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1. Dunne J, Gascoyne DM, Lister TA, Brady HJ, Heidenreich O, Young BD: AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemia. Cancer Res; 2010 May 15;70(10):3985-95
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  • [Title] AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemia.
  • A variety of genetic lesions, including chromosomal translocations, internal tandem duplications, and mutations, have been described in acute myeloid leukemia (AML).
  • AML exhibiting the translocation t(8;21), which fuses the AML1 and ETO genes, has such a characteristic expression profile.
  • One gene whose expression is highly correlated with the presence of the AML1/ETO fusion is POU4F1, which encodes the POU homeodomain transcription factor BRN3A.
  • Here we show using specific siRNA in t(8;21) cells and overexpression studies in progenitor cells that AML1/ETO promotes expression of POU4F1/BRN3A.
  • This effect requires DNA-binding function of AML1/ETO, and accordingly, AML1/ETO is bound to the POU4F1 locus in t(8;21) cells.
  • Functionally, whereas overexpression of Brn3a in murine hematopoietic progenitor cells induces terminal myeloid differentiation, coexpression of AML1/ETO or AML1/ETO9a blocks this effect.
  • Furthermore, Brn3a reduction by shRNA impairs AML1/ETO-induced immortalization of murine progenitors.
  • In summary, we identify POU4F1/BRN3A as a novel potential upregulated AML1/ETO target gene whose dramatically high expression may cooperate with AML1/ETO in t(8;21) cells.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Oncogene Proteins, Fusion / metabolism. Transcription Factor Brn-3A / metabolism
  • [MeSH-minor] Adult. Animals. Base Sequence. Blotting, Western. Cell Differentiation. Chromatin Immunoprecipitation. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Electrophoretic Mobility Shift Assay. Embryonic Stem Cells / cytology. Embryonic Stem Cells / physiology. Fetus. Fluorescent Antibody Technique. Hematopoietic Stem Cells / physiology. Humans. Immunoenzyme Techniques. Liver / cytology. Liver / metabolism. Luciferases / metabolism. Mice. Molecular Sequence Data. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Translocation, Genetic / genetics

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  • (PMID = 20460523.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6789; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / POU4F1 protein, human; 0 / Pou4f1 protein, mouse; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factor Brn-3A; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC2883733; NLM/ UKMS29216
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2. Wang YY, Zhou GB, Yin T, Chen B, Shi JY, Liang WX, Jin XL, You JH, Yang G, Shen ZX, Chen J, Xiong SM, Chen GQ, Xu F, Liu YW, Chen Z, Chen SJ: AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec. Proc Natl Acad Sci U S A; 2005 Jan 25;102(4):1104-9
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  • [Title] AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.
  • To explore the genetic abnormalities that cooperate with AML1-ETO (AE) fusion gene to cause acute myeloid leukemia (AML) with t(8;21), we screened a number of candidate genes and identified 11 types of mutations in C-KIT gene (mC-KIT), including 6 previously undescribed ones among 26 of 54 (48.1%) cases with t(8;21).
  • Therefore, mC-KIT should be a subsequent event on the basis of t(8;21).
  • This may lead to an alternative way of C-KIT activation and may explain the significantly higher C-KIT expression in 81.3% of patients with t(8;21) than in patients with other leukemias.
  • These data strongly suggest that t(8;21) AML follows a stepwise model in leukemogenesis, i.e., AE represents the first, fundamental genetic hit to initiate the disease, whereas activation of the C-KIT pathway may be a second but also crucial hit for the development of a full-blown leukemia.
  • Gleevec also exerted a synergic effect in apoptosis induction with cytarabine, thus providing a potential therapeutic for t(8;21) leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Piperazines / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Apoptosis / drug effects. Benzamides. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. Female. Humans. Imatinib Mesylate. Male. Middle Aged

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  • (PMID = 15650049.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC545849
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3. Schnittger S, Kohl TM, Haferlach T, Kern W, Hiddemann W, Spiekermann K, Schoch C: KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival. Blood; 2006 Mar 1;107(5):1791-9
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  • [Title] KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival.
  • Mutations in codon D816 of the KIT gene represent a recurrent genetic alteration in acute myeloid leukemia (AML).
  • Of these 33 patients, 8 (24.2%) had a t(8;21), which was significantly higher compared with the subgroup without D816 mutations.
  • Analyses of genetic subgroups showed that KIT-D816 mutations were associated with t(8;21)/AML1-ETO and other rare AML1 translocations.
  • In contrast, other activating mutations like FLT3 and NRAS mutations were very rarely detected in AML1-rearranged leukemia.
  • KIT mutations had an independent negative impact on overall (median 304 vs 1836 days; P = .006) and event-free survival (median 244 vs 744 days; P = .003) in patients with t(8;21) but not in patients with a normal karyotype.
  • The KIT-D816 mutations confer a poor prognosis to AML1-ETO-positive AML and should therefore be included in the diagnostic workup.
  • Patients with KIT-D816-positive/AML1-ETO-positive AML might benefit from early intensification of treatment or combination of conventional chemotherapy with KIT PTK inhibitors.
  • [MeSH-major] Amino Acid Substitution. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Point Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Adult. Aged. Cell Line. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Codon / genetics. Disease-Free Survival. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Gene Expression / genetics. Humans. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Retrospective Studies. Translocation, Genetic / genetics

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  • (PMID = 16254134.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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4. Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Liu YR, Shi Y, Dang H, He Q, Lu DP: [Analysis of characteristics of 72 cases of t(8;21) acute myeloid leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):245-8
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  • [Title] [Analysis of characteristics of 72 cases of t(8;21) acute myeloid leukemia].
  • OBJECTIVE: To investigate the laboratorial and clinical characteristics of t(8;21) AML, and to compare the differences between patients with additional chromosomal abnormalities and those without additional aberrations.
  • METHODS: Seventy-two cases of t(8;21) AML were analyzed retrospectively, including features of morphology, initial blood cells, cytogenetic G-banding karyotype, immunophenotype, AML1/ETO fusion gene and clinical outcome.
  • In order to compare the characteristics of patients with additional chromosomal abnormalities with those with t(8;21) alone, these patients were divided into two groups according to their karyotype as follows: Group A included patients with t(8;21) alone; Group B included patients with additional aberrations.
  • There were no obvious differences between these two groups in their features of age distribution, bone marrow blast cells, Auer rods, eosinophilia, immunophenotype, as well as central nervous system leukemia occurrence and complete remission rate of induction, but a male prevalence and a lower initial WBC were observed in Group B.
  • CONCLUSION: Additional chromosomal abnormality is an adverse factor for prognosis of t(8;21) AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 15968311.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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5. Dutta P, Hasan SK, Sazawal S, Kumar B, Bhattacharyya J, Jain M, Tyagi S, Kumar R, Pati HP, Saxena R: AML1-ETO positive AML: first report from India. Indian J Pathol Microbiol; 2007 Jul;50(3):652-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML1-ETO positive AML: first report from India.
  • Translocation (8;21) is associated with few typical morphological features and favorable prognosis.
  • RT-PCR was done for the AML1-ETO fusion transcript in all cases.
  • Overall incidence of AML1-ETO was 28.57% and no correlation was found between AML1-ETO positivity and clinical or hematological parameters except for a direct correlation with absolute blast count (ABC) (a lower ABC in the AML1-ETO positive cases).
  • Interestingly, 1/3 MDS cases were positive for the same fusion transcript and thus, it appears worthwhile to look for AML1-ETO in all cases of MDS with increased blasts.
  • Objective morphological evaluation using a scoring system based on morphological features was not helpful in predicting positivity for AML1-ETO.
  • The effect of this translocation on long-term survival could not be determined by the present study.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / epidemiology. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Incidence. India / epidemiology. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 17883173.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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6. Fortier JM, Payton JE, Cahan P, Ley TJ, Walter MJ, Graubert TA: POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature. Leukemia; 2010 May;24(5):950-7
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  • [Title] POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature.
  • The t(8;21)(q22;q22) translocation, present in approximately 5% of adult acute myeloid leukemia (AML) cases, produces the AML1/ETO (AE) fusion protein.
  • Dysregulation of the Pit/Oct/Unc (POU) domain-containing transcription factor POU4F1 is a recurring abnormality in t(8;21) AML.
  • We observed that AE markedly increases the self-renewal capacity of myeloid progenitors from murine bone marrow or fetal liver and drives the expansion of these cells in liquid culture.
  • POU4F1 is neither necessary nor sufficient for these AE-dependent properties, suggesting that it contributes to leukemia through novel mechanisms.
  • This expression signature was significantly enriched in human t(8;21) AML samples and was sufficient to cluster t(8;21) AML samples in an unsupervised hierarchical analysis.
  • Among the most highly differentially expressed genes, half are known AML1/ETO targets, implying that the unique transcriptional signature of t(8;21) AML is, in part, attributable to POU4F1 and not AML1/ETO itself.
  • These genes provide novel candidates for understanding the biology and developing therapeutic approaches for t(8;21) AML.

