tailieunhanh - osophila as an emerging model to study metastasis

Department of Biochemistry and Molecular Biology and †The Genes and Development Graduate Program, The University of Texas M. D. Anderson Cancer Center, and ‡Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA. Correspondence: Georg Halder. E-mail: ghalder@ comment reviews Published: 25 March 2004 Genome Biology 2004, 5:216 The electronic version of this article is the complete one and can be found online at © 2004 BioMed Central Ltd reports Abstract Metastasis is the primary cause of human cancer-related deaths. Two recent studies describe a system for testing how multiple genetic events synergize to promote neoplastic growth and metastasis in Drosophila, paving. | Minireview Drosophila as an emerging model to study metastasis Madhuri Kango-Singh and Georg Halder 4 Addresses Department of Biochemistry and Molecular Biology and The Genes and Development Graduate Program The University of Texas M. D. Anderson Cancer Center and Program in Developmental Biology Baylor College of Medicine Houston TX 77030 USA. Correspondence Georg Halder. E-mail ghalder@ Published 25 March 2004 Genome Biology 2004 5 216 The electronic version of this article is the complete one and can be found online at http 2004 5 4 216 2004 BioMed Central Ltd Abstract Metastasis is the primary cause of human cancer-related deaths. Two recent studies describe a system for testing how multiple genetic events synergize to promote neoplastic growth and metastasis in Drosophila paving the way for systematic approaches to understanding metastasis using the powerful tools of Drosophila genetics. Modeling metastasis in Drosophila Cancer can be thought of as a genetic disease caused by the accumulation of multiple genetic or epigenetic lesions in tumor-suppressor genes and oncogenes the resulting processes culminate in cell proliferation survival and metastasis colonization of distant sites by tumor cells 1 . But depending on the sequence in which cells accumulate genetic lesions the ensuing tumor progression and metastasis are highly variable even among tumors of the same type 1 . Furthermore only a small fraction of tumor cells achieve metastatic competence suggesting that the combination of required events is acquired only rarely. Our current understanding of the molecular processes leading to metastasis is largely derived from studies of cancer cell lines in vitro xenografts of human tumors and a limited number of transgenic or knockout mouse models 2 3 . These systems may not reflect the normal processes involved in tumorigenesis or as in case of murine models may be too cumbersome to be used for analyzing multiple genetic .