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Blood, 15 January 2008, Vol. 111, No. 2, pp. 790-799. Prepublished online as a Blood First Edition Paper on September 28, 2007; DOI 10.1182/blood-2007-07-098236. This Article Full Text Full Text (PDF) Supplemental Notes, Methods, Figures, and Tables All Versions of this Article: blood-2007-07-098236v1 111/2/790    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Sauvageau, M. Articles by Sauvageau, G. PubMed PubMed Citation Articles by Sauvageau, M. Articles by Sauvageau, G. Related Collections Oncogenes and Tumor Suppressors Gene Expression Genomics Neoplasia Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Quantitative expression profiling guided by common retroviral insertion sites reveals novel and cell type–specific cancer genes in leukemia Martin Sauvageau1,2, Michelle Miller1, Sébastien Lemieux3, Julie Lessard1, Josée Hébert1,4,5, and Guy Sauvageau1,4,5 1 Molecular Genetics of Stem Cells Laboratory, Institute for Research in Immunology and Cancer (IRIC), Montreal, QC; 2 Division of Experimental Medicine, McGill University, Montreal, QC; 3 Functional and Structural Bioinformatics Laboratory, IRIC, Montreal, QC; 4 Leukemia Cell Bank of Quebec and Division of Hematology, Maisonneuve-Rosemont Hospital, Montreal, QC; and 5 Department of Medicine, University of Montreal, QC Proviral insertional mutagenesis is a powerful tool for the discovery of cancer-associated genes. The ability of integrated proviruses to affect gene expression over long distances combined with the lack of methods to determine the expression levels of large numbers of genes in a systematic and truly quantitative manner have limited the identification of cancer genes by proviral insertional mutagenesis. Here, we have characterized a new model of proviral insertional mutagenesis-induced lymphoid tumors derived from Eed Polycomb group gene mutant mice and quantitatively determined the expression levels of all genes within 100 kb of 20 different retroviral common insertion sites (CISs) identified in these tumors. Using high-throughput quantitative reverse transcription–polymerase chain reaction (Q-RT-PCR), we document an average of 13 CIS-associated genes deregulated per tumor, half of which are leukemia subtype–specific, while the others are coordinately deregulated in the majority of tumors analyzed. Interestingly, we find that genes located distantly from common proviral integration sites are as frequently deregulated as proximal genes, with multiple genes affected per integration. Our studies reveal an unsuspected conservation in the group of genes deregulated among phenotypically similar subtypes of lymphoid leukemias, and suggest that identification of common molecular determinants of this disease is within reach. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: What gene have I ID'ed? Rachel J. Bergerson and David A. Largaespada Blood 2008 111: 471-472. [Full Text] [PDF]

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