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References in table
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|<ref>Gronseth CM, McElhone SE, Storer BE, Kroeger KA, Sandhu V, Fero ML, Appelbaum FR, Estey EH, Fang M. Prognostic significance of acquired copy-neutral loss of heterozygosity in acute myeloid leukemia. Cancer 2015;121:2900–8, PMID 26033747</ref><ref>Yi JH, Huh J, Kim HJ, Kim SH, Kim HJ, Kim YK, Sohn SK, MoonJH, Kim SH, Kim KH, Won JH, Mun YC, Kim H, Park J, Jung CW, Kim DH. Adverse prognostic impact of abnormal lesions detected by genome-wide single nucleotide polymorphism array-based karyotyping analysis in acute myeloid leukemia with normal karyotype. J Clin Oncol Offic J Am Soc Clin Oncol, 29 (2011), pp. 4702-4708, [https://www.ncbi.nlm.nih.gov/pubmed/?term=Adverse+prognostic+impact+of+abnormal+lesions+detected+by+genome-wide+single+nucleotide+polymorphism+array-based+karyotyping+analysis+in+acute+myeloid+leukemia+with+normal+karyotype PMID 2208437]</ref><ref>L Bullinger, J Kronke, C Schon, I Radtke, K Urlbauer, UBotzenhardt, V Gaidzik, A Cario, C Senger, RF Schlenk, JRDowning, K Holzmann, K Dohner, H Dohner. Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis. Leukemia, 24 (2010), pp. 438-449, [https://www.ncbi.nlm.nih.gov/pubmed/?term=Identification+of+acquired+copy+number+alterations+and+uniparental+disomies+in+cytogenetically+normal+acute+myeloid+leukemia+using+high-resolution+single-nucleotide+polymorphism+analysis PMID 20016533]</ref><ref>AJ Dunbar, LP Gondek, CL O'Keefe, H Makishima, MS Rataul, HSzpurka, MA Sekeres, Wang XF, MA McDevitt, JP Maciejewski 250K single nucleotide polymorphism array karyotyping identifies acquired uniparental disomy and homozygous mutations, including novel missense substitutions of c-Cbl, in myeloid malignancies. Cancer Res, 68 (2008), pp. 10349-10357, [https://www.ncbi.nlm.nih.gov/pubmed/?term=250K+single+nucleotide+polymorphism+array+karyotyping+identifies+acquired+uniparental+disomy+and+homozygous+mutations%2C+including+novel+missense+substitutions+of+c-Cbl%2C+in+myeloid+malignancies PMID 19074904]</ref><ref>Kronke J, Bullinger L, Teleanu V, Tschurtz F, Gaidzik VI, Kuhn MW, Rucker FG, Holzmann K, Paschka P, Kapp-Schworer S, Spath D, Kindler T, Schittenhelm M, Krauter J, Ganser A, Gohring G, Schlegelberger B, Schlenk RF, Dohner H, Dohner K. Clonal evolution in relapsed NPM1-mutated acute myeloid leukemia. Blood 2013;122:100–8, [https://www.ncbi.nlm.nih.gov/pubmed/?term=Clonal+evolution+in+relapsed+NPM1-mutated+acute+myeloid+leukemia. PMID 23704090]</ref><ref>M Koren-Michowitz, A Sato-Otsubo, A Nagler, T Haferlach, S Ogawa, HP Koeffler. Older patients with normal karyotype acute myeloid leukemia have a higher rate of genomic changes compared to young patients as determined by SNP array analysis. Leukem Res, 36 (2012), pp. 467-473, [https://www.ncbi.nlm.nih.gov/pubmed/22071139 PMID 22071139]</ref><ref>L Bullinger, S Frohling. Array-based cytogenetic approaches in acute myeloid leukemia: clinical impact and biological insights. Sem Oncol, 39 (2012), pp. 37-46, [https://www.ncbi.nlm.nih.gov/pubmed/22289490 PMID 22289490]</ref><ref>Barresi V, Romano A, Musso N, Capizzi C, Consoli C, Martelli MP, Palumbo G, DiRaimondo F, Condorelli DF. Broad copy