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→Recurrent Genomic Alterations in AML Detected by Chromosomal Microarray (Literature Review)
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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>
|<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 name=":12">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 name=":13">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>S Weissmann, T Alpermann, V Grossmann, A Kowarsch, NNadarajah, C Eder, F Dicker, A Fasan, C Haferlach, T Haferlach, WKern, S Schnittger, A Kohlmann. Landscape of TET2 mutations in acute myeloid leukemia. Leukemia, 26 (2012), pp. 934-942, [https://www.ncbi.nlm.nih.gov/pubmed/22116554 PMID 22116554]</ref><ref name=":9">U Bacher, S Weissmann, A Kohlmann, S Schindela, T Alpermann, S Schnittger, W Kern, T Haferlach, C Haferlach. TET2 deletions are a recurrent but rare phenomenon in myeloid malignancies and are frequently accompanied by TET2 mutations on the remaining allele. Br J Haematol, 156 (2012), pp. 67-75, [https://www.ncbi.nlm.nih.gov/pubmed/22017486 PMID 22017486]</ref><ref name=":8" />
|<ref name=":8" /><ref>S Weissmann, T Alpermann, V Grossmann, A Kowarsch, NNadarajah, C Eder, F Dicker, A Fasan, C Haferlach, T Haferlach, WKern, S Schnittger, A Kohlmann. Landscape of TET2 mutations in acute myeloid leukemia. Leukemia, 26 (2012), pp. 934-942, [https://www.ncbi.nlm.nih.gov/pubmed/22116554 PMID 22116554]</ref><ref name=":9">U Bacher, S Weissmann, A Kohlmann, S Schindela, T Alpermann, S Schnittger, W Kern, T Haferlach, C Haferlach. TET2 deletions are a recurrent but rare phenomenon in myeloid malignancies and are frequently accompanied by TET2 mutations on the remaining allele. Br J Haematol, 156 (2012), pp. 67-75, [https://www.ncbi.nlm.nih.gov/pubmed/22017486 PMID 22017486]</ref>
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|<ref name=":10">R Bajaj, Xu F, Xiang B, K Wilcox, AJ Diadamo, R Kumar, APietraszkiewicz, S Halene, Li P. Evidence-based genomic diagnosis characterized chromosomal and cryptic imbalances in 30 elderly patients with myelodysplastic syndrome and acute myeloid leukemia. Mol Cytogenet, 4 (2011), p. 3, [https://www.ncbi.nlm.nih.gov/pubmed/21251322 PMID 21251322]</ref><ref>B Parkin, P Ouillette, M Yildiz, K Saiya-Cork, K Shedden, SN Malek. Integrated genomic profiling, therapy response, and survival in adult acute myelogenous leukemia. Clin Cancer Res Offic J Am Assocr Cancer Res, 21 (2015), pp. 2045-2056, [https://www.ncbi.nlm.nih.gov/pubmed/25652455 PMID 25652455]</ref><ref name=":9" /><ref name=":11">MJ Walter, JE Payton, RE Ries, WD Shannon, H Deshmukh, ZhaoY, J Baty, S Heath, P Westervelt, MA Watson, MH Tomasson, RNagarajan, BP O'Gara, CD Bloomfield, K Mrozek, RR Selzer, TARichmond, J Kitzman, J Geoghegan, PS Eis, R Maupin, RS Fulton, M McLellan, RK Wilson, ER Mardis, DC Link, TA Graubert, JFDiPersio, TJ Ley. Acquired copy number alterations in adult acute myeloid leukemia genomes. Proc Natl Acad Sci USA, 106 (2009), pp. 12950-12955, [https://www.ncbi.nlm.nih.gov/pubmed/19651600 PMID 19651600]</ref><ref name=":7" /><ref name=":8" /><ref>FG Rucker, RF Schlenk, L Bullinger, S Kayser, V Teleanu, H Kett, MHabdank, CM Kugler, K Holzmann, VI Gaidzik, P Paschka, GHeld, M von Lilienfeld-Toal, M Lubbert, S Frohling, T Zenz, JKrauter, B Schlegelberger, A Ganser, P Lichter, K