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6. Zhang L, Wang LS, Xu Y, Xia L, Chen WL, Zheng Y, Chen GQ: Comparative proteomic analysis of human leukemic cells with and without inducible expression of leukemogenic AML1-ETO protein. Chin J Physiol; 2006 Aug 31;49(4):182-91
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  • [Title] Comparative proteomic analysis of human leukemic cells with and without inducible expression of leukemogenic AML1-ETO protein.
  • AML1-ETO is a leukemogenic fusion protein generated by chromosomal translocation t(8;.
  • 21) (q22; q22), one of the most frequent chromosomal abnormalities in acute myeloid leukemia.
  • In this work, we try to explore potential AML1-ETO-targeted proteins through comparing two-dimensional electrophoresis (2DE)-based global protein expression profiles of leukemic U937 cells with and without inducible expression of AML1-ETO.
  • As a result, we identified 14 unique proteins deregulated in AML1-ETO-carrying leukemic cells, including 3 up-regulated such as hairy and enhancer of split 5 (HES5) and 11 down-regulated such as MAT1 (menage a trois-1) and mitogen-activated protein kinase organizer 1 (MORG1).
  • The further investigation on their roles in leukemic cells will uncover new clues to understanding leukemogenic effects of AML1-ETO fusion protein.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia / metabolism. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Proteome / metabolism

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  • (PMID = 17058450.001).
  • [ISSN] 0304-4920
  • [Journal-full-title] The Chinese journal of physiology
  • [ISO-abbreviation] Chin J Physiol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proteome
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7. Zhang LJ, Lu XL, He J, Li Y: [Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia]. Zhonghua Yi Xue Za Zhi; 2006 Aug 29;86(32):2256-60
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  • [Title] [Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia].
  • OBJECTIVE: To study the frequency of mixed lineage leukemia (MLL) gene rearrangements in patients with acute myeloid leukemia (AML) and to determine the significance thereof.
  • METHODS: Conventional cytogenetics (CC) and karyotype analysis were conducted on the bone marrow cells from 58 patients with acute myelocytic leukemia (AML), 47 adults (aged 15 approximately 67) and 11 children (aged 1 approximately 14).
  • Fluorescence in situ hybridization (FISH) using the whole chromosome painting (WCP) probes of the chromosomes 1, 5, 11, 16, 17, and 21 was performed.
  • 17) (q23; q23), -17, -18, +20, +21?
  • ish +21 (wcp21+), der (1) t (1;.
  • ishadd (16) (wcp16+), rea (11) (wcp11+); 55, XY, + markers, ish 11q23 (MLL x 3), +21 (wcp21+); and 46, XY, add (11) (q23) [6]/46, idem, t (15;. 17) (q22;.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 17064570.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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8. Valbuena JR, Medeiros LJ, Rassidakis GZ, Hao S, Wu CD, Chen L, Lin P: Expression of B cell-specific activator protein/PAX5 in acute myeloid leukemia with t(8;21)(q22;q22). Am J Clin Pathol; 2006 Aug;126(2):235-40
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  • [Title] Expression of B cell-specific activator protein/PAX5 in acute myeloid leukemia with t(8;21)(q22;q22).
  • The blasts of acute myeloid leukemia (AML) with t(8;21)(q22;q22) frequently express the B-cell antigen CD19, which is regulated by B cell-specific activator protein (BSAP) encoded by the PAX5 gene, a protein important for B-cell lineage commitment and development.
  • We assessed for BSAP expression in 28 AML cases with t(8;21) and 46 AML cases of other types.
  • CD19 was expressed by 26 (93%) cases of AML with t(8;21) and 1 AML case (2%) without t(8;21).
  • Immunostaining performed on bone marrow biopsy specimens demonstrated BSAP expression in all 28 AML cases with t(8;21): weak, 21; strong, 7.
  • By contrast, BSAP was expressed weakly in only 1 AML case without t(8;21).
  • Oct2 was expressed strongly in 12 of 16 AML cases with t(8;21) and 19 of 46 without t(8;21).
  • These results indicate that silencing of PAX5 is not required for commitment to myeloid differentiation and that BSAP expression in AML is found mainly in cases with t(8;21).
  • [MeSH-major] B-Cell-Specific Activator Protein / metabolism. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / metabolism. Chromosome Banding. Flow Cytometry. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques

