Journal
BLOOD
Volume 113, Issue 8, Pages 1741-1748Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2007-12-130260
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Funding
- National Institutes of Health (NIH, Bethesda, MD) [5R01CA026038-30]
- Inger Foundation, (Greenwich, CT)
- Tom Collier Memorial Regatta Foundation (Los Angeles, CA)
- Parker Hughes Fund (Los Angeles, CA)
- National Health Research Institutes, Miaoli, Taiwan [NHRI-EX96-9434SI]
- Mackay Memorial Hospital, Taipei, Taiwan [MMH-E-96009]
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Acute promyelocytic leukemia (APL) is ahematopoietic 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 (50-K and 250-K 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 chromosomes 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) occurred only 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. (Blood. 2009; 113: 1741-1748)
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