Dohner, HDohner. TP53 alterations in acute myeloid leukemia with complex karyotype correlate with specific copy number alterations, monosomal karyotype, and dismal outcome. Blood, 119 (2012), pp. 2114-2121, [https://www.ncbi.nlm.nih.gov/pubmed/22186996 PMID 22186996]</ref><ref>A Jerez, LP Gondek, AM Jankowska, H Makishima, B Przychodzen, Tiu RV, CL O'Keefe, AM Mohamedali, D Batista, MA Sekeres, MAMcDevitt, GJ Mufti, JP Maciejewski. Topography, clinical, and genomic correlates of 5q myeloid malignancies revisited. J Clin Oncol Offic J Am Soc Clin Oncol, 30 (2012), pp. 1343-1349, [https://www.ncbi.nlm.nih.gov/pubmed/22370328 PMID 22370328]</ref><ref>M Mehrotra, R Luthra, F Ravandi, RL Sargent, BA Barkoh, RAbraham, BM Mishra, LJ Medeiros, KP Patel. Identification of clinically important chromosomal aberrations in acute myeloid leukemia by array-based comparative genomic hybridization. Leukemia Lymph, 55 (2014), pp. 2538-2548, [https://www.ncbi.nlm.nih.gov/pubmed/24446873 PMID 24446873]</ref><ref>Kim MH, J Stewart, C Devlin, Kim YT, E Boyd, M Connor. The application of comparative genomic hybridization as an additional tool in the chromosome analysis of acute myeloid leukemia and myelodysplastic syndromes. Cancer Genet Cytogen, 126 (2001), pp. 26-33, [https://www.ncbi.nlm.nih.gov/pubmed/11343775 PMID 11343775]</ref><ref>Rumi E, Harutyunyan A, Elena C, Pietra D, Klampfl T, Bagien-ski K, Berg T, Casetti I, Pascutto C, Passamonti F, Kralovics R, Cazzola M. Identification of genomic aberrations associated with disease transformation by means of high resolution SNP array analysis in patients with myeloproliferative neoplasm. Am J Hematol 2011;86:974–9, [https://www.ncbi.nlm.nih.gov/pubmed/21953568 PMID 21953568]</ref><ref>LP Gondek, Tiu R, CL O'Keefe, MA Sekeres, KS Theil, JPMaciejewski. Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML. Blood, 111 (2008), pp. 1534-1542, [https://www.ncbi.nlm.nih.gov/pubmed/17954704 PMID 17954704]</ref>
|<ref name=":10">R Bajaj, Xu F, Xiang B, K Wilcox, AJ Diadamo, R Kumar, APietraszkiewicz, S Halene, Li P. Evidence-based genomic diagnosis characterized chromosomal and cryptic imbalances in 30 elderly patients with myelodysplastic syndrome and acute myeloid leukemia. Mol Cytogenet, 4 (2011), p. 3, [https://www.ncbi.nlm.nih.gov/pubmed/21251322 PMID 21251322]</ref><ref name=":14">B Parkin, P Ouillette, M Yildiz, K Saiya-Cork, K Shedden, SN Malek. Integrated genomic profiling, therapy response, and survival in adult acute myelogenous leukemia. Clin Cancer Res Offic J Am Assocr Cancer Res, 21 (2015), pp. 2045-2056, [https://www.ncbi.nlm.nih.gov/pubmed/25652455 PMID 25652455]</ref><ref name=":9" /><ref name=":11">MJ Walter, JE Payton, RE Ries, WD Shannon, H Deshmukh, ZhaoY, J Baty, S Heath, P Westervelt, MA Watson, MH Tomasson, RNagarajan, BP O'Gara, CD Bloomfield, K Mrozek, RR Selzer, TARichmond, J Kitzman, J Geoghegan, PS Eis, R Maupin, RS Fulton, M McLellan, RK Wilson, ER Mardis, DC Link, TA Graubert, JFDiPersio, TJ Ley. Acquired copy number alterations in adult acute myeloid leukemia genomes. Proc Natl Acad Sci USA, 106 (2009), pp. 12950-12955, [https://www.ncbi.nlm.nih.gov/pubmed/19651600 PMID 19651600]</ref><ref name=":7" /><ref name=":8" /><ref name=":15">FG Rucker, RF Schlenk, L Bullinger, S Kayser, V Teleanu, H Kett, MHabdank, CM Kugler, K Holzmann, VI Gaidzik, P Paschka, GHeld, M von Lilienfeld-Toal, M