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  • (PMID = 16891199.001).
  • [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 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
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9. Pullarkat V, Bedell V, Kim Y, Bhatia R, Nakamura R, Forman S, Sun J, Senitzer D, Slovak ML: Neoplastic mast cells in systemic mastocytosis associated with t(8;21) acute myeloid leukemia are derived from the leukemic clone. Leuk Res; 2007 Feb;31(2):261-5
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  • [Title] Neoplastic mast cells in systemic mastocytosis associated with t(8;21) acute myeloid leukemia are derived from the leukemic clone.
  • In systemic mastocytosis with associated clonal, hematological non-mast cell lineage disease (SM-AHNMD), mast cell infiltration of the bone marrow coexists with a hematologic neoplasm, usually of myeloid origin.
  • When SM is associated with AML, the leukemic cells commonly carry the t(8;21)(q22;q22) core binding factor translocation.
  • By target FISH analysis, we demonstrate t(8;21) in the bone marrow mast cells of a patient with systemic mastocytosis associated with t(8;21) AML, thus, proving the origin of these neoplastic mast cells from the leukemic clone.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Mast Cells / pathology. Mastocytosis, Systemic / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Acute Disease. Chromosomes, Human, Pair 21 / genetics. Cytogenetic Analysis / methods. Exons. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence / methods. Middle Aged. Point Mutation. Polymerase Chain Reaction / methods. Proto-Oncogene Proteins c-kit / genetics

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  • (PMID = 16876862.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P 30 CA33572-20; United States / NCI NIH HHS / CA / P01 CA030206-24
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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10. El-Sissy AH, El-Mashari MA, Bassuni WY, El-Swaayed AF: Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia. J Egypt Natl Canc Inst; 2006 Sep;18(3):244-9
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  • [Title] Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia.
  • BACKGROUND: Immunophenotyping improves both accuracy and reproducibility of acute leukemia classification and is considered particularly useful for identifying aberrant lineage association of acute leukemia, biphenotypic and bilineal acute leukemia, as well as monitoring minimal residual disease.
  • THE AIM OF OUR STUDY: Is to determine aberrant lymphoid antigen expression in Saudi acute myeloid leukemia (AML), correlate them with FAB subtypes, evaluate early surface markers CD7 and CD56, and to investigate the role of cytoplasmic CD79a (a B cell marker that is assigned a high score of 2.0 in the WHO classification).
  • CD9 was expressed in 3/6 (50%) of M3 cases, CD7 was expressed in 11.8% and was mostly confined to FAB M1 and M2 and associated with immature antigens CD34, HLA-DR and TdT.
  • CD56 was expressed in 2/7 (28.6%) M2 cases, and was associated with t (8;21) (q22;q22) together with CD19.
  • CD79a was expressed in one case together with CD19, diagnosed as acute biphenotypic leukemia, and was associated with t(8;21) (q22;q22).
  • [MeSH-major] Antigens, CD56 / analysis. Antigens, CD7 / analysis. Antigens, CD79 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / diagnosis


26. Zhu Q, Hu JP, Jia PM, Wang ZY, Tong JH: [cAMP analogue 8-CPT-cAMP inducing differentiation in the M2b subtype of acute myeloid leukemia cell line Kasumi-1]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Feb;16(1):44-7
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  • [Title] [cAMP analogue 8-CPT-cAMP inducing differentiation in the M2b subtype of acute myeloid leukemia cell line Kasumi-1].
  • This study was aimed to investigate the possible effects of cyclic adenosine monophosphate (cAMP) analogue 8-(4-chlorophenylthio) adenosine 3', 5'-cyclic monophosphate (8-CPT-cAMP) on the M(2b) subtype of acute myeloid leukemia (AML-M(2b)) cells.
  • 21) (q22; q22), through which AML1 (acute myeloid leukemia 1) gene on chromosome 21 is fused with ETO (eight twenty-one) gene on chromosome 8, coding correspondent AML1-ETO fusion protein, which plays a crucial role in the leukemogenesis of AML-M(2b).
  • Meanwhile, semi-quantity RT-PCR and Western blot assay were used to detect the degradation of AML1-ETO fusion protein in Kasumi-1 cells before and after the treatment.
  • Furthermore, 8-CPT-cAMP exerted little influence on the expression of AML1-ETO fusion gene and its product in Kasumi-1 cells.
  • This results may provide experimental and theoretical basis for the breakthrough of differentiation-induced therapy extended to another leukemia.

