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Items 1 to 55 of about 55
1. 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
  • [MeSH-minor] Aged. Graft vs Host Disease / diagnosis. Humans. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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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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2. 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.
  • 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%.
  • 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
  • [MeSH-minor] Adolescent. Adult. Aneuploidy. Biomarkers, Tumor / metabolism. Chromosome Deletion. Female. Humans. Male. Prognosis. Sex Chromosomes. Survival Rate. Texas / epidemiology

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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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3. Yin CC, Cortes J, Barkoh B, Hayes K, Kantarjian H, Jones D: t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy. Cancer; 2006 Apr 15;106(8):1730-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy.
  • BACKGROUND: The t(3;21)(q26;q22) translocation is associated with myeloid leukemias and results in a chimeric oncoprotein containing AML1/RUNX1 variably fused to EAP, MDS1, and/or EVI1.
  • METHODS: The current study describes what to the authors' knowledge is the first large case series reported to date of 26 t(3;21)(q26;q22)-associated leukemias, in which 24 cases arose after chemotherapy.
  • Reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to detect fusion transcripts between AML1 and EAP, MDS1, or EVI1, followed by DNA sequencing.
  • RESULTS: In all 16 patients with chronic myeloproliferative disorders, including 14 with chronic myelogenous leukemia (CML), the occurrence of t(3;21) heralded myeloid blast transformation.
  • Eight patients with chronic myeloproliferative disorders (CMPD) were found to have t(3;21) with t(9;22) as the sole cytogenetic abnormality; in 5 other patients this was accompanied by trisomy 8.
  • Among 10 cases of t(3;21)-associated acute myeloid leukemia, 8 were secondary tumors after chemotherapy for other neoplasms that had been treated with regimens including fludarabine and 5-fluorouracil in 3 patients each and etoposide in 2 patients.
  • The immunophenotype of the blasts in all 22 tested cases was similar, with uniform expression of myeloid markers and CD34 and variable expression of CD7 and CD9, but minimal morphological myeloid maturation.
  • RT-PCR followed by DNA sequencing showed that the AML1-/MDS1-/EVI1 (AME) fusion transcript was detected in all 5 cases assessed.
  • Among patients with acute myeloid leukemia/myelodysplastic syndrome, 7 died of disease (at a median of 2 mos) and 2 had persistent leukemia with short follow-up.
  • CONCLUSIONS: Activation of AME through t(3;21) defines a highly aggressive, therapy-related leukemic blast syndrome.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 21 / drug effects. Chromosomes, Human, Pair 3 / drug effects. Hydroxyurea / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Lymphocyte Activation / drug effects. Myeloproliferative Disorders / drug therapy. Oncogene Proteins, Fusion / analysis. Translocation, Genetic / drug effects
  • [MeSH-minor] Adult. Aged. Bone Marrow / pathology. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532439.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; X6Q56QN5QC / Hydroxyurea
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4. Chen CC, Gau JP, Yu YB, Lu CH, Lee KD, You JY: Prognosis and treatment outcome in patients with acute myeloid leukemia with t(8;21)(q22;q22). Adv Ther; 2007 Jul-Aug;24(4):907-20
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  • [Title] Prognosis and treatment outcome in patients with acute myeloid leukemia with t(8;21)(q22;q22).
  • Patients with acute myeloid leukemia (AML) with the t(8;21) karyotype generally have a favorable clinical course, but key prognostic factors remain poorly defined.
  • A total of 22 patients with AML with t(8;21)(q22;q22) were studied.
  • Between patients with t(8-21) and those with a normal karyotype, no significant differences were noted in DFS (median survival, 15.23 vs 12.03 mo; P=.7626) and OS (median survival, 19.17 vs 18.93 mo; P=.7543).
  • Among t(8;21)(q22;q22) patients, no clinical parameters showed a significant impact on DFS.
  • The data presented here suggest that t(8;21)(q22;q22) cytogenetic changes in patients with AML had prognostic significance similar to that in patients with a normal karyotype; patients who harbored either karyotype had parallel clinical outcomes.
  • It is concluded that patients with AML with t(8;21)(q22;q22) would be compromised by treatment approaches that do not include HSCT as postremission therapy.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Hematologic Tests. Hematopoietic Stem Cell Transplantation. Humans. Karyotyping. Male. Middle Aged. Prognosis. Translocation, Genetic. Treatment Outcome