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  • (PMID = 20376082.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / P01 CA101937-010006; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / P30 CA91842
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / POU4F1 protein, human; 0 / Pou4f1 protein, mouse; 0 / RNA, Messenger; 0 / Transcription Factor Brn-3A
  • [Other-IDs] NLM/ NIHMS183891; NLM/ PMC2868953
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7. Klymenko S, Trott K, Atkinson M, Bink K, Bebeshko V, Bazyka D, Dmytrenko I, Abramenko I, Bilous N, Misurin A, Zitzelsberger H, Rosemann M: Aml1 gene rearrangements and mutations in radiation-associated acute myeloid leukemia and myelodysplastic syndromes. J Radiat Res; 2005 Jun;46(2):249-55
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  • [Title] Aml1 gene rearrangements and mutations in radiation-associated acute myeloid leukemia and myelodysplastic syndromes.
  • Several studies suggested a causal link between AML1 gene rearrangements and both radiation-induced acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS).
  • Fifty-three AML samples were analyzed for the presence of AML1 abnormalities using fluorescent in-situ hybridization (FISH) and reverse transcription polymerase chain reaction (RT-PCR).
  • AML1/ETO translocations were found in 9 of 29 spontaneous AML but only in 1 of 24 radiation-associated AML cases.
  • This difference between translocation frequencies is statistically significant in the age-unstratified cohorts (p=0.015).
  • AML1 mutation status was assessed in 5 clean-up workers at Chernobyl NPP with MDS, or AML following MDS, by direct sequencing of genomic DNA from the coding region (exon 3 through 8).
  • In one patient who developed MDS following an acute radiation syndrome, a hexanucleotide duplication of CGGCAT in exon 8 was found, inserted after base position 1502.
  • Our results suggest that AML1 gene translocations are infrequent in radiation-induced leukemogenesis but are consistent with the idea that radiation may contribute to the development of MDS through AML1 gene mutation.
  • [MeSH-major] Chernobyl Nuclear Accident. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / metabolism. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Radiation-Induced / metabolism. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Causality. Core Binding Factor Alpha 2 Subunit. DNA Mutational Analysis. Female. Gene Frequency. Humans. Incidence. Male. Middle Aged. Power Plants. Radioactive Hazard Release. Risk Assessment / methods. Risk Factors. Translocation, Genetic / genetics. Translocation, Genetic / radiation effects. Ukraine / epidemiology


8. Vundinti BR, Kerketta L, Madkaikar M, Jijina F, Ghosh K: Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22. Indian J Cancer; 2008 Jan-Mar;45(1):30-2
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  • [Title] Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22.
  • The t(8;21)(q22;q22) is one of the most frequent chromosomal abnormality associated with acute myeloid leukemia (AML) M2 sub type.
  • The additional chromosomal abnormalities including structural and numerical are frequently reported with the translocation, t (8;21)(q22;q22).
  • We report a case of AML-M2 with t(X;8;21)(p22;q22;q22) associated with loss of Y chromosome.
  • Using a dual color fluorescence in situ hybridization (FISH) analysis with ETO and AML1 probes, we demonstrated an ETO/AML1 fusion signal on the derivative chromosome 8 and one ETO signal on derivative Chromosome Xp22.
  • Hence, this three way translocation involving X chromosome might be associated with poor prognosis.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Fatal Outcome. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18453738.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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9. Miao YQ, Chen ZX, He J, Cen JN, Bao XJ, Qiu QC, Zhang DE, Yan M: [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jan;28(1):27-9
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  • [Title] [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype].
  • OBJECTIVE: To investigate the expression of AML1/ETO9a isoform in the acute myeloid leukemia (AML)-M2 patients.
  • METHODS: Expressions of AML1/ETO fusion gene and AML1/ETO9a isoform were detected by using reverse transcriptase-polymerase chain reaction (RT-PCR) in leukemia patients, MDS patients, leukemia cell lines and healthy subjects.
  • RESULT: In 30 newly diagnosed AML-M2 patients 15 were found to express AML1/ETO9a isoform, while the rest including 20 AML-M2CR, 18 other subtypes of AML, 5 chronic myelogenous leukemia (CML), 3 myelodysplastic syndromes (MDS), 3 leukemia cell lines (NB4, KG-1, K562) and 5 healthy subjects were AML1/ETO9a negative.
  • Among the 15 AML/ETO9a isoform expressing cases, 13 were demonstrated t(8;21) translocation and AML1/ETO expression.
  • CONCLUSION: Isoform AML1/ETO9a was correlated to AML/M2, and it may promote the development of leukemia in combination with the AML1/ETO fusion gene.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Gene Expression. Humans. Karyotyping. Male. Middle Aged. Protein Isoforms / genetics. Protein Isoforms / metabolism

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  • (PMID = 17649722.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
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10. Kuchenbauer F, Schnittger S, Look T, Gilliland G, Tenen D, Haferlach T, Hiddemann W, Buske C, Schoch C: Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1-ETO. Br J Haematol; 2006 Sep;134(6):616-9
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  • [Title] Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1-ETO.
  • AML1-ETO collaborates with further genetic abnormalities to induce acute myeloid leukaemia (AML).
  • We analysed 99 patients with an AML1-ETO rearrangement for additional aberrations.
  • Frequent genetic abnormalities were, loss of a sex chromosome (56/99, 56.5%) and del(9)(q22) (24/99, 24.2%).
  • Further molecular abnormalities were FLT3 mutations (3/87, 3.4%), AML1 (1/26, 3.8%) and PU1 (1/14, 7.1%).
  • These clinical findings support the model that AML1-ETO collaborates with other genetic alterations, such as mutations of receptor tyrosine kinases, to induce AML.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid. Male. Middle Aged

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  • (PMID = 16938118.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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11. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • Conventional cytogenetic studies have shown a complex cytogenetic abnormality, notably and surprisingly, a t(8;21)(q22;q22) translocation.
  • Interphase and metaphase fluorescent in situ hybridization have revealed a RUNX1/RUNX1T1 fusion signal on derivative chromosome 8 but not on chromosome 21, confirming the unbalanced translocation between chromosomes 8q22 and 21q22 involving both the RUNX1 and RUNX1T1 genes.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Cytogenetics. Fatal Outcome. Female. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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12. Jiao B, Wu CF, Liang Y, Chen HM, Xiong SM, Chen B, Shi JY, Wang YY, Wang JH, Chen Y, Li JM, Gu LJ, Tang JY, Shen ZX, Gu BW, Zhao WL, Chen Z, Chen SJ: AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2. Leukemia; 2009 Sep;23(9):1598-604
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  • [Title] AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2.
  • AML1-ETO fusion gene is generated from chromosomal translocation t(8;21) mainly in acute myeloid leukemia M2 subtype (AML-M2).
  • Its spliced variant transcript, AML1-ETO9a, rapidly induces leukemia in murine model.
  • To evaluate its clinical significance, AML1-ETO9a expression was assessed in 118 patients with t(8;21) AML-M2, using qualitative and nested quantitative reverse transcriptase (RT)-PCR methods.
  • These cases were accordingly divided into the AML1-ETO9a-H group (n=86, positive for qualitative RT-PCR, with higher level of AML1-ETO9a by quantitative RT-PCR) and the AML1-ETO9a-L group (n=32, negative for qualitative RT-PCR, with lower but still detectable level of AML1-ETO9a by quantitative RT-PCR).
  • C-KIT expression was significantly increased in the AML1-ETO9a-H group, as compared with the AML1-ETO9a-L group.
  • Of the 36 patients harboring C-KIT mutations, 32 patients overexpressed AML1-ETO9a (P=0.0209).
  • Clinically, AML1-ETO9a-H patients exhibited significantly elevated white blood cells count, less bone marrow aberrant myelocytes, increased CD56 but decreased CD19 expression (P=0.0451, P=0.0479, P=0.0149 and P=0.0298, respectively).
  • Moreover, AML1-ETO9a overexpression was related to short event-free and overall survival time (P=0.0072 and P=0.0076, respectively).
  • Taken together, these data suggest that AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged