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  • (PMID = 18315898.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Thionucleotides; 41941-66-6 / 8-((4-chlorophenyl)thio)cyclic-3',5'-AMP; E0399OZS9N / Cyclic AMP
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27. Moore SD, Offor O, Ferry JA, Amrein PC, Morton CC, Dal Cin P: ELF4 is fused to ERG in a case of acute myeloid leukemia with a t(X;21)(q25-26;q22). Leuk Res; 2006 Aug;30(8):1037-42
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  • [Title] ELF4 is fused to ERG in a case of acute myeloid leukemia with a t(X;21)(q25-26;q22).
  • We report a novel chromosomal translocation in AML, t(X;21)(q25-26;q22), resulting in a fusion transcript between two ETS domain family members, ELF4 (at Xq25) and ERG (at 21q22).
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, X / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion. Trans-Activators / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Chromosome Mapping / methods. Fatal Outcome. Female. Humans. In Situ Hybridization, Fluorescence / methods. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Translocation, Genetic

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  • (PMID = 16303180.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006516
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ELF4 protein, human; 0 / ERG protein, human; 0 / Oncogene Proteins, Fusion; 0 / Trans-Activators; 0 / Transcription Factors
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28. Kim J, Park TS, Song J, Lee KA, Hong DJ, Min YH, Cheong JW, Choi JR: Detection of FUS-ERG chimeric transcript in two cases of acute myeloid leukemia with t(16;21)(p11.2;q22) with unusual characteristics. Cancer Genet Cytogenet; 2009 Oct 15;194(2):111-8
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  • [Title] Detection of FUS-ERG chimeric transcript in two cases of acute myeloid leukemia with t(16;21)(p11.2;q22) with unusual characteristics.
  • Reciprocal t(16;21)(p11;q22) is a rare chromosomal abnormality in acute myeloid leukemia (AML).
  • Here we report two cases of AML with t(16;21)(p11.2;q22) showing unusual characteristics, and address the clinical, hematological, and molecular aspects of leukemia with t(16;21), along with a review of the literature.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic

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  • (PMID = 19781443.001).
  • [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 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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29. Kalogianni DP, Bravou V, Christopoulos TK, Ioannou PC, Zoumbos NC: Dry-reagent disposable dipstick test for visual screening of seven leukemia-related chromosomal translocations. Nucleic Acids Res; 2007;35(4):e23
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  • [Title] Dry-reagent disposable dipstick test for visual screening of seven leukemia-related chromosomal translocations.
  • We report the first dry-reagent, disposable, dipstick test for molecular screening of seven chromosomal translocations associated with acute and chronic leukemia.
  • Biotinylated amplified DNA is hybridized with a dA-tailed probe and applied to the strip, which contains oligo(dT)-conjugated gold nanoparticles in dry form.
  • We studied the: t(9;22)(q34;q11), t(15;17)(q22;q21), t(11;17)(q23;q21), t(5;17)(q32;q21), t(11;17)(q13;q21), t(8,21)(q22;q22) and inv(16)(p13;q22) that generate the BCR-ABL, PML-RARa, PLZF-RARa, NPM-RARa, NuMA-RARa, AML1-ETO and CBFbeta-MYH11 fusion genes, respectively.
  • [MeSH-major] Leukemia / diagnosis. Nucleic Acid Hybridization / methods. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Humans. Indicators and Reagents. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myeloid / diagnosis. Leukemia, Promyelocytic, Acute / diagnosis. Polymerase Chain Reaction. Reproducibility of Results

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  • (PMID = 17251199.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; 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 / Indicators and Reagents; 0 / Oncogene Proteins, Fusion; 0 / abl-bcr fusion protein, human; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC1851627
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30. Mrózek K, Marcucci G, Paschka P, Bloomfield CD: Advances in molecular genetics and treatment of core-binding factor acute myeloid leukemia. Curr Opin Oncol; 2008 Nov;20(6):711-8
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  • [Title] Advances in molecular genetics and treatment of core-binding factor acute myeloid leukemia.
  • PURPOSE OF REVIEW: Core-binding factor (CBF) acute myeloid leukemia (AML) is among the most common cytogenetic subtypes of AML, being detected in approximately 13% of adults with primary disease.
  • Although CBF-AML is associated with a relatively favorable prognosis, only one-half of the patients are cured.
  • Herein we review recent discoveries of genetic and epigenetic alterations in CBF-AML that may represent novel prognostic markers and therapeutic targets and lead to improvement of the still disappointing clinical outcome of these patients.
  • RECENT FINDINGS: Several acquired gene mutations and gene-expression and microRNA-expression changes that occur in addition to t(8;21)(q22;q22) and inv(16)(p13q22)/t(16;16)(p13;q22), the cytogenetic hallmarks of CBF-AML, have been recently reported.
  • Alterations that may represent cooperative events in CBF-AML leukemogenesis include mutations in the KIT, FLT3, JAK2 and RAS genes, haploinsufficiency of the putative tumor suppressor genes TLE1 and TLE4 in t(8;21)-positive patients with del(9q), MN1 overexpression in inv(16) patients, and epigenetic and posttranscriptional silencing of CEBPA.
  • Genome-wide gene-expression and microRNA-expression profiling identifying subgroups of CBF-AML patients with distinct molecular signatures, different clinical outcomes, or both, have also been reported.
  • SUMMARY: Progress has been made in delineating the genetic basis of CBF-AML that will likely result in improved prognostication and development of novel, risk-adapted therapeutic approaches.