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  • (PMID = 17901040.001).
  • [ISSN] 0741-238X
  • [Journal-full-title] Advances in therapy
  • [ISO-abbreviation] Adv Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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5. 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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6. 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] United States
  • [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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7. Chung HJ, Chi HS, Cho YU, Lee EH, Jang S, Park CJ, Seo EJ: [Prognostic effect of cytoplasmic CD79a expression in acute myeloid leukemia with t(8;21)]. Korean J Lab Med; 2007 Dec;27(6):388-93
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  • [Title] [Prognostic effect of cytoplasmic CD79a expression in acute myeloid leukemia with t(8;21)].
  • BACKGROUND: Although cytoplasmic CD79a (cytCD79a) is a highly lineage-specific marker of B lymphoid cells and plays an important role in the diagnosis of acute leukemia, its clinical significance is not fully understood.
  • We aimed to investigate the relationship between cytCD79a positivity and survival probability, and to evaluate the prognostic value of cytCD79a expression in AML with t(8;21) (q22;q22).
  • METHODS: A total of 68 cases of AML with t(8;21)(q22;q22) were diagnosed based on conventional morphology, cytochemistry, flow cytometrty, and cytogenetic and molecular genetic analysis.
  • RESULTS: Five patients among 68 AML with t(8;21)(q22;q22) revealed cytCD79a positive reaction; scores for myeloid lineage/B-lymphoid lineage were 5/3-3.5.
  • The survival probability of the cytCD79a expression group was significantly lower than classical AML with t(8;21)(q22;q22) (P=0.0001).
  • CONCLUSIONS: These findings emphasize the necessity of investigating cytCD79a, especially in AML with t(8;21)(q22;q22), for a different clinical prognostic value.
  • [MeSH-major] Antigens, CD79 / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytoplasm / metabolism. Female. Humans. Male. Middle Aged. Prognosis. Survival Analysis

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  • (PMID = 18160827.001).
  • [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 / Antigens, CD79
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8. 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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9. 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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10. 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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11. Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Zhang Y, Liu YR, Shi HL, Lu DP: Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22). Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Oct;13(5):733-40
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  • [Title] Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22).
  • The translocation t (8;. 21) (q22;.
  • q22) frequently associated with additional chromosomal aberrations is one of the most recurrent chromosomal abnormalities in AML.
  • On the other hand, some reports also showed poor prognosis in AML patients with t (8; 21), and the associated bad-prognosis factors have not been strongly established to date.
  • 21) AML in China, 75 Chinese AML patients with t (8;.
  • 21) were retrospectively analyzed.
  • In multivariate analyses of prognostic factors, karyotype, extramedullary leukemia, age and post-remission therapy were of prognostic value for OS.
  • Patients with additional chromosomal anomalies had shorter survival compared to those with t (8;.
  • 21) only (P = 0.019), no matter which kind of additional karyotype it was.
  • Extramedullary leukemia was an adverse prognostic factor (P = 0.012).
  • It is concluded that Chinese AML patients with t (8;.
  • 21) had some different characteristics as compared with patients from other countries, a relatively poor outcome was observed in our patients, especially in those with extramedullary leukemia or additional chromosomal abnormalities.
  • 21) AML in China, especially to those with adverse prognostic factors.

