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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 (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.

Titel:	Hidden abnormalities and novel classification of t(15;17) acute promyelocytic leukemia (APL) based on genomic alterations.
Autor/in / Beteiligte Person:	Akagi, T ; Shih, LY ; Kato, M ; Kawamata, N ; Yamamoto, G ; Sanada, M ; Okamoto, R ; Miller, CW ; Liang, DC ; Ogawa, S ; Koeffler, HP
Link:	Full Text Finder (Volltext)
Zeitschrift:	Blood, Jg. 113 (2009-02-19), Heft 8, S. 1741-8
Veröffentlichung:	2021- : [New York] : Elsevier ; <i>Original Publication</i>: New York, Grune & Stratton [etc.], 2009
Medientyp:	academicJournal
ISSN:	1528-0020 (electronic)
DOI:	10.1182/blood-2007-12-130260
Schlagwort:	Adolescent Adult Aged Child Female Gene Dosage Gene Expression Regulation, Leukemic Genomics Humans Leukemia, Promyelocytic, Acute pathology Loss of Heterozygosity genetics Male Middle Aged Polymorphism, Single Nucleotide Tumor Cells, Cultured Young Adult fms-Like Tyrosine Kinase 3 genetics Chromosomes, Human, Pair 15 Chromosomes, Human, Pair 17 Leukemia, Promyelocytic, Acute genetics Oligonucleotide Array Sequence Analysis Oncogene Proteins, Fusion genetics Translocation, Genetic
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Language: English [Blood] 2009 Feb 19; Vol. 113 (8), pp. 1741-8. <i>Date of Electronic Publication: </i>2008 Dec 23. MeSH Terms: Chromosomes, Human, Pair 15* ; Chromosomes, Human, Pair 17* ; Oligonucleotide Array Sequence Analysis* ; Translocation, Genetic* ; Leukemia, Promyelocytic, Acute / genetics ; Oncogene Proteins, Fusion / genetics ; Adolescent ; Adult ; Aged ; Child ; Female ; Gene Dosage ; Gene Expression Regulation, Leukemic ; Genomics ; Humans ; Leukemia, Promyelocytic, Acute / pathology ; Loss of Heterozygosity / genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Tumor Cells, Cultured ; Young Adult ; fms-Like Tyrosine Kinase 3 / genetics References: Blood. 2005 Jun 15;105(12):4792-9. (PMID: 15718420) ; Blood. 2005 Sep 15;106(6):2113-9. (PMID: 15951308) ; Genes Chromosomes Cancer. 2008 Sep;47(9):729-39. (PMID: 18506749) ; Genes Chromosomes Cancer. 2005 Nov;44(3):334-7. (PMID: 16015648) ; Cancer Res. 2005 Jan 15;65(2):375-8. (PMID: 15695375) ; Haematologica. 2000 Jan;85(1):31-4. (PMID: 10629588) ; Am J Hum Genet. 2007 Jul;81(1):114-26. (PMID: 17564968) ; Blood. 1991 Mar 1;77(5):1080-6. (PMID: 1995093) ; Nature. 1998 Feb 19;391(6669):815-8. (PMID: 9486655) ; Cancer Res. 2005 Jul 15;65(14):6071-9. (PMID: 16024607) ; Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2551-6. (PMID: 9122233) ; Blood. 1999 May 15;93(10):3167-215. (PMID: 10233871) ; Cancer Res. 2005 Oct 15;65(20):9152-4. (PMID: 16230371) ; Blood. 1984 Feb;63(2):254-9. (PMID: 6362749) ; Nature. 1990 Oct 11;347(6293):558-61. (PMID: 2170850) ; Br J Haematol. 2007 Sep;138(5):603-15. (PMID: 17686054) ; Cancer. 2003 Sep 15;98(6):1206-16. (PMID: 12973844) ; Blood. 2008 Jan 15;111(2):776-84. (PMID: 17890455) ; Blood. 2005 Jul 1;106(1):265-73. (PMID: 15769897) ; Haematologica. 2009 Feb;94(2):213-23. (PMID: 19144660) ; Br J Haematol. 2002 Mar;116(4):744-57. (PMID: 11886377) ; Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8. (PMID: 12060771) ; Blood. 2005 May 1;105(9):3699-706. (PMID: 15650056) ; Blood. 2006 Sep 1;108(5):1708-15. (PMID: 16675706) ; N Engl J Med. 1993 Jul 15;329(3):177-89. (PMID: 8515790) ; Cancer. 2008 Mar 15;112(6):1296-305. (PMID: 18246537) ; Leukemia. 2005 Jul;19(7):1153-60. (PMID: 15889156) ; Nature. 2007 Apr 12;446(7137):758-64. (PMID: 17344859) ; Blood. 2003 Apr 15;101(8):3188-97. (PMID: 12515727) ; Cell. 1991 Aug 23;66(4):675-84. (PMID: 1652369) ; Blood. 2008 Aug 1;112(3):814-21. (PMID: 18490517) ; Genes Chromosomes Cancer. 2002 Nov;35(3):261-70. (PMID: 12353268) ; J Clin Oncol. 2005 Dec 20;23(36):9234-42. (PMID: 16275934) ; Oncogene. 2005 Jun 9;24(25):4129-37. (PMID: 15806161) ; Blood. 1997 Jan 15;89(2):376-87. (PMID: 9002938) ; Blood. 2002 Apr 15;99(8):2985-91. (PMID: 11929790) ; Blood. 2002 Jan 1;99(1):310-8. (PMID: 11756186) ; Blood. 2007 Feb 1;109(3):1202-10. (PMID: 17053054) ; Leuk Lymphoma. 2008 Jun;49(6):1178-83. (PMID: 18452069) ; Br J Haematol. 2007 Apr;137(1):64-75. (PMID: 17359372) ; Oncogene. 2006 Mar 13;25(11):1594-601. (PMID: 16550159) Grant Information: R01 CA026038 United States CA NCI NIH HHS; 5R01CA026038-30 United States CA NCI NIH HHS Substance Nomenclature: 0 (Oncogene Proteins, Fusion) ; 0 (promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein) ; EC 2.7.10.1 (FLT3 protein, human) ; EC 2.7.10.1 (fms-Like Tyrosine Kinase 3) Entry Date(s): Date Created: 20081226 Date Completed: 20090401 Latest Revision: 20211020 Update Code: 20240513 PubMed Central ID: PMC2647673

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Hidden abnormalities and novel classification of t(15;17) acute promyelocytic leukemia (APL) based on genomic alterations.