76. Fan L, Wu YJ, Zhang JF, Qiu HR, Qiao C, Wang R, Yang H, Xu W, Li JY: [Immunophenotypic analysis of acute myeloid leukemia with t(8;21)]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1410-3
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  • [Title] [Immunophenotypic analysis of acute myeloid leukemia with t(8;21)].
  • This study was aimed to investigate laboratorial characteristics of immunophenotyping and concurrent karyotypic aberrations in acute myeloid leukemia with t(8;21)(q22;q22).
  • A total number of 47 AML patients with t(8;21) were enrolled in this study and immunophenotypic antigens were detected by multiparameter flow cytometry.
  • The results indicated that the additional karyotypic aberrations were found in 21 out of 47 AML patients with t(8;21) (q22;q22 (44.68%), single karyotypic aberration was observed in 26 out of 47 AML patients with t(8;21) (q22;q22) (55.32%).
  • Myeloid markers of CD13 and CD33 were 93.6% and 87.2%, and there were nearly no expression of T lineage antigens (CD2, CD3, CD5 and CD7) detected in t(8;21)-AML.
  • CD19, one of a pan-B markers was found in 66.0% of all 47 t(8;21)-AML patients as well as CD56(66.7%), which was significant higher than other B lineage antigens (CD20 and CD22).
  • It is concluded that AML with t(8;21) displays an exclusive immunophenotyping with significantly high expression of CD19 and CD56 as well as precursor cell markers (CD34, CD117 and HLA-DR) and combination detection of CD34/CD19/CD56 may become a predictive indicator of t(8;21) (q22;q22) cytogenetic abnormality.

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  • (PMID = 21176340.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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77. 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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78. Chang WR, Park IJ, Lee HW, Park JS, Kim HC, Kim HJ, Han JH, Cho SR: [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts]. Korean J Lab Med; 2009 Oct;29(5):390-5
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  • [Title] [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts].
  • Many AML-associated chromosomal abnormalities, such as t(8;21), t(15;17), inv(16), t(9;11), t(9;22) and t(6;9) are well known.
  • The chromosomal aberration of t(16;21)(p11;q22) in AML is rare and it is known to be associated with poor prognosis, young age (median age, 22 yr), and involvement of various subtypes of the French-American-British classification.
  • We report here 2 AML patients with t(16;21)(p11;q22), proved by conventional cytogenetics and/or reverse transcription (RT)-PCR.
  • One patient was a 24 yr-old male with acute myelomonocytic leukemia.
  • His karyotype was 46,XY,t(16;21)(p11;q22),del(18)(p11.2) and RT-PCR revealed the TLS/FUS-ERG fusion transcripts.
  • The other patient was a 72 yr-old male with acute myeloid leukemia without maturation.
  • His karyotype was 45,XY,-16,add(21)(q22) and the presence of t(16;21)(p11;q22) was detected by RT-PCR.
  • We suggest that the presence of t(16;21)(p11;q22) and/or TLS/FUS-ERG fusion transcripts has to be considered in cases of AML with erythrophagocytosis.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic

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  • (PMID = 19893346.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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79. Bacher U, Schnittger S, Kern W, Trenn G, Weisser M, Haferlach T, Schoch C: Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22). Cancer Genet Cytogenet; 2006 Jul 15;168(2):172-4
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  • [Title] Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22).
  • We here report on an 48-year-old male patient with a primary diagnosis of acute myeloid leukemia (AML)-M2 with t(8;21)(q22;q22), who developed complete hematologic and molecular remission after induction chemotherapy.
  • Thirteen months later, he relapsed and showed an AML-M2 with t(3;21)(q26;q22).
  • Retrospectively, polymerase chain reaction (PCR) for AML1-EVI1 and EVI1 overexpression was performed on bone marrow and peripheral blood samples taken at diagnosis and during the first year after the first manifestation of AML to quantify the AML1-EVI1-positive clone.
  • In a bone marrow sample taken 25 days from diagnosis, PCR for AML1-EVI1 was negative, and EVI1 expression, as assessed by quantitative real-time PCR, was within the same range as that of healthy controls.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Humans. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Proto-Oncogenes / genetics. Recurrence. Transcription Factors / genetics