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  • (PMID = 19458628.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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13. Al Bahar S, Adriana Z, Pandita R: A novel variant translocation t(6;8;21)(p22;q22;q22) leading to AML/ETO fusion in acute myeloid leukemia. Gulf J Oncolog; 2009 Jan;(5):56-9
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  • [Title] A novel variant translocation t(6;8;21)(p22;q22;q22) leading to AML/ETO fusion in acute myeloid leukemia.
  • Acute myeloid leukemia associated with translocation t(8;21) and the underlying AML1-ETO gene fusion is considered as a distinct type of leukemia with characteristic morphologic features.
  • Variant and masked forms of the classic translocation t(8;21) are uncommon and their clinicopathologic features are less well characterized.
  • We report here a patient with a masked translocation involving chromosomes 6,8 and 21.
  • Chromosomal study at diagnosis initially reported the karyotype as translocation between chromosomes 6 and 8 without visible involvement of chromosome 21.
  • However, fluorescence in situ hybridization studies revealed the involvement of chromosome 21 in the translocation and presence of the AML1-ETO chimeric gene.
  • The complex rearrangement t(6;8;21) observed in our patient was not previously described and could be not detected without combination of techniques.
  • Our case illustrates the challenge of recognizing complex aberrations that occur with variant t(8;21) and further reinforces the utility of fluorescence in situ hybridization applications in more accurate characterization of chromosome abnormalities which can lead to more precise therapeutic stratification.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence

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  • (PMID = 20084788.001).
  • [ISSN] 2078-2101
  • [Journal-full-title] The Gulf journal of oncology
  • [ISO-abbreviation] Gulf J Oncolog
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Kuwait
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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14. He G, Wu D, Sun A, Xue Y, Jin Z, Qiu H, Tang X, Miao M, Fu Z, Ma X, Wang X, Chen Z, Ruan C: B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22). Int J Hematol; 2008 Mar;87(2):132-6
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  • [Title] B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22).
  • By analyzing the characteristics of morphology, immune phenotype, chromosome karyotype and clinical manifestations of six cases of B-lymphoid and myeloid lineages biphenotypic acute leukemia (BAL) with t(8;21)(q22;q22), a new subgroup of BAL was reported.
  • Immunophenotype revealed B-lymphoid and myeloid lineages positive, together with frequent and high expression of CD34 and CD33, and weak expression of HLA-DR.
  • In addition to t(8;21) chromosomal translocation, deletion of Y chromosome and complex chromosome abnormalities were also found.
  • Chemotherapy for myeloid and lymphoid leukemia simultaneously produced good response in the patients.
  • BAL with t(8; 21)(q22;.
  • q22) might be a new subgroup of BAL, and it was suggested that the leukemia clone with t(8;21)(q22;q22) might have originated from an early phase of hematopoiesis, and AML1/ETO fusion gene might be related to differentiation of B lymphocyte.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Antigens, CD / metabolism. Antigens, CD79 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 18288568.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD79A protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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15. Yamagata T, Maki K, Mitani K: Runx1/AML1 in normal and abnormal hematopoiesis. Int J Hematol; 2005 Jul;82(1):1-8
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  • [Title] Runx1/AML1 in normal and abnormal hematopoiesis.
  • Runx1/AML1 (also known as CBFA2 and PEBP23B) is a Runt family transcription factor critical for normal hematopoiesis.
  • Runx1 not only is critical for definitive hematopoiesis in the fetus but also is required for normal megakaryocytic maturation and T-lymphocyte and B-lymphocyte development in adult mice.
  • Runx1 has been identified in leukemia-associated chromosomal translocations, including t(8;21) (Runx1-ETO/MTG8), t(16;21) (Runx1-MTG16), t(3;21) (Runx1-Evi1), t(12;21) (TEL-Runx1), and t(X;21) (Runx1-Fog2).
  • However, expression of the fusion protein is not sufficient by itself to cause leukemia and likely requires additional events for leukemogenesis.
  • Point mutations in a Runx1 allele cause haploinsufficiency and a biallelic null for Runx1, which are associated with familial platelet disorder with a propensity for acute myeloid leukemia (FPD/AML) and AML-M0, respectively.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. Hematopoiesis / genetics. Hematopoiesis / physiology. Leukemia / genetics. Leukemia / physiopathology
  • [MeSH-minor] Animals. Fetal Development. Humans. Mice. Point Mutation. Transcription, Genetic / physiology. Translocation, Genetic

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  • (PMID = 16105753.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
  • [Number-of-references] 81
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16. Bae SY, Kim JS, Ryeu BJ, Lee KN, Lee CK, Kim YK, Lim CS, Cho Y, Choi CW, Ryu SW, Yoon SY: Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases. Cancer Genet Cytogenet; 2010 May;199(1):31-7
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  • [Title] Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases.
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for approximately 3% of all t(8;21)(q22;q22) found in patients with acute myeloid leukemia (AML).
  • The clinicopathologic features of AML with the variant t(8;21) have not been well established.
  • We report three cases of AML with variants of t(8;21) characterized, respectively, by derivative 8 with the interstitial inverted insertion of 21q and concurrent monosomy 21, t(8;18;21)(p22;q11.3;q22), and t(2;21;8)(q11.2;q22;q22).
  • Fluorescence in situ hybridization or reverse transcriptase-polymerase chain reaction assay confirmed the presence of RUNX1-RUNX1T1 gene (previously AML1-ETO) rearrangements.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Base Sequence. Chromosome Painting. DNA Mutational Analysis. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Young Adult

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20417866.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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17. Kozlov I, Beason K, Yu C, Hughson M: CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity. Cancer Genet Cytogenet; 2005 Nov;163(1):62-7
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  • [Title] CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity.
  • Acute leukemias that express antigens associated with more than one lineage have been classified as acute lymphocytic leukemia with myeloid markers, acute myeloid leukemia with lymphoid markers, or biphenotypic acute leukemia (BAL).
  • It has only recently begun to be reported in biphenotypic acute leukemias.
  • Cases of acute leukemia submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to leukemia and lymphoma panels.
  • Both cases were differentiated FAB AML-M2 and demonstrated the t(8;21) with cytogenetics and the AML1/ETO rearrangement with fluorescence in situ hybridization (FISH).
  • Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-cell differentiation, represented the aberrant presence of a B-cell antigen in leukemias of distinct myeloid linage.
  • [MeSH-major] Antigens, CD79 / genetics. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / genetics. Antigens, CD / immunology. B-Lymphocytes / immunology. Blast Crisis. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. T-Lymphocytes / immunology

