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Blood, 19 February 2009, Vol. 113, No. 8, pp. 1741-1748. Prepublished online as a Blood First Edition Paper on December 23, 2008; DOI 10.1182/blood-2007-12-130260. This Article Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2007-12-130260v1 113/8/1741    most recent Alert me when this article is cited Alert me if a correction is posted 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 Akagi, T. Articles by Koeffler, H P. Search for Related Content PubMed PubMed Citation Articles by Akagi, T. Articles by Koeffler, H P. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 20, 2007 Accepted November 16, 2008 Hidden abnormalities and novel classification of t(15;17) APL based on genomic alterations Tadayuki Akagi*, Lee-Yung Shih, Motohiro Kato, Norihiko Kawamata, Go Yamamoto, Masashi Sanada, Ryoko Okamoto, Carl W Miller, Der-Cherng Liang, Seishi Ogawa, and H Phillip Koeffler Division of Hematology and Oncology, Cedar-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA, United States Division of Hematology-Oncology, Department of Internal Medicine, Chang Gung University, Taipei, Taiwan Department of Hematology and Oncology, University of Tokyo, Tokyo, Japan The 21st century COE program, Graduate School of Medicine, University of Tokyo, Tokyo, Japan Division of Pediatric Hematology-Oncology, Mackay Memorial Hospital, Taipei, Taiwan * Corresponding author; email: tadayuki{at}staff.kanazawa-u.ac.jp. Acute promyelocytic leukemia (APL) is a hematopoietic malignant disease characterized by the chromosomal translocation t(15;17), resulting in the formation of the PML-RARA gene. Here, 47 t(15;17) APL samples were analyzed with high-density single-nucleotide polymorphism microarray (50K and 250K SNP-chips) using the new algorithm AsCNAR (allele-specific copy-number analysis using anonymous references). Copy-number-neutral loss of heterozygosity (CNN-LOH) was identified at chromosome 10q (3 cases), 11p (3 cases) and 19q (1 case). Twenty-eight samples (60%) did not have an obvious alteration (normal-copy-number [NC] group). Nineteen samples (40%) showed either one or more genomic abnormalities: 8 samples (17%) had trisomy 8 either with or without an additional duplication, deletion, or CNN-LOH (+8 group); and 11 samples (23%) had genomic abnormalities without trisomy 8 (other abnormalities group). These chromosomal abnormalities were acquired somatic mutations. Interestingly, FLT3-ITD mutations (11/47 cases) only occurred in the group with no genomic alteration (NC group). Taken together, these results suggest that the pathway of development of APL differs in each group: FLT3-ITD, trisomy 8, and other genomic changes. Here, we showed for the first time hidden abnormalities and novel disease-related genomic changes in t(15;17) APL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Akagi, L.-Y. Shih, S. Ogawa, J. Gerss, S. R. Moore, R. Schreck, N. Kawamata, D.-C. Liang, M. Sanada, Y. Nannya, et al. Single nucleotide polymorphism genomic arrays analysis of t(8;21) acute myeloid leukemia cells Haematologica, September 1, 2009; 94(9): 1301 - 1306. [Abstract] [Full Text] [PDF] M. J. Walter, J. E. Payton, R. E. Ries, W. D. Shannon, H. Deshmukh, Y. Zhao, J. Baty, S. Heath, P. Westervelt, M. A. Watson, et al. Acquired copy number alterations in adult acute myeloid leukemia genomes PNAS, August 4, 2009; 106(31): 12950 - 12955. [Abstract] [Full Text] [PDF]

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