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  • (PMID = 16843110.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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80. 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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81. Gong JY, Liu XP, Li CW, Zhao XC, Dai Y, Qin S, Xiao JG, Huang Q, Xu FY, Wang F, Cui W, Liu SH, Wang JX: [Clinical and laboratory study of a complex translocation t (6; 21; 8) (p22; q22; q22) in two patients with acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):314-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical and laboratory study of a complex translocation t (6; 21; 8) (p22; q22; q22) in two patients with acute myeloid leukemia].
  • OBJECTIVE: To investigate the clinical and laboratory characteristics of a complex translocation t (6; 21;.
  • 8) (p22; q22;.
  • q22) in two patients with acute myeloid leukemia.
  • The complex translocation was assayed by fluorescence in situ hybridization (FISH) with a dual-color AML1/ETO-specific probe.
  • AML1/ETO chimeric transcript was detected by reverse transcription polymerase chain reaction (RT-PCR).
  • 21) (p22; q22; q22), which was confirmed by interphase and metaphase FISH and AML1/ETO fusion transcript was detected by RT-PCR.
  • CONCLUSION: The t (6; 21;.
  • 8) (p22; q22;.
  • q22) is a rare variant of complex translocation of t (8;.
  • 21) (q22; q22).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16875580.001).
  • [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] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [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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82. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Iyer RR, Parikh EH, Shukla SN, Shah PM, Bakshi SR: A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21). Indian J Hum Genet; 2008 Jan;14(1):20-2
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  • [Title] A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21).
  • t(8;21)(q22;q22) is the most frequently observed karyotypic abnormality associated with acute myeloid leukemia (AML), specifically in FAB-M2.
  • Short-term unstimulated bone marrow (BM) and peripheral blood lymphocyte culture showed 47,XX, +4,t(8;21) in all metaphase plates; and interphase and metaphase results of AML-ETO fusion was positive and trisomy of 4 was confirmed with WCP probes.
  • Trisomy 4 in AML with t(8;21) is a rare numerical abnormality.

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  • (PMID = 20300287.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2840780
  • [Keywords] NOTNLM ; Acute myeloid leukemia / cytogenetics / fluorescence in situ hybridization
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83. Mrózek K, Bloomfield CD: Clinical significance of the most common chromosome translocations in adult acute myeloid leukemia. J Natl Cancer Inst Monogr; 2008;(39):52-7
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  • [Title] Clinical significance of the most common chromosome translocations in adult acute myeloid leukemia.
  • Acquired genetic alterations such as balanced and unbalanced chromosome aberrations and submicroscopic gene mutations and changes in gene expression strongly affect pretreatment features and prognosis of adults with acute myeloid leukemia (AML).
  • The most frequent chromosome/molecular rearrangements, that is, t(8;21)(q22;q22)/RUNX1-RUNX1T1 and inv(16)(p13q22)/t(16;16)(p13;q22)/CBFB-MYH11 characteristic of core-binding factor (CBF) AML and t(15;17)(q22;q12-21)/PML-RARA characteristic of acute promyelocytic leukemia (APL), confer favorable clinical outcome when patients receive optimal treatment, that is, regimens that include high-dose cytarabine for CBF AML and all-trans-retinoic acid and/or arsenic trioxide for APL.
  • Recently, mutations in such genes as KIT in CBF AML and FLT3 in APL have been correlated with clinical features and/or outcome of patients with these AML subtypes, and microarray gene expression profiling has been successfully used for diagnostic purposes and to provide biologic insights.
  • These data underscore the value of genetic testing for common translocations for diagnosis, prognostication, and, increasingly, selecting therapy in acute leukemia.
  • [MeSH-major] Chromosomes, Human / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18648004.001).
  • [ISSN] 1052-6773
  • [Journal-full-title] Journal of the National Cancer Institute. Monographs
  • [ISO-abbreviation] J. Natl. Cancer Inst. Monographs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA16058
  • [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 / Core Binding Factors
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8
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4. Andreeva SV, Drozdova VD, Kavardakova NV: [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia]. Tsitol Genet; 2010 May-Jun;44(3):41-52
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  • [Title] [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia].
  • Analysis of chromosomal abnormalities in bone marrow cells in 116 children with diagnosis of acute myeloid leukemia (AML) was performed.
  • The most abundant among them were numerical abnormalities of chromosomes 8, 9, and 21 as well as secondary structural abnormalities in region 12p12, 9p22, 9q22, 9q34, 11q14-23, and 16q22.
  • The high frequency of evolution was established at t(15;17)(q22;q22) and the absence at inv(16)(p13q22).
  • Conception of abnormality clone evolution was proposed at some stages: I--appearance of balanced rearrangement; II--trisomy; III--lose of chromosomal material.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics