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  • [CommentIn] Cancer Genet Cytogenet. 2007 Apr 1;174(1):76-7 [17350472.001]
  • (PMID = 16271957.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 04079A1RDZ / Cytarabine
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18. Huang L, Abruzzo LV, Valbuena JR, Medeiros LJ, Lin P: Acute myeloid leukemia associated with variant t(8;21) detected by conventional cytogenetic and molecular studies: a report of four cases and review of the literature. Am J Clin Pathol; 2006 Feb;125(2):267-72
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  • [Title] Acute myeloid leukemia associated with variant t(8;21) detected by conventional cytogenetic and molecular studies: a report of four cases and review of the literature.
  • Acute myeloid leukemia (AML) with the t(8;21) (q22;q22) creating the AML1-ETO fusion gene is a distinct type of AML generally associated with a favorable prognosis.
  • The clinicopathologic features of AML carrying variant t(8;21) are less well characterized.
  • We report 4 cases of AML characterized by ins(8;21)(q22;q22q22), t(1;21;8)(q25;q22;q22), t(8;11;21)(q22;q13;q22), and t(4;21;8;12)(q31.3;q22;q22;q15), respectively.
  • Fluorescence in situ hybridization or reverse transcriptase-polymerase chain reaction assay confirmed the presence of AML1-ETO or its transcripts in 3 cases assessed.
  • Each neoplasm had morphologic characteristics of AML associated with the t(8;21).
  • We conclude that cases of AML with variant t(8;21) display morphologic, immunophenotypic, and clinical features similar to classical cases.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Humans. Immunophenotyping. Male. Middle Aged. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16393685.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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19. Gustafson SA, Lin P, Chen SS, Chen L, Abruzzo LV, Luthra R, Medeiros LJ, Wang SA: Therapy-related acute myeloid leukemia with t(8;21) (q22;q22) shares many features with de novo acute myeloid leukemia with t(8;21)(q22;q22) but does not have a favorable outcome. Am J Clin Pathol; 2009 May;131(5):647-55
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  • [Title] Therapy-related acute myeloid leukemia with t(8;21) (q22;q22) shares many features with de novo acute myeloid leukemia with t(8;21)(q22;q22) but does not have a favorable outcome.
  • To determine if therapy-related acute myeloid leukemia (t-AML) with t(8;21)(q22;q22) [t-AML-t(8;21)] harbors similar characteristic clinicopathologic features as de novo AML-t(8;21) (q22;q22), we studied 13 cases of t-AML-t(8;21) and 38 adult cases of de novo AML-t(8;21) diagnosed and treated at our hospital (1995-2008).
  • Of 13 t-AML-t(8;21) cases, 11 had previously received chemotherapy with or without radiation for malignant neoplasms and 2 received radiation alone.
  • Compared with patients with de novo AML-t(8;21), patients with t-AML-t(8;21) were older (P = .001) and had a lower WBC count (P = .039), substantial morphologic dysplasia, and comparable CD19/CD56 expression.
  • The AML1-ETO (RUNX1-RUNX1T1) fusion was demonstrated in all 10 cases assessed.
  • With a median follow-up of 13 months, 10 patients with t-AML-t(8;21) died; the overall survival was significantly inferior to that of patients with de novo AML-t(8;21) (19 months vs not reached; P = .002).
  • These findings suggest that t-AML-t(8;21) shares many features with de novo AML-t(8;21)(q22;q22), but affected patients have a worse outcome.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Age Factors. Aged. Aged, 80 and over. Combined Modality Therapy. Core Binding Factor Alpha 2 Subunit / metabolism. Female. Humans. Male. Middle Aged. Oncogene Proteins, Fusion / metabolism. Prognosis. Survival Rate. Texas / epidemiology. Time Factors

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  • (PMID = 19369623.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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20. Kelly MJ, Meloni-Ehrig AM, Manley PE, Altura RA: Poor outcome in a pediatric patient with acute myeloid leukemia associated with a variant t(8;21) and trisomy 6. Cancer Genet Cytogenet; 2009 Feb;189(1):48-52
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  • [Title] Poor outcome in a pediatric patient with acute myeloid leukemia associated with a variant t(8;21) and trisomy 6.
  • RUNX1T1/RUNX1 (formerly ETO/AML1) is a molecular marker that is usually associated with a favorable outcome in both pediatric and adult patients with acute myeloid leukemia (AML).
  • The patient's karyotype at the time of diagnosis was 46,X,-X,t(4;21;8)(q25;q22;q22),+6.
  • Cytogenetic analysis at second relapse showed evidence of clonal evolution in the form of a highly complex karyotype with numeric and structural abnormalities in addition to the t(4;21;8) and trisomy 6 detected in the diagnostic sample.
  • Trisomy 6 is an uncommon cytogenetic abnormality in myeloid diseases.
  • The presence of this novel variant of t(8;21)(q22;q22) associated with trisomy 6 may have abrogated the usual favorable prognosis associated with RUNX1T1/RUNX1 in AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics. Trisomy / genetics

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  • (PMID = 19167612.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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21. Cheng CK, Li L, Cheng SH, Lau KM, Chan NP, Wong RS, Shing MM, Li CK, Ng MH: Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemia. Blood; 2008 Oct 15;112(8):3391-402
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  • [Title] Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemia.
  • RUNX3/AML2 is a Runt domain transcription factor like RUNX1/AML1 and RUNX2/AML3.
  • In this study on 73 acute myeloid leukemia (AML) patients (44 children and 29 adults), we first showed that high RUNX3 expression among childhood AML was associated with a shortened event-free survival, and RUNX3 was significantly underexpressed in the prognostically favorable subgroup of AML with the t(8;21) and inv(16) translocations.
  • We further demonstrated that this RUNX3 repression was mediated not by P2 methylation, but RUNX1-ETO and CBFbeta-MYH11, the fusion products of t(8;21) and inv(16), via a novel transcriptional mechanism that acts directly or indirectly in collaboration with RUNX1, on 2 conserved RUNX binding sites in the P1 promoter.
  • In in vitro studies, ectopically expressed RUNX1-ETO and CBFbeta-MYH11 also inhibited endogenous RUNX3 expression.
  • Taken together, RUNX3 was the first transcriptional target found to be commonly repressed by the t(8;21) and inv(16) fusion proteins and might have an important role in core-binding factor AML.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 3 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Transcription, Genetic. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged

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  • (PMID = 18663147.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / Runx3 protein, human
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22. He GS, Zhou L, Wu DP, Xue YQ, Zhu MQ, Liu DD, Sun AN, Jin ZM, Qiu HY, Miao M, Tang XW, Fu ZZ, Ma X, Wang XL: [Abnormal expression of cCD79a/cCD22 in acute myeloid leukemia with t (8;21)]. Zhonghua Xue Ye Xue Za Zhi; 2006 Mar;27(3):187-9
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  • [Title] [Abnormal expression of cCD79a/cCD22 in acute myeloid leukemia with t (8;21)].
  • OBJECTIVE: To report abnormal expression of cCD79a/cCD22 in four cases of acute myeloid leukemia (AML) with t (8;21).
  • METHODS: The characteristics of morphology, immunophenotype, chromosome karyotype (MIC) and clinical manifestations of 4 AML patients with t (8;21) expressing cCD79a/cCD22 were analyzed.
  • (5) morphology showed acute myeloid leukemia with high percentage of blast cells;.
  • (6) B-lymphoid and myeloid immunophenotype, and high expression of CD34;.
  • (8) positive for AML1/ETO fusion gene;.
  • (9) response well to chemotherapy regimen which simultaneously treated myeloid and lymphocytic leukemia.
  • CONCLUSION: Abnormal expression of cCD79a/cCD22 in AML with t (8;21) (q22;q22) suggested that this kind of leukemia might be related with abnormal expression gene of B cell.
  • [MeSH-major] Antigens, CD79 / metabolism. Leukemia, Myeloid, Acute / genetics. Sialic Acid Binding Ig-like Lectin 2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Female. Humans. Immunophenotyping. Male. Middle Aged. Translocation, Genetic. Young Adult

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  • (PMID = 16792922.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD79; 0 / Sialic Acid Binding Ig-like Lectin 2
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23. Zhang J, Liu Z, Shao H, Ma Y, Tong H, Wang Y: Laboratory study of a complex translocation t(2;8;21) (p12;q22;q22) in a patient with acute myelogenous leukemia. Leuk Lymphoma; 2008 Oct;49(10):1925-8
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  • [Title] Laboratory study of a complex translocation t(2;8;21) (p12;q22;q22) in a patient with acute myelogenous leukemia.
  • The t(2;8;21) is a complex translocation of t(8;21), and is very rare.
  • To investigate the laboratory characteristics of a complex translocation t(2;8;21)(p12;q22;q22) in a patient with acute myelogenous leukemia (AML-M2), bone marrow smears were prepared for morphological analysis.
  • AML1/ETO chimera transcription was detected by reverse transcriptase polymerase chain reaction (RT-PCR), and laboratory test results were studied with multifactorial analysis method.
  • In this case, the chromosomal analysis (R-banding) demonstrated a complex translocation t(2;8;21)(p12;q22;q22).
  • With combined evidence from morphological and immunophenotypic results, the patient was diagnosed as AML-M2. t(2;8;21)(p12;q22;q22) was considered a rare complex translocation of t(8;21).
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Bone Marrow Examination. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / analysis. Cytogenetic Analysis. Female. Humans. Oncogene Proteins, Fusion / analysis