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  • (PMID = 16277833.001).
  • [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] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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12. 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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13. Yamamoto K, Sada A, Kawano Y, Katayama Y, Shimoyama M, Matsui T: Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement. Cancer Genet Cytogenet; 2010 Sep;201(2):122-7
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  • [Title] Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement.
  • We describe here a new case of therapy-related acute leukemia with t(1;21)(p36;q22).
  • Chromosome analysis showed 46,XY,t(1;21)(p36.3;q22)[11]/49,sl,+8,+16,+20[9].
  • Fluorescence in situ hybridization demonstrated that RUNX1 signals at 21q22 were split onto the der(1)t(1;21) and der(21)t(1;21).
  • Immunophenotypic analyses revealed that blasts were positive for CD19, CD79a, and cytCD22, as well as MPO, CD13, and CD33, fulfilling the diagnostic criteria of mixed phenotype acute leukemia, B/myeloid.
  • Thus, acute leukemia with t(1;21) and RUNX1 rearrangement could be associated with B/myeloid mixed phenotype as well as previous topoisomerase II inhibitor therapy and poor prognoses.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fatal Outcome. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682397.001).
  • [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 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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14. Jekarl DW, Kim M, Lim J, Kim Y, Han K, Lee AW, Kim HJ, Min WS: CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22). Int J Hematol; 2010 Sep;92(2):306-13
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  • [Title] CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22).
  • The translocation t(16;21)(p11;q22) is rare, occurs with an incidence of 1%, in acute myeloid leukemia (AML), forming TLS/FUS-ERG fusion transcript, and it is known to cause the hemophagocytosis and vacuolation of leukemic cells.
  • As previously reported cases numbered less than 60, we aimed to identify the clinical and genetic aspects of AML with t(16;21).
  • Among 1,277 patients diagnosed with de novo and secondary AML, 12 AML patients with t(16;21) were retrospectively evaluated (0.94%, 12/1,277).
  • AML with t(16;21) expressed CD56 with a median value of 45% (7.8-87%), and the rate of hemophagocytosis plus vacuolation of leukemic cells was 2.9% (2.0-9.0%).
  • AML with t(16;21) expressed CD13, CD33, CD34, CD117, CD56, HLA-DR, and cytoplasmic myeloperoxidase.
  • AML with t(16;21) showed a very low rate of complete remission after induction chemotherapy (8.3%), and high relapse (75%) and mortality (75%) rates.
  • AML with t(16;21) exhibited a distinct morphology with frequent CD56 expression and a poor prognosis.
  • [MeSH-major] Antigens, CD56 / analysis. Cytophagocytosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Translocation, Genetic
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Female. Humans. Male. Middle Aged. Prognosis. Young Adult

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  • (PMID = 20694842.001).
  • [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] United States
  • [Chemical-registry-number] 0 / Antigens, CD56
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15. 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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16. Ma Y, Tong HX, Deng X, Zhao Y, Liu ZG, Zhang JH: [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):12-6
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  • [Title] [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)].
  • This study was purposed to investigate the acute myeloid leukemia with complex karyotype t(2;21;8)(p12;q22;q22) (AML-M(2)) by using morphologic, immunologic, cytogenetic and molecular biologic classification technique (MICM) and to analyze the MICM characteristics of AML-M(2) and their diagnostic significance.
  • The FAB typing of bone marrow cells (BMCs) was performed by Wright-Giemsa staining and histochemical staining of BM smears; the immunophenotype of leukemic cells was detected by flow cytometry; the karyotypes of chromosome samples prepared by short-term (48 hours) conventional culture of fresh BMCs were analyzed by RHG banding technique; the FISH signaling in mitotic metaphase was determined by dual color and dual fusion AML/ETO probe and chromosome painting probe, and was compared with results of conventional cytogenetic assay; the AML/ETO fusion transcripts were detected by nested RT-PCR.
  • The complex karyotype t(2;21;8)(p12;q22;q22) was detected by cytogenetic analysis combined with FISH in both two cases and AML1/ETO fusion transcripts were found by RT-PCR as well.
  • It is concluded that application of MICM has an important significance for correct diagnostic typing of AML-M2 with complex karyotype variant of t(8; 21)(p12;q22;q22).

