficiency caused genomic instability in normal cells and, on a p53-deficient background, early onset of various tumors including more mature B lymphomas. Most H2AX(delta/delta)p53(-/-) or H2AX(+/delta)p53(-/-) B lineage lymphomas harbored chromosome 12 (IgH)/15 (c-myc) translocations with hallmarks of either aberrant V(D)J or class switch recombination. In contrast, H2AX(delta/delta)p53(-/-) thymic lymphomas had clonal translocations that did not involve antigen receptor loci and which likely occurred during cellular expansion. Thus, H2AX helps prevent aberrant repair of both programmed and general DNA breakage and, thereby, functions as a dosage-dependent suppressor of genomic instability and tumors in mice. Notably, H2AX maps to a cytogenetic region frequently altered in human cancers, possibly implicating similar functions in man. .

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