Lubbert, S Frohling, T Zenz, JKrauter, B Schlegelberger, A Ganser, P Lichter, K Dohner, HDohner. TP53 alterations in acute myeloid leukemia with complex karyotype correlate with specific copy number alterations, monosomal karyotype, and dismal outcome. Blood, 119 (2012), pp. 2114-2121, [https://www.ncbi.nlm.nih.gov/pubmed/22186996 PMID 22186996]</ref><ref>A Jerez, LP Gondek, AM Jankowska, H Makishima, B Przychodzen, Tiu RV, CL O'Keefe, AM Mohamedali, D Batista, MA Sekeres, MAMcDevitt, GJ Mufti, JP Maciejewski. Topography, clinical, and genomic correlates of 5q myeloid malignancies revisited. J Clin Oncol Offic J Am Soc Clin Oncol, 30 (2012), pp. 1343-1349, [https://www.ncbi.nlm.nih.gov/pubmed/22370328 PMID 22370328]</ref><ref>M Mehrotra, R Luthra, F Ravandi, RL Sargent, BA Barkoh, RAbraham, BM Mishra, LJ Medeiros, KP Patel. Identification of clinically important chromosomal aberrations in acute myeloid leukemia by array-based comparative genomic hybridization. Leukemia Lymph, 55 (2014), pp. 2538-2548, [https://www.ncbi.nlm.nih.gov/pubmed/24446873 PMID 24446873]</ref><ref>Kim MH, J Stewart, C Devlin, Kim YT, E Boyd, M Connor. The application of comparative genomic hybridization as an additional tool in the chromosome analysis of acute myeloid leukemia and myelodysplastic syndromes. Cancer Genet Cytogen, 126 (2001), pp. 26-33, [https://www.ncbi.nlm.nih.gov/pubmed/11343775 PMID 11343775]</ref><ref>Rumi E, Harutyunyan A, Elena C, Pietra D, Klampfl T, Bagien-ski K, Berg T, Casetti I, Pascutto C, Passamonti F, Kralovics R, Cazzola M. Identification of genomic aberrations associated with disease transformation by means of high resolution SNP array analysis in patients with myeloproliferative neoplasm. Am J Hematol 2011;86:974–9, [https://www.ncbi.nlm.nih.gov/pubmed/21953568 PMID 21953568]</ref><ref name=":16">LP Gondek, Tiu R, CL O'Keefe, MA Sekeres, KS Theil, JPMaciejewski. Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML. Blood, 111 (2008), pp. 1534-1542, [https://www.ncbi.nlm.nih.gov/pubmed/17954704 PMID 17954704]</ref>
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|<ref name=":3" /><ref name=":4" /><ref>A Tyybakinoja, E Elonen, H Vauhkonen, J Saarela, S Knuutila. Single nucleotide polymorphism microarray analysis of karyotypically normal acute myeloid leukemia reveals frequent copy number neutral loss of heterozygosity. Haematologica, 93 (2008), pp. 631-632, [https://www.ncbi.nlm.nih.gov/pubmed/18379011 PMID 18379011]</ref>
|<ref name=":3" /><ref name=":4" /><ref name=":17">A Tyybakinoja, E Elonen, H Vauhkonen, J Saarela, S Knuutila. Single nucleotide polymorphism microarray analysis of karyotypically normal acute myeloid leukemia reveals frequent copy number neutral loss of heterozygosity. Haematologica, 93 (2008), pp. 631-632, [https://www.ncbi.nlm.nih.gov/pubmed/18379011 PMID 18379011]</ref>
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|<ref>Huh J, Jung CW, Kim HJ, Kim YK, Moon JH, Sohn SK, Kim HJ, Min WS, Kim DH. Different characteristics identified by single nucleotide polymorphism array analysis in leukemia suggest the need for different application strategies depending on disease category. Genes Chromos cancer, 52 (2013), pp. 44-55, [https://www.ncbi.nlm.nih.gov/pubmed/23023762 PMID 23023762]</ref><ref name=":7" /><ref name=":8" /><ref>ME McNerney, CD Brown, X Wang, ET Bartom, S Karmakar, CBandlamudi, Yu S, Ko J, BP Sandall, T Stricker, J Anastasi, RLGrossman, JM Cunningham, MM Le Beau, KP White. CUX1 is a haploinsufficient tumor suppressor gene on chromosome 7 frequently inactivated in acute myeloid leukemia. Blood, 121 (2013), pp. 975-983, [https://www.ncbi.nlm.nih.gov/pubmed/23212519 PMID 23212519]</ref>