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  • (PMID = 19236738.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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17. 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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18. 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).
  • The chimeric transcript FUS-ERG formed by this translocation which causes the replacement of RNA-binding domain of FUS (alias TLS) with the DNA-binding domain of ERG, and this event is thought to be responsible for leukemogenesis.
  • 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
  • [MeSH-minor] Adult. Aged. Base Sequence. Cytogenetic Analysis. DNA Mutational Analysis. Female. Humans. Male. RNA, Messenger / genetics. RNA, Messenger / isolation & purification

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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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19. 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.
  • 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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20. 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.


21. Nanri T, Matsuno N, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N: Mutations in the receptor tyrosine kinase pathway are associated with clinical outcome in patients with acute myeloblastic leukemia harboring t(8;21)(q22;q22). Leukemia; 2005 Aug;19(8):1361-6
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  • [Title] Mutations in the receptor tyrosine kinase pathway are associated with clinical outcome in patients with acute myeloblastic leukemia harboring t(8;21)(q22;q22).
  • AML1-MTG8 generated by t(8;21) contributes to leukemic transformation, but additional events are required for full leukemogenesis.
  • We examined whether mutations in the receptor tyrosine kinase (RTK) pathway could be the genetic events that cause acute myeloblastic leukemia (AML) harboring t(8;21).
  • Mutations in the second tyrosine kinase domain, juxtamembrane (JM) domain and exon 8 of the C-KIT gene were observed in 10, one and three of 37 AML patients with t(8;21), respectively.
  • These results suggest that activating mutations in the RTK pathway play a role in part as an additional event leading to the development of t(8;21) AML.
  • Furthermore, the 6-year relapse-free survival in patients with mutations was 18% compared to 60% in those without mutations (P=0.0340), indicating that RTK mutations are associated with the clinical outcome in t(8;21) AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Disease-Free Survival. Female. Genes, ras. Humans. Male. Middle Aged. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-kit / genetics. Recurrence. Tandem Repeat Sequences. Translocation, Genetic. Treatment Outcome. fms-Like Tyrosine Kinase 3

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  • [Copyright] Leukemia (2005) 19, 1361-1366.
  • (PMID = 15902284.001).
  • [ISSN] 0887-6924
  • [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 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. 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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24. 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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25. 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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26. 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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27. Owatari S, Otsuka M, Uozumi K, Takeshita T, Hanada S: Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Jan;85(1):32-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma.
  • We identified 2 cases of secondary acute myeloid leukemia (AML) following adult T-cell leukemia/lymphoma (ATL) in patients who had previously received chemotherapy.
  • The cases were diagnosed as AML M4 with eosinophilia and AML M2, with the chromosomal abnormalities inv(16)(p13q22) and t(8;21)(q22;q22), respectively.
  • In our hospital, only these 2 cases of secondary AML accompanying ATL were identified among 90 cases of acute- or lymphoma-type ATL diagnosed from October 1999 to July 2006.
  • The frequency of coexisting AML and ATL is lower than that reported for acute leukemia coexisting with other lymphoid malignancies.
  • The low frequency of secondary leukemia with ATL may be associated with the short survival times of ATL patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Acute Disease. Alkylating Agents / therapeutic use. Anthracyclines / therapeutic use. Chromosome Aberrations. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / chemically induced. Male. Middle Aged. Podophyllotoxin / therapeutic use