85. 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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86. Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B: Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study. Blood; 2008 Feb 1;111(3):1575-83
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  • [Title] Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
  • Children with Down syndrome (DS) have a markedly increased risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these leukemias, we analyzed 215 DS-ALLs and 189 DS-AMLs.
  • Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-cell precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
  • Unlike DS-ALL, the common translocations associated with non-DS-AML were rare in DS-AML, which instead were characterized by the frequent presence of dup(1q), del(6q), del(7p), dup(7q), +8, +11, del(16q), and +21.
  • This series of DS leukemias-the largest to date-reveals that DS-ALL is a heterogeneous disorder that comprises both t(12;21) and HeH as well as DS-related abnormalities.
  • Furthermore, this analysis confirms that DS-AML is a distinct entity, originating through other genetic pathways than do non-DS-AMLs, and suggests that unbalanced changes such as dup(1q), +8, and +21 are involved in the leukemogenic process.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


87. Lin P, Chen L, Luthra R, Konoplev SN, Wang X, Medeiros LJ: Acute myeloid leukemia harboring t(8;21)(q22;q22): a heterogeneous disease with poor outcome in a subset of patients unrelated to secondary cytogenetic aberrations. Mod Pathol; 2008 Aug;21(8):1029-36
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  • [Title] Acute myeloid leukemia harboring t(8;21)(q22;q22): a heterogeneous disease with poor outcome in a subset of patients unrelated to secondary cytogenetic aberrations.
  • Acute myeloid leukemia with t(8;21)(q22;q22) is a distinct type of leukemia considered to have a favorable prognosis.
  • We studied 56 patients with acute myeloid leukemia associated with t(8;21) and correlated clinicopathologic, cytogenetic and molecular findings with outcome to identify markers of prognosis.
  • There were 31 men and 25 women, with a median age of 38 years (range 4-76).
  • Most patients (39/56, 70%) had chromosomal aberrations in addition to t(8;21), with loss of a sex chromosome (39%) being most common followed by del(9q)(q21-22) (11%) and trisomy 8 (7%).
  • The 5-year overall survival rate of patients with mutated leukemia was 20%.
  • Leukocytosis or CD56 expression did not correlate with a poor survival nor did the levels of CD19 expression predict c-KIT mutation status.
  • We conclude that acute myeloid leukemia associated with t(8;21) is a heterogeneous disease with poor survival in a subset of patients unrelated to common secondary cytogenetic aberrations.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 18536654.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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88. Agerstam H, Lilljebjörn H, Lassen C, Swedin A, Richter J, Vandenberghe P, Johansson B, Fioretos T: Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome. Genes Chromosomes Cancer; 2007 Jul;46(7):635-43
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  • [Title] Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome.
  • EMS is associated with a high risk of transformation to acute myeloid leukemia (AML), but the mechanisms underlying the disease progression are unknown.
  • In the present study, we have investigated a case of EMS harboring a t(8;22)(p11;q11)/BCR-FGFR1 rearrangement as well as a t(9;21)(q34;q22) at the time of AML transformation.
  • FISH and RT-PCR analyses revealed that the t(9;21) leads to a fusion gene consisting of the 5' part of RUNX1 (exons 1-4) fused to repetitive sequences of a gene with unknown function on chromosome 9, adding 70 amino acids to RUNX1 exon 4.
  • The t(9;21) hence results in a truncation of RUNX1.
  • No point mutations were found in the other RUNX1 allele.
  • The most likely functional outcome of the rearrangement was haploinsufficiency of RUNX1, which thus may be one mechanism by which EMS transforms to AML.
  • [MeSH-major] Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Gene Fusion. Myeloproliferative Disorders / genetics