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  • (PMID = 18949616.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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24. Khandanpour C, Thiede C, Valk PJ, Sharif-Askari E, Nückel H, Lohmann D, Horsthemke B, Siffert W, Neubauer A, Grzeschik KH, Bloomfield CD, Marcucci G, Maharry K, Slovak ML, van der Reijden BA, Jansen JH, Schackert HK, Afshar K, Schnittger S, Peeters JK, Kroschinsky F, Ehninger G, Lowenberg B, Dührsen U, Möröy T: A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia. Blood; 2010 Mar 25;115(12):2462-72
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  • [Title] A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia.
  • The GFI1 gene encodes a transcriptional repressor, which regulates myeloid differentiation.
  • We report here that a variant allele of GFI1 (GFI1(36N)) is associated with acute myeloid leukemia (AML) in white subjects with an odds ratio of 1.6 (P < 8 x 10(-5)).
  • We observed that both GFI1 variants maintain the same activity as transcriptional repressors but differ in their regulation by the AML1/ETO (RUNX1/RUNX1T1) fusion protein produced in AML patients with a t(8;21) translocation.
  • AML1/ETO interacts and colocalizes with the more common GFI1(36S) form in the nucleus and inhibits its repressor activity.
  • As a consequence, AML1/ETO does not colocalize with GFI1(36N) and is unable to inhibit its repressor activity.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. COS Cells. Cell Nucleus / metabolism. Cercopithecus aethiops. Core Binding Factor Alpha 2 Subunit / metabolism. Female. Gene Frequency. Genetic Variation. HeLa Cells. Humans. Linkage Disequilibrium. Male. Mice. Middle Aged. NIH 3T3 Cells. Oncogene Proteins, Fusion / metabolism. Translocation, Genetic. Young Adult

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  • (PMID = 20075157.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA101140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / GFI1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2919174
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25. Serrano E, Carnicer MJ, Lasa A, Orantes V, Pena J, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias. Leuk Res; 2008 Jun;32(6):944-53
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  • [Title] Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by an abnormal proliferation of the myeloid precursors and a maturation block.
  • The most common chromosomal lesions in AML are the t(8;21) and inv(16).
  • To better understand the leukemogenic mechanism of these fusion proteins, we performed gene expression studies in samples from (8;21), AML1 mutated and inv(16) patients, as well as from the Kasumi-1 cell line and a U937 cell line expressing the AML1-ETO fusion gene.
  • We found a tight link between Inv(16) and mutant AML1 samples.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. DNA Methylation. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Biomarkers, Tumor / genetics. Chromatin Assembly and Disassembly. Chromosome Inversion / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. DNA Modification Methylases / antagonists & inhibitors. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Histone Deacetylase Inhibitors. Humans. Hydroxamic Acids / pharmacology. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Oncogene Proteins, Fusion / genetics. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic. Tumor Cells, Cultured. U937 Cells

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  • (PMID = 18206229.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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26. Li CW, Bo LJ, Dai Y, Liu XP, Qin S, Liu SH, Wang JX: [Application of dual-color fluorescence in situ hybridization in acute myeloid leukemia with t (8; 21)]. Zhonghua Xue Ye Xue Za Zhi; 2006 Jan;27(1):32-5
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  • [Title] [Application of dual-color fluorescence in situ hybridization in acute myeloid leukemia with t (8; 21)].
  • OBJECTIVE: To investigate the utilities of dual-color fluorescence in situ hybridization (FISH) in diagnosis and monitor of treatment in acute myeloid leukemia (AML) with t (8; 21).
  • 21) AML were positive for AML1/ETO in FISH assay.
  • Three cases were positive for AML/ETO by FISH although two of them lacked t (8;.
  • 21) by CCA and one negative for AML1/ETO by RT-PCR.
  • Six cases with complex karyotype abnormalities were confirmed to be AML1/ETO positive by the successive R-banding and FISH assay, and the involved genes were clearly visualized in FISH image.
  • 21) AML diagnosed.
  • 21) by CCA were positive by FISH.
  • 21) AML and minimal residual disease (MRD) monitoring.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 16732938.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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27. Najima Y, Ohashi K, Kawamura M, Onozuka Y, Yamaguchi T, Akiyama H, Sakamaki H: Molecular monitoring of BAALC expression in patients with CD34-positive acute leukemia. Int J Hematol; 2010 May;91(4):636-45
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  • [Title] Molecular monitoring of BAALC expression in patients with CD34-positive acute leukemia.
  • Recent studies have shown that high BAALC expression predicts an adverse prognosis and may define an important risk factor in acute myeloid leukemia patients with normal karyotype.
  • We performed, using real-time quantitative reverse transcriptase polymerase chain reaction (RQ-PCR), the molecular analysis of BAALC gene as a possible minimal residual disease (MRD) marker in 45 patients with newly diagnosed acute leukemia.
  • Comparative monitoring of MRD by RQ-PCR for the Wilms' tumor gene 1(WT1) or specific translocation markers demonstrated that BAALC had similar kinetics as WT1, AML1/ETO and minor BCR/ABL, but not PML/RARA.
  • Quantitation of BAALC gene expression made it possible to assess MRD in patients with CD34-positive acute leukemia.
  • [MeSH-major] Biomarkers, Tumor / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Neoplasm Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / metabolism. Disease-Free Survival. Female. Gene Expression Regulation, Leukemic. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm, Residual / genetics. Neoplasm, Residual / mortality. Predictive Value of Tests. Prognosis. RNA, Messenger / genetics. Risk Factors. Translocation, Genetic. Young Adult

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  • (PMID = 20376583.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BAALC protein, human; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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28. Udayakumar AM, Alkindi S, Pathare AV, Raeburn JA: Complex t(8;13;21)(q22;q14;q22)--a novel variant of t(8;21) in a patient with acute myeloid leukemia (AML-M2). Arch Med Res; 2008 Feb;39(2):252-6
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  • [Title] Complex t(8;13;21)(q22;q14;q22)--a novel variant of t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for about 3% of all t(8;21)(q22;q22) in acute myeloid leukemia (AML) patients.
  • We report a case of AML-M2 with t(8;13;21)(q22;q14;q22), not reported earlier.
  • Using a dual-color fluorescence in situ hybridization (FISH) analysis with ETO and AML1 probes, we demonstrate an ETO/AML1 fusion signal on the derivative chromosome 8.
  • Whole chromosome painting probes were used for chromosomes 8 and 13, to demonstrate the three-way translocation t(8;13;21)(q22;q14;q22).
  • Involvement of chromosome region 13q14 has never been reported earlier, although region 13q12 as a variant in AML with t(8;21) has been reported earlier.
  • [MeSH-major] Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Humans. In Situ Hybridization, Fluorescence. Male. Oman. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 18164974.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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29. Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z: Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2). Cancer Genet Cytogenet; 2009 Jan 15;188(2):95-8
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  • [Title] Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Acute myeloid leukemia with maturation (AML-M2 based on the French-American-British classification) is often accompanied by typical chromosomal changes such as t (8;21)(q22;q22).
  • We report a case of a 31-year-old female with a positive RUNX1/CBFA2T1 (alias AML1/ETO) fusion gene and a karyotype with a t(2;21;8)(p12;q22;q22).
  • Although variant translocations involving chromosome region 2p12 have never been reported before, we suppose this translocation may be responsible for the clinical manifestation and prognosis of this case.
  • The role of this complex variant translocation, as well as the possible formation mechanism, prognostic factors, and morphologic changes are discussed.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebral Hemorrhage / complications. Core Binding Factor Alpha 2 Subunit / genetics. Cytarabine / administration & dosage. Fatal Outcome. Female. Humans. Karyotyping. Mitoxantrone / administration & dosage. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • [RetractionIn] Cancer Genet Cytogenet. 2009 Jul;192(1):54 [19489159.001]
  • (PMID = 19100512.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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30. Bug G, Schwarz K, Schoch C, Kampfmann M, Henschler R, Hoelzer D, Ottmann OG, Ruthardt M: Effect of histone deacetylase inhibitor valproic acid on progenitor cells of acute myeloid leukemia. Haematologica; 2007 Apr;92(4):542-5
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  • [Title] Effect of histone deacetylase inhibitor valproic acid on progenitor cells of acute myeloid leukemia.
  • Here, VPA maintains a significantly higher proportion of CD34+ LPC and colony forming units compared to control cultures in six AML samples, but selectively reduces leukemic cell numbers in another AML sample with expression of AML1/ETO.
  • [MeSH-major] Hematopoietic Stem Cells / drug effects. Histone Deacetylase Inhibitors. Leukemia, Myeloid / pathology. Neoplasm Proteins / antagonists & inhibitors. Neoplastic Stem Cells / drug effects. Valproic Acid / adverse effects
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / analysis. Cell Culture Techniques / methods. Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line, Tumor / cytology. Cell Line, Tumor / drug effects. Chromosomes, Human, Pair 21 / ultrastructure. Chromosomes, Human, Pair 8 / ultrastructure. Core Binding Factor Alpha 2 Subunit / analysis. Core Binding Factor Alpha 2 Subunit / physiology. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / physiology. Translocation, Genetic. Tumor Stem Cell Assay