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  • (PMID = 17261499.001).
  • [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 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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28. 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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29. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Paschka P, Marcucci G, Ruppert AS, Mrózek K, Chen H, Kittles RA, Vukosavljevic T, Perrotti D, Vardiman JW, Carroll AJ, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B: Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study. J Clin Oncol; 2006 Aug 20;24(24):3904-11
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  • [Title] Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study.
  • PURPOSE: To analyze the prognostic impact of mutated KIT (mutKIT) in core-binding factor acute myeloid leukemia (AML) with inv(16)(p13q22) and t(8;21)(q22;q22).
  • PATIENTS AND METHODS: Sixty-one adults with inv(16) and 49 adults with t(8;21), assigned to postremission therapy with repetitive cycles of higher dose cytarabine were analyzed for mutKIT in exon 17 (mutKIT17) and 8 (mutKIT8) by denaturing high-performance liquid chromatography and direct sequencing at diagnosis.
  • Among patients with t(8;21), 22% had mutKIT (18% with mutKIT17 and 4% with sole mutKIT8).
  • In t(8;21), mutKIT predicted higher CIR (P = .017; 5-year CIR, 70% v 36%), but did not influence OS.
  • We also confirm the adverse impact of mutKIT on relapse risk in t(8;21) AML.
  • [MeSH-major] Chromosome Inversion. Leukemia, Myeloid / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Chromatography, High Pressure Liquid. Female. Humans. Male. Middle Aged. Multivariate Analysis. Predictive Value of Tests. Prognosis. Survival Analysis

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  • (PMID = 16921041.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00233454
  • [Grant] United States / NCI NIH HHS / CA / CA02599; United States / NCI NIH HHS / CA / CA03927; United States / NCI NIH HHS / CA / CA04326; United States / NCI NIH HHS / CA / CA04457; United States / NCI NIH HHS / CA / CA07968; United States / NCI NIH HHS / CA / CA08025; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA11028; United States / NCI NIH HHS / CA / CA11789; United States / NCI NIH HHS / CA / CA12011; United States / NCI NIH HHS / CA / CA12046; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA21060; United States / NCI NIH HHS / CA / CA26806; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA31983; United States / NCI NIH HHS / CA / CA32291; United States / NCI NIH HHS / CA / CA35279; United States / NCI NIH HHS / CA / CA35406; United States / NCI NIH HHS / CA / CA37135; United States / NCI NIH HHS / CA / CA41287; United States / NCI NIH HHS / CA / CA45418; United States / NCI NIH HHS / CA / CA47545; United States / NCI NIH HHS / CA / CA47555; United States / NCI NIH HHS / CA / CA47559; United States / NCI NIH HHS / CA / CA47577; United States / NCI NIH HHS / CA / CA47642; United States / NCI NIH HHS / CA / CA74811; United States / NCI NIH HHS / CA / CA77298; United States / NCI NIH HHS / CA / CA77406; United States / NCI NIH HHS / CA / CA77440; United States / NCI NIH HHS / CA / CA77597; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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32. 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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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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
  • [MeSH-minor] Adult. Chromosome Inversion. Core Binding Factors / genetics. Humans

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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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34. 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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35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The cytogenetic-risk classifications differ somewhat for younger adult patients and those aged 60 years or older.
  • 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.

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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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36. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • FISH analysis was performed utilizing commercially available DNA probes, including whole chromosome painting probes, locus specific probes, and specific and dual color/multiple color translocation fusion probes.
  • RESULTS: Six out of the 58 patients (10.3%) were found to have MLL gene rearrangements, either an extra signal of MLL gene or a disruption of MLL gene due to a translocation or deletion or duplication.
  • 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;.
  • Because MLL gene arrangements due to translocation or other structural changes are associated with poor response to chemotherapy and poor prognosis, routine testing for this gene rearrangement should be provided to all newly diagnosed patients with AML.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. In Situ Hybridization, Fluorescence. Infant. Middle Aged

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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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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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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38. Paschka P: Core binding factor acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):410-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Core binding factor acute myeloid leukemia.
  • Core binding factor (CBF) acute myeloid leukemia (AML) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult de novo AML cases.
  • Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16) AML, thereby supporting the notion that they represent two distinct biologic and clinical entities.
  • [MeSH-major] Chromosome Inversion. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual / diagnosis. Prognosis

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  • (PMID = 18692691.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors
  • [Number-of-references] 76
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39. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm, Residual. Saudi Arabia

