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Blood, 1 October 2005, Vol. 106, No. 7, pp. 2498-2505. Prepublished online as a Blood First Edition Paper on June 16, 2005; DOI 10.1182/blood-2004-12-4840. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-12-4840v1 106/7/2498    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Du, Y. Articles by Copeland, N. G. Search for Related Content PubMed PubMed Citation Articles by Du, Y. Articles by Copeland, N. G. Related Collections Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Cooperating cancer-gene identification through oncogenic-retrovirus–induced insertional mutagenesis Yang Du, Sally E. Spence, Nancy A. Jenkins, and Neal G. Copeland From the Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick, MD. Multiple cooperating mutations that deregulate different signaling pathways are required to induce cancer. Identifying these cooperating mutations is a prerequisite for developing better combinatorial therapies for treating cancer. Here we show that cooperating cancer mutations can be identified through oncogenic-retrovirus-induced insertional mutagenesis. Among 13 myeloid leukemias induced by transplanting into mice bone marrow cells infected in vitro with a replication-defective retrovirus carrying the Sox4 oncogene, 9 contained insertional mutations at known or suspected cancer genes. This likely occurred because rare bone marrow cells, in which the oncogenic retrovirus happened to integrate and in which it mutated a cooperating cancer gene, were selected because the host harbored a cooperating cancer mutation. Cooperativity between Sox4 and another gene, Mef2c, was subsequently confirmed in transplantation studies, in which deregulated Mef2c expression was shown to accelerate the myeloid leukemia induced by Sox4. Insertional mutagenesis of cooperating cancer genes by a defective oncogenic retrovirus provides a new method for identifying cooperating cancer genes and could aid in the development of better therapies for treating cancer. 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