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  • (PMID = 17394134.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [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 2 Subunit; 0 / DNA, Complementary; 0 / RUNX1 protein, human
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89. Fenske TS, Pengue G, Graubert TA: Dominant negative effects of the AML1/ETO fusion oncoprotein. Cell Cycle; 2005 Jan;4(1):33-6
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  • [Title] Dominant negative effects of the AML1/ETO fusion oncoprotein.
  • The t(8;21)(q22;q22) translocation, present in 10-15% of acute myeloid leukemia (AML) cases results in the production of the AML1/ETO fusion protein.
  • Expression of AML1/ETO in patients or mouse models is not sufficient to induce AML.
  • Despite convincing evidence that AML1/ETO is directly involved in the pathogenesis of AML, the underlying mechanism is not well understood.
  • Genetic and biochemical experiments suggest that AML1/ETO is a dominant inhibitor of the core binding factor (CBF) transcription complex that includes AML1 (RUNX1), the N-terminal fusion partner in the t(8;21).
  • We generated and recently characterized a novel strain of transgenic mice in which the AML1/ETO cDNA was inserted into the Ly-6A gene that encodes Sca1, a well-characterized marker of murine hematopoietic stem cells.
  • We have confirmed this finding at the mRNA level and suggest that this phenotype is a consequence of dominant inhibition of transgene expression by AML1/ETO.
  • The dominant negative characteristics of AML1/ETO may be important for AML pathogenesis and may provide a molecular target for therapeutic intervention.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. Leukemia, Myeloid / etiology. Oncogene Proteins, Fusion / physiology
  • [MeSH-minor] Acute Disease. Animals. Ataxin-1. Ataxins. Core Binding Factor alpha Subunits / genetics. Core Binding Factor alpha Subunits / physiology. DNA, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, Dominant. Genes, Neoplasm. Hematopoiesis / genetics. Humans. Mice. Mice, Transgenic. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / physiology. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Translocation, Genetic

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  • (PMID = 15611635.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / ATXN1 protein, human; 0 / Ataxin-1; 0 / Ataxins; 0 / Atxn1 protein, mouse; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor alpha Subunits; 0 / DNA, Neoplasm; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion
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90. Mikulasovich M, LeBlanc A, Scalise A, Manwani D, Keyzner A, Najfeld V: Duplication and triplication of der(21)t(8;21)(q22;q22) in acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Jan 15;188(2):83-7
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  • [Title] Duplication and triplication of der(21)t(8;21)(q22;q22) in acute myeloid leukemia.
  • We report on two patients with complicons resulting in duplication der(21)t(8;21)(q22;q22), triplication in the form of isochromosome of der(21)t(8;21), and four copies of ETO-AML1 fusion.
  • Duplication of der(21) was present at diagnosis as a minor cell population in one patient, while the presence of isoderivative (21)t(8;21) characterized the relapse cells of the second patient.
  • Due to the rarity of these cases, literature search of other reported cases of complicons may be taken as evidence that duplication and triplication of ETO-AML1 may be a poor prognostic indicator, regardless of whether it is present at diagnosis or relapse.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Core Binding Factor Alpha 2 Subunit / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Isochromosomes. Karyotyping. Middle Aged. Proto-Oncogene Proteins / genetics. Remission Induction. Transcription Factors / genetics

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  • (PMID = 19100510.001).
  • [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 / 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
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91. 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).
  • Morphologically, the AML M2 subtype according to the French-American-British (FAB) classification was present.
  • 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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92. 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.
  • Analysis of RUNX1T1 expression in human embryonic and fetal tissues suggests a role of RUNX1T1 in brain and heart development and support the notion that disruption of the RUNX1T1 gene is associated with the patient's phenotype.


93. Tsuji T, Takatsu N, Nosaka K, Kawakita T, Nanri T, Horikawa K, Mitsuya H, Asou N: Extramedullary tumors presenting double vision in patients with t(8;21)(q22;q22) acute myeloid leukemia lacking mutations in the receptor tyrosine kinase genes KIT or FLT3. Leuk Res; 2010 Dec;34(12):e320-2
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  • [Title] Extramedullary tumors presenting double vision in patients with t(8;21)(q22;q22) acute myeloid leukemia lacking mutations in the receptor tyrosine kinase genes KIT or FLT3.
  • [MeSH-major] Blast Crisis. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Diplopia. Leukemia, Myeloid, Acute. Paranasal Sinus Neoplasms. Proto-Oncogene Proteins c-kit. Translocation, Genetic. fms-Like Tyrosine Kinase 3