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  • (PMID = 17671534.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Antigens, CD79; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
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40. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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41. Yang L, Zhang Y, Zhang MR, Xiao ZJ: [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations]. Zhonghua Yi Xue Za Zhi; 2005 Aug 31;85(33):2312-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].
  • OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.
  • METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.
  • The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.
  • 21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.
  • 17) (q22; q11)/PML-RARalpha fusion gene, all significantly higher than those in the controls (49.4% and 13.7% respectively).
  • 21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.
  • 17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.
  • CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.
  • 21) (q22; q22)/AML-ETO fusion gene and t (15;.
  • 17) (q22; q11)/PML-RARalpha fusion gene.
  • [MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Gene Frequency. Genotype. Humans. Male. Middle Aged. NAD(P)H Dehydrogenase (Quinone) / genetics. Translocation, Genetic. Young Adult

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  • (PMID = 16321221.001).
  • [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] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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42. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
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  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • The various aberrations observed were t(8;21)(q22;q22) (5.2%); t(15;17) (q22;q11-21) (9%); t(9;22)(q34;q11)(1.7%); t(14;17)(q32;q11.2)(0.5%); inv(16)(p13;q22)(1.7%); 11q23 rearrangements (4%); monosomy 7 (2.2%) and 22 (1.1%); deletion of 9q (q22q34) (5.1%), 5q (q13q33) (0.5%) and 13q (q13q31) (0.5%); common trisomies like +8 (5.6%), +16 (1.7%), +22 (1.1%), +21 (0.5%), +13 (0.5%), +11 (0.5%), +3 (0.5%); hyperdiploidy (3.4%); hypodiploidy (1.1%); complex karyotype (4%); and other structural abnormalities (4.5%).
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Humans. India. Infant. Karyotyping. Male. Middle Aged

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  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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43. Grimwade D, Hills RK, Moorman AV, Walker H, Chatters S, Goldstone AH, Wheatley K, Harrison CJ, Burnett AK, National Cancer Research Institute Adult Leukaemia Working Group: Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials. Blood; 2010 Jul 22;116(3):354-65
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  • [Title] Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials.
  • Diagnostic karyotype provides the framework for risk-stratification schemes in acute myeloid leukemia (AML); however, the prognostic significance of many rare recurring cytogenetic abnormalities remains uncertain.
  • In multivariable analysis, t(15;17)(q22;q21), t(8;21)(q22;q22), and inv(16)(p13q22)/t(16;16)(p13;q22) were the only abnormalities found to predict a relatively favorable prognosis (P < .001).
  • In patients with t(15;17) treated with extended all-trans retinoic acid and anthracycline-based chemotherapy, additional cytogenetic changes did not have an impact on prognosis.
  • Similarly, additional abnormalities did not have a significant adverse effect in t(8;21) AML; whereas in patients with inv(16), the presence of additional changes, particularly +22, predicted a better outcome (P = .004).
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols. Bone Marrow Transplantation. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Cohort Studies. Cytogenetic Analysis. Female. Great Britain. Humans. Karyotyping. Male. Middle Aged. Multivariate Analysis. Mutation. Nuclear Proteins / genetics. Prognosis. Risk Factors. Survival Analysis. Translocation, Genetic. Treatment Outcome. Young Adult. fms-Like Tyrosine Kinase 3 / genetics


44. 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.
  • 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.