neutral loss of heterozygosity regions and rare recurring copy number abnormalities in normal karyotype acute myeloid leukemia genomes. Genes Chromos Cancer 2010;49:1014–23., [https://www.ncbi.nlm.nih.gov/pubmed/20725993 PMID 20725993]</ref><ref>T Akagi, S Ogawa, M Dugas, N Kawamata, G Yamamoto, YNannya, M Sanada, CW Miller, Yung A, S Schnittger, T Haferlach, C Haferlach, HP Koeffler. Frequent genomic abnormalities in acute myeloid leukemia/myelodysplastic syndrome with normal karyotype. Haematologica, 94 (2009), pp. 213-223, [https://www.ncbi.nlm.nih.gov/pubmed/19144660 PMID 19144660]</ref>
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|<ref name=":0">Gronseth CM, McElhone SE, Storer BE, Kroeger KA, Sandhu V, Fero ML, Appelbaum FR, Estey EH, Fang M. Prognostic significance of acquired copy-neutral loss of heterozygosity in acute myeloid leukemia. Cancer 2015;121:2900–8, PMID 26033747</ref><ref name=":1">Yi JH, Huh J, Kim HJ, Kim SH, Kim HJ, Kim YK, Sohn SK, MoonJH, Kim SH, Kim KH, Won JH, Mun YC, Kim H, Park J, Jung CW, Kim DH. Adverse prognostic impact of abnormal lesions detected by genome-wide single nucleotide polymorphism array-based karyotyping analysis in acute myeloid leukemia with normal karyotype. J Clin Oncol Offic J Am Soc Clin Oncol, 29 (2011), pp. 4702-4708, [https://www.ncbi.nlm.nih.gov/pubmed/?term=Adverse+prognostic+impact+of+abnormal+lesions+detected+by+genome-wide+single+nucleotide+polymorphism+array-based+karyotyping+analysis+in+acute+myeloid+leukemia+with+normal+karyotype PMID 2208437]</ref><ref name=":2">L Bullinger, J Kronke, C Schon, I Radtke, K Urlbauer, UBotzenhardt, V Gaidzik, A Cario, C Senger, RF Schlenk, JRDowning, K Holzmann, K Dohner, H Dohner. Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis. Leukemia, 24 (2010), pp. 438-449, [https://www.ncbi.nlm.nih.gov/pubmed/?term=Identification+of+acquired+copy+number+alterations+and+uniparental+disomies+in+cytogenetically+normal+acute+myeloid+leukemia+using+high-resolution+single-nucleotide+polymorphism+analysis PMID 20016533]</ref><ref name=":3">AJ Dunbar, LP Gondek, CL O'Keefe, H Makishima, MS Rataul, HSzpurka, MA Sekeres, Wang XF, MA McDevitt, JP Maciejewski 250K single nucleotide polymorphism array karyotyping identifies acquired uniparental disomy and homozygous mutations, including novel missense substitutions of c-Cbl, in myeloid malignancies. Cancer Res, 68 (2008), pp. 10349-10357, [https://www.ncbi.nlm.nih.gov/pubmed/?term=250K+single+nucleotide+polymorphism+array+karyotyping+identifies+acquired+uniparental+disomy+and+homozygous+mutations%2C+including+novel+missense+substitutions+of+c-Cbl%2C+in+myeloid+malignancies PMID 19074904]</ref><ref>Kronke J, Bullinger L, Teleanu V, Tschurtz F, Gaidzik VI, Kuhn MW, Rucker FG, Holzmann K, Paschka P, Kapp-Schworer S, Spath D, Kindler T, Schittenhelm M, Krauter J, Ganser A, Gohring G, Schlegelberger B, Schlenk RF, Dohner H, Dohner K. Clonal evolution in relapsed NPM1-mutated acute myeloid leukemia. Blood 2013;122:100–8, [https://www.ncbi.nlm.nih.gov/pubmed/?term=Clonal+evolution+in+relapsed+NPM1-mutated+acute+myeloid+leukemia. PMID 23704090]</ref><ref>M Koren-Michowitz, A Sato-Otsubo, A Nagler, T Haferlach, S Ogawa, HP Koeffler. Older patients with normal karyotype acute myeloid