JBC Ideal method for primary cell transfection

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Originally published In Press as doi:10.1074/jbc.M208353200 on September 12, 2002

J. Biol. Chem., Vol. 277, Issue 48, 46289-46297, November 29, 2002
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Prevalent Involvement of Illegitimate V(D)J Recombination in Chromosome 9p21 Deletions in Lymphoid Leukemia*

Yukiko KitagawaDagger §, Kaoru InoueDagger §, Shigeru SasakiDagger , Yasuhide Hayashi||, Yoshinobu Matsuo**, Michael R. LieberDagger Dagger , Hideaki Mizoguchi§, Jun YokotaDagger §§, and Takashi KohnoDagger

From the Dagger  Biology Division, National Cancer Center Research Institute, Tokyo 1040045, Japan, the § Department of Hematology, Tokyo Women's Medical University, Tokyo 1628666, Japan, the || Department of Pediatrics, Graduate School of Medicine, University of Tokyo, Tokyo 1038655, Japan, ** Fujisaki Cell Center, Hayashibara Biochemical Laboratories, Okayama 7028006, Japan, and Dagger Dagger  Norris Comprehensive Cancer Center, University of Southern California School of Medicine, Los Angeles, California 90089

To understand molecular pathways underlying 9p21 deletions, which lead to inactivation of the p16/CDKN2A, p14/ARF, and/or p15/CDKN2B genes, in lymphoid leukemia, 30 breakpoints were cloned from 15 lymphoid leukemia cell lines. Seventeen (57%) breakpoints were mapped at five breakpoint cluster sites, BCS-LL1 to LL5, each of <15 bp. Two breakpoint cluster sites were located within the ARF and CDKN2B loci, respectively, whereas the remaining three were located >100 kb distal to the CDKN2A, ARF, and CDKN2B loci. The sequences of breakpoint junctions indicated that deletions in the 11 (73%) cell lines were mediated by illegitimate V(D)J recombination targeted at the five BCS-LL and six other sites, which contain sequences similar to recombination signal sequences for V(D)J recombination. An extrachromosomal V(D)J recombination assay indicated that BCS-LL3, at which the largest number of breakpoints (i.e. five breakpoints) was clustered, has a V(D)J recombination potential 150-fold less than the consensus recombination signal sequence. Three other BCS-LLs tested also showed V(D)J recombination potential, although it was lower than that of BCS-LL3. These results indicated that illegitimate V(D)J recombination, which was targeted at several ectopic recombination signal sequences widely distributed in 9p21, caused a large fraction of 9p21 deletions in lymphoid leukemia.

* This study was supported in part by Grants-in-Aid from the Ministry of Health, Labor, and Welfare for the 2nd Term Comprehensive 10-Year Strategy for Cancer Control; the Program for Promotion of Fundamental Studies in Health Sciences of the Organization for Pharmaceutical Safety and Research of Japan; the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Sagawa Foundation for Promotion of Cancer Research; and the Foundation for Promotion of Cancer Research.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by the Research Resident Fellowship from the Foundation for Promotion of Cancer Research.

§§ To whom correspondence should be addressed: Biology Division, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104-0045, Japan. Tel.: 81-3-3547-5272; Fax: 81-3-3542-0807; E-mail: jyokota@gan2.ncc.go.jp.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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