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  • (PMID = 18841055.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / R01CA102031
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Number-of-references] 81
  • [Other-IDs] NLM/ NIHMS202765; NLM/ PMC3677535
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45. Burmeister T, Gökbuget N, Schwartz S, Fischer L, Hubert D, Sindram A, Hoelzer D, Thiel E: Clinical features and prognostic implications of TCF3-PBX1 and ETV6-RUNX1 in adult acute lymphoblastic leukemia. Haematologica; 2010 Feb;95(2):241-6
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  • [Title] Clinical features and prognostic implications of TCF3-PBX1 and ETV6-RUNX1 in adult acute lymphoblastic leukemia.
  • BACKGROUND: The t(9;22) and t(4;11) chromosomal translocations, which generate the BCR-ABL and MLL-AF4 fusion genes, define high-risk subtypes of acute lymphoblastic leukemia in adults.
  • However, the prognostic impact of other rarer fusion genes is less well established in adult acute lymphoblastic leukemia than in the childhood form.
  • DESIGN AND METHODS: In the context of the German Multicenter Therapy Study Group for Adult Acute Lymphoblastic Leukemia (GMALL) we used reverse transcriptase polymerase chain reaction to investigate 441 cases of BCR-ABL- and MLL-AF4-negative B-precursor acute lymphoblastic leukemia for the TCF3-PBX1 (E2A-PBX1) and ETV6-RUNX1 (TEL-AML1) fusion transcripts generated by the t(1;19)(q23;p13.3) and t(12;21)(p13;q22) translocations.
  • Both are well-known molecular alterations in pediatric acute lymphoblastic leukemia in which they have favorable prognostic implications.
  • RESULTS: We identified 23 adult patients with TCF3-PBX1 and ten with ETV6-RUNX1.
  • CONCLUSIONS: In contrast to previous suggestions, adult patients with TCF3-PBX1-positive acute lymphoblastic leukemia do not appear to have a worse outcome than their negative counterparts.
  • [MeSH-major] Oncogene Proteins, Fusion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Cell Line. Core Binding Factor Alpha 2 Subunit. Female. Fusion Proteins, bcr-abl. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19713226.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TCF3-PBX1 fusion protein, human; 0 / TEL-AML1 fusion protein; 0 / abl-bcr fusion protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2817026
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46. 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
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Chromosome Aberrations / classification. Chromosomes, Human / genetics. Cytogenetics. Female. Genome, Human / genetics. Humans. Infant. Infant, Newborn. Karyotyping. Male


47. Jost E, Lorenzen J, Haage P, Bos G, Beelen D, Galm O, Gehbauer G, Osieka R: Heart and muscle involvement by extra-medullary myeloid leukemia: a case report and review of the literature. Leuk Lymphoma; 2005 Dec;46(12):1819-24
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  • [Title] Heart and muscle involvement by extra-medullary myeloid leukemia: a case report and review of the literature.
  • Extra-medullary myeloid tumours (EMT) have been described after curative treatment for acute myeloid leukaemia (AML) in increasing numbers after allogeneic stem cell transplantation.
  • This study reports a case of EMT in muscles and the heart 1.5 years after allogeneic transplantation for an AML with t(8;21)(q22;23) who achieved a complete remission by use of an idarubicine-based combination chemotherapy.
  • [MeSH-major] Leukemia, Myeloid / pathology. Muscle, Skeletal / pathology. Myocardium / pathology
  • [MeSH-minor] Adult. Graft vs Host Disease. Humans. Magnetic Resonance Imaging. Male. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 16263587.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 28
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48. Lane S, Saal R, Mollee P, Jones M, Grigg A, Taylor K, Seymour J, Kennedy G, Williams B, Grimmett K, Griffiths V, Gill D, Hourigan M, Marlton P: A &gt;or=1 log rise in RQ-PCR transcript levels defines molecular relapse in core binding factor acute myeloid leukemia and predicts subsequent morphologic relapse. Leuk Lymphoma; 2008 Mar;49(3):517-23
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  • [Title] A >or=1 log rise in RQ-PCR transcript levels defines molecular relapse in core binding factor acute myeloid leukemia and predicts subsequent morphologic relapse.
  • Core binding factor acute myeloid leukemia (CBF AML), with t(8;21)(q22;q22), inv(16)(p13q22) or t(16;16)(p13;q22) and the associated fusion gene transcripts AML1/ETO or CBFbeta/MYH11, has a favourable clinical prognosis although significant numbers of patients still suffer relapse.
  • However, a >or=1 log(10) rise at any stage in transcript level relative to the level from a remission bone marrow sample correlated with inferior leukemia free survival (LFS) and imminent morphologic relapse (hazard ratio 8.6).
  • [MeSH-major] Core Binding Factors. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Neoplasm, Residual / diagnosis. Predictive Value of Tests. RNA, Messenger / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Bone Marrow Examination. Child. Cohort Studies. Female. Follow-Up Studies. Humans. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Recurrence