leukemia have a higher rate of genomic changes compared to young patients as determined by SNP array analysis. Leukem Res, 36 (2012), pp. 467-473, [https://www.ncbi.nlm.nih.gov/pubmed/22071139 PMID 22071139]</ref><ref name=":4">L Bullinger, S Frohling. Array-based cytogenetic approaches in acute myeloid leukemia: clinical impact and biological insights. Sem Oncol, 39 (2012), pp. 37-46, [https://www.ncbi.nlm.nih.gov/pubmed/22289490 PMID 22289490]</ref><ref>Barresi V, Romano A, Musso N, Capizzi C, Consoli C, Martelli MP, Palumbo G, DiRaimondo F, Condorelli DF. Broad copy neutral loss of heterozygosity regions and rare recurring copy number abnormalities in normal karyotype acute myeloid leukemia genomes. Genes Chromos Cancer 2010;49:1014–23., [https://www.ncbi.nlm.nih.gov/pubmed/20725993 PMID 20725993]</ref><ref name=":5">T Akagi, S Ogawa, M Dugas, N Kawamata, G Yamamoto, YNannya, M Sanada, CW Miller, Yung A, S Schnittger, T Haferlach, C Haferlach, HP Koeffler. Frequent genomic abnormalities in acute myeloid leukemia/myelodysplastic syndrome with normal karyotype. Haematologica, 94 (2009), pp. 213-223, [https://www.ncbi.nlm.nih.gov/pubmed/19144660 PMID 19144660]</ref>
 
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|<ref name=":0" /><ref name=":6">M Gupta, M Raghavan, RE Gale, C Chelala, C Allen, G Molloy, TChaplin, DC Linch, JB Cazier, Young BD. Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia. Genes Chromos Cancer, 47 (2008), pp. 729-739, [https://www.ncbi.nlm.nih.gov/pubmed/18506749 PMID 18506749]</ref><ref>T McKerrell, T Moreno, H Ponstingl, N Bolli, JM Dias, G Tischler, V Colonna, B Manasse, A Bench, D Bloxham, B Herman, DFletcher, N Park, MA Quail, N Manes, C Hodkinson, J Baxter, JSierra, T Foukaneli, AJ Warren, Chi J, P Costeas, R Rad, B Huntly, C Grove, Ning Z, C Tyler-Smith, I Varela, M Scott, J Nomdedeu, VMustonen, GS Vassiliou. Development and validation of a comprehensive genomic diagnostic tool for myeloid malignancies. Blood, 128 (2016), pp. e1-e9, [https://www.ncbi.nlm.nih.gov/pubmed/27121471 PMID 27121471]</ref>
 
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|<ref name=":3" /><ref>B Parkin, H Erba, P Ouillette, D Roulston, A Purkayastha, J Karp, M Talpaz, L Kujawski, S Shakhan, Li C, K Shedden, SN Malek. Acquired genomic copy number aberrations and survival in adult acute myelogenous leukemia. Blood, 116 (2010), pp. 4958-4967, [https://www.ncbi.nlm.nih.gov/pubmed/20729466 PMID 20729466]</ref><ref>J Flach, F Dicker, S Schnittger, S Schindela, A Kohlmann, THaferlach, W Kern, C Haferlach. An accumulation of cytogenetic and molecular genetic events characterizes the progression from MDS to secondary AML: an analysis of 38 paired samples analyzed by cytogenetics, molecular mutation analysis and SNP microarray profiling. Leukemia, 25 (2011), pp. 713-718, [https://www.ncbi.nlm.nih.gov/pubmed/21233836 PMID 21233836]</ref>
 
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|<ref name=":11" /><ref>E Kjeldsen. Oligo-based high-resolution aCGH analysis enhances routine cytogenetic diagnostics in haematological malignancies. Cancer Genom Proteom, 12 (2015), pp. 301-337, [https://www.ncbi.nlm.nih.gov/pubmed/26543079 PMID 26543079]</ref>
 
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