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  • (PMID = 17488665.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antigens, CD34; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Histone Deacetylase Inhibitors; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 614OI1Z5WI / Valproic Acid
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31. Zhu YL, Zhang Y, Zhu P, Yang Y, Du JW, Liu J: [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):236-9
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  • [Title] [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia].
  • OBJECTIVE: To assess the value of common fusion genes analysis in the diagnosis and classification of leukemia by multiplex RT-PCR.
  • METHODS: The multiplex RT-PCR, including 8 parallel PCR reactions, could screen 86 mRNA breakpoints or splice variants at the same time, which was important for the diagnosis and prognosis of leukemia.
  • Bone marrow samples from 161 cases of leukemia and 8 cases of myelodysplastic syndrome (MDS) were involved in the study.
  • The distribution of common fusion genes in leukemia was analyzed by the method mentioned above in combination with clinical and morphological features.
  • RESULTS: Ten fusion genes were detected in 115 cases of leukemia, including AML1/ETO, PML/RAR alpha, PLZF/RAR alpha, dupMLL, MLL/AF6, MLL/AF10, CBFbeta/MYH11, BCR/ABL, Hox11, and EVI1 BCR/ABL was positive in all the 52 cases of chronic myeloid leukemia; PML/RAR alpha was found in 21 of 25 acute promyelocytic leukemia (APL), and PLZF/RAR alpha was detected in one case of APL.
  • Sixteen cases of 17 AML1/ETO-positive acute leukemia (AL) belonged to FAB-M2 subtype, and one case was mixed leukemia.
  • MLL aberrations were found in 16 AL, in which all MLL/AF6 translocation existed in M5 subtype with classic monoblastic characters.
  • Furthermore, BCR/ABL was detected in 5 acute lymphoblastic leukemia (ALL) cases.
  • Fusion genes were also found in 2 MDS cases, of which AML1/ETO positive-MDS-RAEB progressed to AML rapidly.
  • CONCLUSION: Screening of common fusion genes by multiplex RT-PCR is an important tool which could provide useful and reliable molecular genetic information for the diagnosis and treatment of leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15968309.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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32. Ma L, Xue YQ, Pan JL, He J, Wu YF, Cen JN, Wen BZ: [Detection of fusion genes associated with specific translocations in acute leukemia patients with normal karyotypes by using multiplex RT-PCR]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):228-31
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  • [Title] [Detection of fusion genes associated with specific translocations in acute leukemia patients with normal karyotypes by using multiplex RT-PCR].
  • This study was aimed to explore the usefulness of multiplex reverse transcription-polymerase chain reaction (multiplex RT-PCR) in detection of fusion genes associated with specific translocations in acute leukemia (AL) patients with normal karyotypes.
  • The results showed that 4 types of fusion genes such as PML/RARA, AML1/ETO, CBFbeta/MYH11, BCR/ABL were detected in 8 (21.6%) patients by multiplex RT-PCR.
  • In conclusion, multiplex RT-PCR is useful in detection of fusion genes associated with specific translocations in acute leukemia (AL) with normal karyotypes and it would refine the karyotype analysis.
  • When the normal karyotypes were detected in acute leukemia patients by conventional cytogenetic method, the multiplex RT-PCR should be performed for them.

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  • (PMID = 16638186.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
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33. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
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  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • A substantial proportion of cases exhibiting recurrent reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • We discuss the relevance of GEM AML from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models; through to the valuable retroviral-mediated gene transfer models.
  • The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all AML cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis

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  • (PMID = 18264136.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 111
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34. Aoki T, Miyamoto T, Yoshida S, Yamamoto A, Yamauchi T, Yoshimoto G, Mori Y, Kamezaki K, Iwasaki H, Takenaka K, Harada N, Nagafuji K, Teshima T, Akashi K: Additional acquisition of t(1;21)(p32;q22) in a patient relapsing with acute myelogenous leukemia with NUP98-HOXA9. Int J Hematol; 2008 Dec;88(5):571-4
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  • [Title] Additional acquisition of t(1;21)(p32;q22) in a patient relapsing with acute myelogenous leukemia with NUP98-HOXA9.
  • We report a 29-year-old Japanese male with acute myelogenous leukemia (AML)-M4 with a cryptic t(7;11)(p15;p15), in which a chimeric NUP98-HOXA9 fusion was detected by polymerase chain reaction analysis and a chromosomal analysis showed 46,XY.
  • However, 6 months after transplantation, the patient relapsed; NUP98-HOXA9 was detected again and karyotypic analysis revealed 46,XY, t(1;21)(p32;q22).
  • Fluorescent in situ hybridization (FISH) analysis using an AML1-ETO translocation dual probe, showed that the 21q22 breakpoint involved AML1 locus.
  • A retrospective FISH analysis showed that t(1;21) was absent at onset.
  • This is the first reported case with AML who had a cryptic t(7;11)(p15;p15), and additionally acquired t(1;21)(p32;q22) at relapse.
  • [MeSH-major] Chromosomes, Human / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Asian Continental Ancestry Group. Humans. Japan. Male. Recurrence. Stem Cell Transplantation. Time Factors. Transplantation, Autologous

