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Prepublished online as a Blood First Edition Paper on June 5, 2003; DOI 10.1182/blood-2002-12-3817. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-12-3817v1 102/7/2321    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 Greaves, M. F. Articles by Ford, A. M. Search for Related Content PubMed PubMed Citation Articles by Greaves, M. F. Articles by Ford, A. M. Related Collections Oncogenes and Tumor Suppressors Review Articles Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 October 2003, Vol. 102, No. 7, pp. 2321-2333 REVIEW ARTICLES Leukemia in twins: lessons in natural history Mel F. Greaves, Ana Teresa Maia, Joseph L. Wiemels, and Anthony M. Ford From the Leukaemia Research Fund Centre, Institute of Cancer Research, London, United Kingdom. Identical infant twins with concordant leukemia were first described in 1882, and since that time many such pairs of infants and older children have been described. It has long been recognized that this situation offers a unique opportunity to identify aspects of the developmental timing, natural history, and molecular genetics of pediatric leukemia in general. We reviewed both the older literature and more recent molecular biologic studies that have uncovered the basis of concordance of leukemia. Molecular markers of clonality, including unique, genomic fusion gene sequences, have provided unequivocal evidence that twin pairs of leukemia have a common clonal origin. The only plausible basis for this, first suggested more than 40 years ago, is that following initiation of leukemia in one twin fetus, clonal progeny spread to the co-twin via vascular anastomoses within a single, monochorionic placenta. This explanation has been endorsed by the identification of clonotypic gene fusion sequences in archived neonatal blood spots of individuals who subsequently developed leukemia. These analyses of twin leukemias have thrown considerable light on the natural history of disease. They reveal a frequent prenatal origin and an early or initiating role for chromosome translocations. Further, they provide evidence for a variable and often protracted latency and the need, in childhood acute lymphoblastic leukemia (ALL)/acute myeloblastic leukemia (AML), for further postnatal exposures and/or genetic events to produce clinical disease. We argue that these insights provide a very useful framework for attempts to understand etiologic mechanisms. (Blood. 2003;102:2321-2333) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Crump, B. Coiffier, E. D. Jacobsen, L. Sun, J. L. Ricker, H. Xie, S. R. Frankel, S. S. Randolph, and B. D. Cheson Phase II trial of oral vorinostat (suberoylanilide hydroxamic acid) in relapsed diffuse large-B-cell lymphoma Ann. Onc., May 1, 2008; 19(5): 964 - 969. [Abstract] [Full Text] [PDF] D. Hong, R. Gupta, P. Ancliff, A. Atzberger, J. Brown, S. Soneji, J. Green, S. Colman, W. Piacibello, V. Buckle, et al. 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