|<ref name=":18">Huh J, Jung CW, Kim HJ, Kim YK, Moon JH, Sohn SK, Kim HJ, Min WS, Kim DH. Different characteristics identified by single nucleotide polymorphism array analysis in leukemia suggest the need for different application strategies depending on disease category. Genes Chromos cancer, 52 (2013), pp. 44-55, [https://www.ncbi.nlm.nih.gov/pubmed/23023762 PMID 23023762]</ref><ref name=":7" /><ref name=":8" /><ref>ME McNerney, CD Brown, X Wang, ET Bartom, S Karmakar, CBandlamudi, Yu S, Ko J, BP Sandall, T Stricker, J Anastasi, RLGrossman, JM Cunningham, MM Le Beau, KP White. CUX1 is a haploinsufficient tumor suppressor gene on chromosome 7 frequently inactivated in acute myeloid leukemia. Blood, 121 (2013), pp. 975-983, [https://www.ncbi.nlm.nih.gov/pubmed/23212519 PMID 23212519]</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>
|<ref name=":11" /><ref name=":19">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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|<ref name=":10" /><ref name=":2" /><ref name=":14" /><ref name=":11" /><ref name=":7" /><ref name=":8" /><ref name=":15" /><ref name=":5" /><ref name=":16" /><ref name=":19" /><ref>Paulsson K, Heidenblad M, Strombeck B, Staaf J, Jonsson G, Borg A, Fioretos T, Johansson B. High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration. Leukemia 2006;20:840–6. [https://www.ncbi.nlm.nih.gov/pubmed/16498392 PMID 16498392]</ref><ref>Feurstein S, Rucker FG, Bullinger L, Hofmann W, Manuk-jan G, Gohring G, Lehmann U, Heuser M, Ganser A, Dohner K, Schlegelberger B, Steinemann D. Haploinsufficiency of ETV6 and CDKN1B in patients with acute myeloid leukemia and complex karyotype. BMC Genom 2014;15:784. [https://www.ncbi.nlm.nih.gov/pubmed/25213837 PMID 25213837]</ref><ref>Zhang R, Kim YM, Wang X, Li Y, Lu X, Sternenberger AR, Li S, Lee JY. Genomic copy number variations in the myelodysplastic syndrome and acute myeloid leukemia patients with del(5q) and/or -7/del(7q). Int J Med Sci 2015;12:719–26, [https://www.ncbi.nlm.nih.gov/pubmed/26392809 PMID 26392809]</ref><ref>Wall M, Rayeroux KC, MacKinnon RN, Zordan A, Campbell LJ. ETV6 deletion is a common additional abnormality in patients with myelodysplastic syndromes or acute myeloid leukemia and monosomy 7. Haematologica 2012;97:1933–6., [https://www.ncbi.nlm.nih.gov/pubmed/22875624 PMID 22875624]</ref>
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|<ref name=":0" /><ref name=":18" /><ref name=":1" /><ref name=":2" /><ref>Tiu RV, LP Gondek, CL O'Keefe, Huh J, MA Sekeres, P Elson, MAMcDevitt, Wang XF, MJ Levis, JE Karp, AS Advani, JP Maciejewski. New lesions detected by single nucleotide polymorphism array-based chromosomal analysis have important clinical impact in acute myeloid leukemia. J Clin Oncol Off J Am Soc Clin Oncol, 27 (2009), pp. 5219-5226, [https://www.ncbi.nlm.nih.gov/pubmed/19770377 PMID 19770377]</ref><ref name=":6" /><ref name=":8" /><ref name=":3" /><ref name=":12" /><ref name=":13" /><ref name=":4" /><ref name=":5" /><ref name=":17" />
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