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  • (PMID = 19005624.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / NUP98-HOXA9 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion
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35. Kawakami K, Nishii K, Hyou R, Watanabe Y, Nakao M, Mitani H, Murata T, Monma F, Yamamori S, Hosokai N, Miura I: A case of acute myeloblastic leukemia with a novel variant of t(8;21)(q22;q22). Int J Hematol; 2008 Jan;87(1):78-82
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  • [Title] A case of acute myeloblastic leukemia with a novel variant of t(8;21)(q22;q22).
  • We encountered a case of acute myeloblastic leukemia (AML), with extramedullary leukemia (EML) and a masked type of the variant translocation t(8;21)(q22;q22).
  • The initial karyotypic interpretation was t(8;9)(q22;q34) on G-banding.
  • Multiplex-fluorescence in situ hybridization (multiplex-FISH) analysis revealed a three-way translocation involving chromosomes 8, 9, and 21, and identified a masked type of variant t(8;21)q22;q22) translocation.
  • The karyotype was finally determined as 45,X,-Y,der(8)t(8;21)(q22;q22), der(9)(8;9)(q22;q34), and der(21)t(9;21)(q34;q22).
  • Results of FISH using the AML1/ETO probe and detection of the AML1/ETO fusion transcripts by reverse transcriptase-polymerase chain reaction (RT-PCR) support the karyotype as well as the sequence of the PCR product.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Hematopoiesis, Extramedullary / genetics. Humans. Male. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 18224418.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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36. Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R: Haematological & molecular profile of acute myelogenous leukaemia in India. Indian J Med Res; 2009 Mar;129(3):256-61
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  • [Title] Haematological & molecular profile of acute myelogenous leukaemia in India.
  • BACKGROUND & OBJECTIVE: Recurrent balanced translocations are generally recognized to be a major parameter for prognostication in acute myeloid leukaemia (AML).
  • The chromosomal translocation t(15;17) results in PML/RARalpha fusion gene, t(8;21) results in AML1/ETO fusion gene and Inv 16 generates CBFbeta/MYH11 fusion gene.
  • RT-PCR was performed to identify PML/RARalpha, AML1/ETO, CBFbeta/MYH11 and FLT3 nternal tandem duplication (ITD).
  • AML1-ETO fusion transcript was detected in 16 of 56 patients with no correlation with clinical or haematological parameters.
  • FLT3 internal tandem duplication (ITD) mutation was predominant in acute promyelocytic leukaemia patients with bcr3 isoform.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Genetic Predisposition to Disease / epidemiology. Humans. India / epidemiology. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Prevalence. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19491417.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 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
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37. Zhang Y, Rowley JD: Chromatin structural elements and chromosomal translocations in leukemia. DNA Repair (Amst); 2006 Sep 8;5(9-10):1282-97
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  • [Title] Chromatin structural elements and chromosomal translocations in leukemia.
  • Recurring chromosome abnormalities are strongly associated with certain subtypes of leukemia, lymphoma and sarcomas.
  • Chromosome translocations are frequently observed in both de novo and therapy-related acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS).
  • The mechanisms that result in such chromosome translocations in leukemia and other cancers are largely unknown.
  • Genomic breakpoints in all the common chromosome translocations in leukemia, including t(4;11), t(9;11), t(8;21), inv(16), t(15;17), t(12;21), t(1;19) and t(9;22), have been cloned.
  • Genomic breakpoints tend to cluster in certain intronic regions of the relevant genes including MLL, AF4, AF9, AML1, ETO, CBFB, MYHI1, PML, RARA, TEL, E2A, PBX1, BCR and ABL.
  • However, whereas the genomic breakpoints in MLL tend to cluster in the 5' portion of the 8.3 kb breakpoint cluster region (BCR) in de novo and adult patients and in the 3' portion in infant leukemia patients and t-AML patients, those in both the AML1 and ETO genes occur in the same clustered regions in both de novo and t-AML patients.
  • Strong in vivo topo II cleavage sites and DNase I hypersensitive sites often co-localize with each other and also with many of the BCRs in most of these genes, whereas SARs are associated with BCRs in MLL, AF4, AF9, AML1, ETO and ABL, but not in the BCR gene.
  • In addition, the BCRs in MLL, AML1 and ETO have the lowest free energy level for unwinding double strand DNA.
  • Virtually all chromosome translocations in leukemia that have been analyzed to date show no consistent homologous sequences at the breakpoints, whereas a strong non-homologous end joining (NHEJ) repair signature exists at all of these chromosome translocation breakpoint junctions; this includes small deletions and duplications in each breakpoint, and micro-homologies and non-template insertions at genomic junctions of each chromosome translocation.
  • Surprisingly, the size of these deletions and duplications in the same translocation is much larger in de novo leukemia than in therapy-related leukemia.
  • We propose a non-homologous chromosome recombination model as one of the mechanisms that results in chromosome translocations in leukemia.
  • [MeSH-major] Chromatin / genetics. DNA Topoisomerases, Type II / genetics. Leukemia / genetics. Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 16893685.001).
  • [ISSN] 1568-7864
  • [Journal-full-title] DNA repair
  • [ISO-abbreviation] DNA Repair (Amst.)
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84405
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromatin; EC 3.1.21.1 / Deoxyribonuclease I; EC 5.99.1.3 / DNA Topoisomerases, Type II
  • [Number-of-references] 122
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38. Pan JL, Xue YQ, Qiu HY, Zhang J, Wu YF, Wang Y, Shen J, Zhu YJ: [Clinical and experimental retrospective analysis on acute leukemia with trisomy 4 cell]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Aug;24(4):369-72
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  • [Title] [Clinical and experimental retrospective analysis on acute leukemia with trisomy 4 cell].
  • OBJECTIVE: To explore the clinical and experimental features of acute leukemia (AL) with trisomy 4.
  • METHODS: A retrospective analysis on the clinical and laboratory data of 21 cases of AL with trisomy 4 was performed.
  • 21) revealed by karyotypic analysis were detected by dual-color FISH using t (8;.
  • 21) translocation probe to confirm the AML1/ETO rearrangement.
  • M2 was the most frequent Franch-American-British(FAB) subtype in this series (9/21 cases).
  • Among 15 cases received immunophenotypic analysis, 11 cases showed CD34 positivity and 6 cases co-expressed myeloid and lymphocyte antigens.
  • 21) was found in 8 cases.
  • 21) had AML1/ETO rearrangement.
  • [MeSH-major] Chromosomes, Human, Pair 4 / genetics. Leukemia / genetics. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping / methods. Male. Middle Aged. Young Adult

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  • (PMID = 17680522.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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39. Ruiz-Argüelles GJ, Morales-Toquero A, Manzano C, Ruiz-Delgado GJ, Jaramillo P, Gonzalez-Carrillo ML, Reyes-Núñez V: t(8;21) (q22;q22) acute myelogenous leukemia in Mexico: a single institution experience. Hematology; 2006 Aug;11(4):235-8
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  • [Title] t(8;21) (q22;q22) acute myelogenous leukemia in Mexico: a single institution experience.
  • We analyze the prevalence and clinical features of a group of patients with t(8;21) (q22;q22) acute myeloblastic leukemia, identified in a single institution in México over a 10-year period.
  • According to the French-American-British (FAB) morphological classification of leukemia, the morphology was M2 in four cases, M4 in three cases, M3 in one case and M0 in one.
  • In addition to the myeloid markers, lymphoid markers were identified in 6 patients.
  • In this single-center experience in México, we found that the t(8;21) (q22;q22) variant of leukemia was more frequent than in Caucasian populations, that the co-expression of lymphoid markers in the blast cells is very frequent and that this malignancy is associated with a relatively good prognosis.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Peripheral Blood Stem Cell Transplantation / statistics & numerical data. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Cytarabine / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Mexico / epidemiology. Middle Aged. Prevalence. Prospective Studies. Remission Induction. Salvage Therapy. Transplantation, Autologous / statistics & numerical data. Transplantation, Homologous / statistics & numerical data. Treatment Outcome

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  • (PMID = 17178661.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 04079A1RDZ / Cytarabine; 80168379AG / Doxorubicin
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40. Sekiguchi N, Watanabe T, Kobayashi Y, Inokuchi C, Kim SW, Yokota Y, Tanimoto K, Matsuno Y, Tobinai K: The application of molecular analyses for primary granulocytic sarcoma with a specific chromosomal translocation. Int J Hematol; 2005 Oct;82(3):210-4
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  • [Title] The application of molecular analyses for primary granulocytic sarcoma with a specific chromosomal translocation.
  • Primary GS is well known to frequently develop into acute myeloid leukemia (AML).
  • Fluorescence in situ hybridization analysis detected the AML1/MTG8 fusion gene in neoplastic cells obtained from her cerebrospinal fluid specimen and the epidural mass.
  • The AML1/MTG8 fusion gene transcript was also detected by a nested reverse transcriptase-polymerase chain reaction analysis of mononuclear cells from the bone marrow, although leukemic cells were not recognized in a microscopical examination of the patient's bone marrow.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Sarcoma, Myeloid / genetics. Spinal Neoplasms / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / administration & dosage. Combined Modality Therapy. Cytarabine / administration & dosage. DNA Mutational Analysis. Female. Hemibody Irradiation. Humans

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  • (PMID = 16207593.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 04079A1RDZ / Cytarabine
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41. Park TS, Song J, Lee KA, Min YH, Lee SG, Park Y, Kim J, Lee EY, Choi JR: Paracentric inversion-associated t(8;21) variant in de novo acute myelogenous leukemia: characteristic patterns of conventional cytogenetics, FISH, and multicolor banding analysis. Cancer Genet Cytogenet; 2008 May;183(1):72-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paracentric inversion-associated t(8;21) variant in de novo acute myelogenous leukemia: characteristic patterns of conventional cytogenetics, FISH, and multicolor banding analysis.
  • Acute myelogenous leukemia (AML) with t(8;21)(q22;q22) demonstrates unique clinico-pathologic disease entity in patients with hematologic malignancies.
  • The t(8;21), which results in fusion of the AML1 gene on 21q22 and the ETO gene on 8q22 on a molecular level, is one of the most common nonrandom chromosomal changes, and it is found in about 5-12% of patients with AML.
  • Among these cases, complex variants involving chromosomes 8 and 21, as well as a third or fourth chromosome, account for approximately 6-10% of patients with an AML1/ETO chimeric gene, and about 100 variant cases with AML1/ETO fusion transcript have been reported in the literature.
  • Here, we describe a rare case report of reciprocal paracentric inversion-associated t(8;21) variant in a 28-year old male patient with de novo AML.
  • This report emphasizes the value of "conventional" cytogenetics, as well as "newly developed" molecular cytogenetic methods in the diagnosis of rare complex t(8;21) variant in patients with AML.
  • [MeSH-major] Centromere / genetics. Chromosome Inversion. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Chromosome Banding / methods. Humans. In Situ Hybridization, Fluorescence / methods. Male. Middle Aged

