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Alterations of the Double-Strand Break Repair Gene MRE11 in Cancer¹

Departments of Molecular Pathology [T. F., T. S., K. M.] and Cancer Cytogenetics [N. K.], Research Institute for Radiation Biology and Medicine, and 2nd Department of Surgery [M. T., T. K., T. A.], Hiroshima University, Hiroshima 734-8553, Japan, and 1st Department of Surgery, Kinki University School of Medicine, Osaka 589-8511, Japan [H. I., M. W., M. Y.]

MRE11 plays a role in DNA double-strand break repair. Hypomorphic mutations of MRE11 have been demonstrated in ataxia-telangiectasia (AT)-like disorder. ATM mutations play a causal role in AT and have been demonstrated in lymphoid malignancies in patients without AT histories. By analogy with the relationship of ATM to lymphoid malignancies, it is probable that alterations of MRE11 are associated with tumor formation. We performed a mutation analysis of MRE11 in 159 unselected primary tumors. Three missense mutations at conserved positions were found in breast and lymphoid tumors. Additionally, an aberrant transcript without genomic mutation was found in a breast tumor. These findings suggest an occasional role for MRE11 alterations in the development of primary tumors.

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