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Mutations of a novel human RAD54 homologue, RAD54B, in primary cancer

Oncogene volume 18, pages 3422–3426 (1999)Cite this article

Abstract

Association of breast tumor susceptibility gene products BRCA1 and BRCA2 with the RAD51 recombination protein suggested that cancer could arise through defects in recombination. The identification of NBS1, responsible for Nijmegen breakage syndrome, from the MRE11/RAD50 recombination protein complex also supports this hypothesis. However, our mutation analysis revealed that known members of the RAD52 epistasis group are rarely mutated in human primary cancer. Here we describe the isolation of a novel member of the SNF2 superfamily, characterized with sequence motifs similar to those in DNA and RNA helicases. The gene, designated RAD54B, is significantly homologous to the RAD54 recombination gene. The expression of RAD54B was high in testis and spleen, which are active in meiotic and mitotic recombination. These findings suggest that RAD54B may play an active role in recombination processes in concert with other members of the RAD52 epistasis group. RAD54B maps to human chromosome 8q21.3-q22 in a region associated with cancer-related chromosomal abnormalities. Homozygous mutations at highly conserved positions of RAD54B were observed in human primary lymphoma and colon cancer. These findings suggest that some cancers arise through alterations of the RAD54B function.

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Acknowledgements

We thank T Nishioka for photographic work. This work was supported by Grants-in-Aid for Cancer Research from the Ministry of Education, Science and Culture, Japan, and by Tsuchiya Medical Research Foundation, GenBank accession No. AF112481.

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Authors and Affiliations

  1. Department of Molecular Pathology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, 734, Minami-Ku, Hiroshima, Japan

    Tomoki Hiramoto, Tae Nakanishi, Tatsuro Sumiyoshi, Toshikatsu Fukuda & Kiyoshi Miyagawa

  2. Department of Developmental Biology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, 734, Minami-Ku, Hiroshima, Japan

    Tomoki Hiramoto, Kiyoshi Miyagawa & Kenji Kamiya

  3. First Department of Internal Medicine, Hiroshima University School of Medicine, 1-2-3 Kasumi, 734, Minami-Ku, Hiroshima, Japan

    Tomoki Hiramoto, Koji Sumii & Goro Kajiyama

  4. Department of Radiation Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, 734, Minami-Ku, Hiroshima, Japan

    Shinya Matsuura, Hiroshi Tauchi & Kenshi Komatsu

  5. Human Genetics Unit, Molecular Medicine Unit, University of Edinburgh, Western General Hospital, EH4 2XU, Edinburgh, UK

    Yoshiro Shibasaki

  6. First Department of Surgery, Kinki University School of Medicine, 377-3 Ohno-higashi, Osaka-sayama, Osaka, 589, Japan

    Hiroki Inui, Masahiro Watatani & Masayuki Yasutomi

  7. Department of Cancer Cytogenetics, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, 734, Minami-Ku, Hiroshima, Japan

    Nanao Kamada

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  1. Tomoki Hiramoto
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Hiramoto, T., Nakanishi, T., Sumiyoshi, T. et al. Mutations of a novel human RAD54 homologue, RAD54B, in primary cancer. Oncogene 18, 3422–3426 (1999). https://doi.org/10.1038/sj.onc.1202691

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