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  • [Copyright] Copyright 2008 Elsevier Inc.
  • (PMID = 18474302.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
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42. Zhang L, Tümer Z, Møllgård K, Barbi G, Rossier E, Bendsen E, Møller RS, Ullmann R, He J, Papadopoulos N, Tommerup N, Larsen LA: Characterization of a t(5;8)(q31;q21) translocation in a patient with mental retardation and congenital heart disease: implications for involvement of RUNX1T1 in human brain and heart development. Eur J Hum Genet; 2009 Aug;17(8):1010-8
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  • [Title] Characterization of a t(5;8)(q31;q21) translocation in a patient with mental retardation and congenital heart disease: implications for involvement of RUNX1T1 in human brain and heart development.
  • The chromosome break points of the t(8;21)(q21.3;q22.12) translocation associated with acute myeloid leukemia disrupt the RUNX1 gene (also known as AML1) and the RUNX1T1 gene (also known as CBFA2T3, MTG8 and ETO) and generate a RUNX1-RUNX1T1 fusion protein.
  • Molecular characterization of the translocation break points in a t(5;8)(q32;q21.3) patient with mild-to-moderate mental retardation and congenital heart disease revealed that one of the break points was within the RUNX1T1 gene.
  • [MeSH-major] Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 8. Heart Defects, Congenital / genetics. Intellectual Disability / genetics. Proto-Oncogene Proteins / physiology. Transcription Factors / physiology. Translocation, Genetic
  • [MeSH-minor] Adult. Animals. Brain / embryology. Brain / metabolism. Heart / embryology. Humans. Male. Mice. Myocardium / metabolism


43. Tajeddine N, Millard I, Gailly P, Gala JL: Real-time RT-PCR quantification of PRAME gene expression for monitoring minimal residual disease in acute myeloblastic leukaemia. Clin Chem Lab Med; 2006;44(5):548-55
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  • [Title] Real-time RT-PCR quantification of PRAME gene expression for monitoring minimal residual disease in acute myeloblastic leukaemia.
  • RESULTS: In paediatric acute myeloid leukaemia (AML) (n=22) and acute lymphoblastic leukaemia (ALL) (n=17), and in adult AML (n=20), abnormal PRAME expression was found in 41%, 35% and 40% of cases, respectively.
  • To assess the sensitivity of PRAME for monitoring MRD, PRAME-positive t(8;21) AML samples with detectable AML1/ETO expression by conventional RT-PCR (n=17) were assessed for quantitative expression of AML1/ETO and PRAME.

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  • (PMID = 16681423.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / PRAME protein, human
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44. Leroy H, de Botton S, Grardel-Duflos N, Darre S, Leleu X, Roumier C, Morschhauser F, Lai JL, Bauters F, Fenaux P, Preudhomme C: Prognostic value of real-time quantitative PCR (RQ-PCR) in AML with t(8;21). Leukemia; 2005 Mar;19(3):367-72
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  • [Title] Prognostic value of real-time quantitative PCR (RQ-PCR) in AML with t(8;21).
  • Despite the favorable prognosis of patients with acute myeloid leukemia (AML) with t(8;21)(q22;q22) translocation, relapses still occur in about 30% of the cases but no initial factors can strongly predict the risk of relapse.
  • We prospectively monitored AML1-ETO rearrangement by real-time quantitative PCR (RQ-PCR) in 21 patients uniformly treated in our center.
  • At diagnosis, levels of AML1-ETO transcript showed large variations and there was a trend for a higher relapse rate in patients with high pretreatment expression levels (P=0.065).
  • Comparison of BM and PB samples showed similar sensitivity for detecting AML1-ETO transcript.
  • In conclusion, RQ-PCR appears to be an early predictive factor of the relapse risk in AML with t(8;21).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / therapeutic use. Disease-Free Survival. Female. Gene Rearrangement. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Regression Analysis. Sensitivity and Specificity. Survival Rate. Translocation, Genetic / genetics

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  • (PMID = 15674426.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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45. Kokate P, Ahmad F, Dalvi R, Das BR, Mandava S: Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype. Cancer Genet Cytogenet; 2008 Jul;184(1):52-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype.
  • Acute myeloid leukemia (AML) is a clinically and molecularly heterogeneous disease characterized by the aberrant proliferation of myeloid stem cells, reduced apoptosis and blockage in cellular differentiation.
  • Cytogenetic as well as FISH analysis revealed a complex translocation involving four chromosomes, with the karyotype 45,-Y,der(X)t(X;8)(p21;q22),der(8)t(8;21)(q22;q22),ins(15;21)(q15;q22.2q22.3),der(21)t(8;21)(q22;q22).
  • The breakpoints at 8q22 and 21q22 suggested a rearrangement of the RUNX1T1 (alias ETO) and RUNX1 (previously AML1) genes, respectively.
  • Using a dual-color FISH test with RUNX1T1 and RUNX1 probes, we demonstrated an RUNX1/RUNX1T1 fusion signal on the derivative chromosome 8, establishing this translocation as a novel complex variant of t(8;21)(q22;q22).
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male

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  • (PMID = 18558290.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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46. Chen SJ, Chen LJ, Zhou GB: [Basic and clinical studies of the gene product-targeting therapy based on leukemogenesis--editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Feb;13(1):1-8
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  • In the last twenty years, using all-trans retinoic acid (ATRA) as a differentiation inducer, Shanghai Institute of Hematology has achieved an important breakthrough in the treatment of acute promyelocytic leukemia (APL), which realized the theory of reversing phenotype of cells and provided a successful model of differentiation therapy in cancers.
  • Our group first discovered in the world the variant chromosome translocation t(11;17)(q23;q21) of APL, and cloned the PML-RAR alpha, PLZF-RAR alpha and NPM-RAR alpha fusion genes corresponding to the characterized chromosome translocations t(15;17); t(11;17) and t(5;17) in APL.
  • The ability of ATRA to modify the recruitment of nuclear receptor co-repressor with PML-RAR alpha but not PLZF-RAR alpha caused by the variant chromosome translocation elucidated the therapeutic mechanism of ATRA from the molecular level and provides new insight into transcription-modulating therapy.
  • This is the best clinical effect achieved in treating adult acute leukemia to this day, possibly making APL the first adult curable leukemia.
  • Combination of Gleevec and arsenic agents in treating chronic myeloid leukemia has already make a figure both in clinical and laboratory research, aiming at counteracting the abnormal tyrosine kinase activity of ABL and the degradating BCR-ABL fusion protein.
  • In acute myeloid leukemia M(2b), using new target therapy degradating AML1-ETO fusion protein and reducing the abnormal tyrosine kinase activity of c-kit will also lead to new therapeutic management in acute leukemias.

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  • (PMID = 15748426.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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47. Tamaki H, Yoshihara S, Fujioka T, Kawakami M, Oka Y, Ogawa H: Molecular detection of AML1-MTG8-positive cells in peripheral blood from a patient with isolated extramedullary relapse of t(8;21) acute myeloid leukemia. Leukemia; 2009 Feb;23(2):424-6
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  • [Title] Molecular detection of AML1-MTG8-positive cells in peripheral blood from a patient with isolated extramedullary relapse of t(8;21) acute myeloid leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / analysis. Leukemia, Myeloid, Acute / diagnosis. Oncogene Proteins, Fusion / analysis. Polymerase Chain Reaction / methods
  • [MeSH-minor] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Female. Humans. Molecular Diagnostic Techniques. Recurrence. Translocation, Genetic. Young Adult

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  • (PMID = 18719617.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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48. Wong KF, Siu LL, Wong WS: Aleukaemic acute myeloid leukaemia with t(8;21)(q22;q22). Br J Haematol; 2009 Aug;146(4):345
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aleukaemic acute myeloid leukaemia with t(8;21)(q22;q22).
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Core Binding Factor Alpha 2 Subunit / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Sarcoma, Myeloid / complications

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  • (PMID = 19222479.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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