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  • (PMID = 20701971.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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94. 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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  • [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.
  • The present report describes the results of hematological, cytogenetic, and fluorescence in situ hybridization (FISH) analysis in a 25-year-old man diagnosed with AML-M2.
  • 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

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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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95. Oh SH, Park TS, Choi JR, Kim J, Song SA, Lee JY, Shin JH, Kim HR, Lee JN: A novel three-way t(7;21;8)(q11.2;q22;q22) in a patient with acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Dec;195(2):195-7
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  • [Title] A novel three-way t(7;21;8)(q11.2;q22;q22) in a patient with acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 19963126.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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96. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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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97. Mrózek K, Bloomfield CD: Chromosome aberrations, gene mutations and expression changes, and prognosis in adult acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2006;:169-77
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  • [Title] Chromosome aberrations, gene mutations and expression changes, and prognosis in adult acute myeloid leukemia.
  • Pretreatment clinical features and prognosis of patients with acute myeloid leukemia (AML) are strongly influenced by acquired genetic alterations in leukemic cells, which include microscopically detectable chromosome aberrations and, increasingly, submicroscopic gene mutations and changes in gene expression.
  • In many instances, patients with specific cytogenetic findings, e.g., those with a normal karyotype or those with either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22) [collectively referred to as core-binding factor (CBF) AML] can be further subdivided into prognostic categories based on the presence or absence of particular gene mutations or changes in gene expression.
  • In this article, we briefly review major cytogenetic prognostic categories and discuss molecular genetic findings of prognostic significance in two of the largest cytogenetic groups of patients with AML, namely AML with a normal karyotype and CBF AML.

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  • (PMID = 17124057.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA77658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 48
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98. Schafhausen P, Dierlamm J, Bokemeyer C, Bruemmendorf TH, Bacher U, Zander AR, Schnittger S, Hochhaus A: Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib. Cancer Genet Cytogenet; 2009 Feb;189(1):63-7
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  • [Title] Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Oncogene Proteins, Fusion / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Translocation, Genetic / genetics
  • [MeSH-minor] Benzamides. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Imatinib Mesylate. Karyotyping. Middle Aged

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  • (PMID = 19167615.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [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; 8A1O1M485B / Imatinib Mesylate
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99. Tretiak NM, Vakul'chuk OM, Kalinina SIu: [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)]. Lik Sprava; 2008 Jan-Feb;(1-2):89-96
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  • [Title] [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)].
  • 3 patients with secondary acute non-lymphoblastic leucosis have been observed.
  • The cytogenetic analysis revealed pathologic karyotypes: 46, XY,+8, t(8;21), inv 16.


100. Li HY, Yue H, Wei XD, Zhu XH, Zhang YL, Zhang LN, Liu YY, Wang P, Fang BJ, Li YF, Song YP: [The efficacy of high-dose cytarabine for patients with t(8;21) AML and with normal karyotype AML]. Zhonghua Xue Ye Xue Za Zhi; 2008 Feb;29(2):110-2
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  • [Title] [The efficacy of high-dose cytarabine for patients with t(8;21) AML and with normal karyotype AML].
  • OBJECTIVE: To compare the efficacy of high-dose cytarabine (HD-Ara-C) based chemotherapy for post-remission treatment in patients with t(8;21) (q22;q22) AML-M2 and those with normal karyotype AML-M2.
  • METHODS: AML-M2 patients were grouped into with (21 cases) or without (23 cases) t(8;21) (q22;q22) karyotype groups.
  • After achieved remission by induction therapy, all patients received four cycles of HD-Ara-C (3 mg/m2 per 12 hours by three-hour infusion day 1 to day 3) with either mitoxantrone (7 mg m(-2) d(-1)) or aclarubicin (30 mg m(-2) d(-1)) or etoposide (70 mg m(-2) d(-1)) for 3d as post-remission treatment.
  • RESULTS: Relapse rate in the t(8;21) and the normal karyotype groups was 29% and 57% respectively (P<0.05); 3 year disease-free survival (DFS) rate was 71% and 43% respectively (P < 0.05).
  • CONCLUSION: Four cycles of high-dose cytarabine based combination chemotherapy as post-remission treatment improves long-term disease-free survival in patients with t(8;21) (q22;q22) AML-M2.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Karyotyping. Male. Middle Aged. Treatment Outcome. Young Adult

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  • (PMID = 18681312.001).
  • [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] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine
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