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  • (PMID = 18297529.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; 0 / RNA, Messenger
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49. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


50. Heald B, Hilden JM, Zbuk K, Norton A, Vyas P, Theil KS, Eng C: Severe TMD/AMKL with GATA1 mutation in a stillborn fetus with Down syndrome. Nat Clin Pract Oncol; 2007 Jul;4(7):433-8
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  • BACKGROUND: A 34-year-old woman was referred for evaluation of a recent stillborn male fetus, gestational age 27 6/7 weeks, found to have congenital myeloid leukemia at autopsy.
  • INVESTIGATIONS: Immunoperoxidase staining of placental tissue, fluorescence in situ hybridization of paraffin-embedded sections of the placenta using probes for t(12;21)(p13;q22), t(8;21)(q22;q22) and t/del(11q23), cytogenetic analysis of fetal tissue (tendon), sequence analysis of GATA1 in placental leukemic cells, and parental chromosome studies.
  • DIAGNOSIS: Down syndrome with in utero onset of GATA1 mutation-positive severe transient myeloproliferative disorder/acute megakaryoblastic leukemia.
  • [MeSH-major] Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Myeloproliferative Disorders / genetics. Stillbirth
  • [MeSH-minor] Adult. Autopsy. Female. Humans. Infant, Newborn. Mutation / genetics. Pregnancy

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  • (PMID = 17597708.001).
  • [ISSN] 1743-4262
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
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51. Lück SC, Russ AC, Du J, Gaidzik V, Schlenk RF, Pollack JR, Döhner K, Döhner H, Bullinger L: KIT mutations confer a distinct gene expression signature in core binding factor leukaemia. Br J Haematol; 2010 Mar;148(6):925-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Core binding factor (CBF) leukaemias, characterized by either inv(16)(p13.1q22) or t(8;21)(q22;q22), constitute acute myeloid leukaemia (AML) subgroups with favourable prognosis.
  • [MeSH-major] Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / genetics. Young Adult

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  • (PMID = 20064158.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; 0 / Neoplasm Proteins; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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52. 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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53. Imagawa J, Harada Y, Yoshida T, Sakai A, Sasaki N, Kimura A, Harada H: Giant granulocytic sarcoma of the vagina concurrent with acute myeloid leukemia with t(8;21)(q22;q22) translocation. Int J Hematol; 2010 Oct;92(3):553-5
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  • [Title] Giant granulocytic sarcoma of the vagina concurrent with acute myeloid leukemia with t(8;21)(q22;q22) translocation.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Sarcoma, Myeloid / complications. Vagina / pathology. Vaginal Neoplasms / complications
  • [MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging. Translocation, Genetic


54. Iwanaga E, Nanri T, Matsuno N, Kawakita T, Mitsuya H, Asou N: A JAK2-V617F activating mutation in addition to KIT and FLT3 mutations is associated with clinical outcome in patients with t(8;21)(q22;q22) acute myeloid leukemia. Haematologica; 2009 Mar;94(3):433-5
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  • [Title] A JAK2-V617F activating mutation in addition to KIT and FLT3 mutations is associated with clinical outcome in patients with t(8;21)(q22;q22) acute myeloid leukemia.
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Substitution. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Kaplan-Meier Estimate. Male. Mutation

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  • [Cites] Leukemia. 2005 Aug;19(8):1361-6 [15902284.001]
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  • (PMID = 19181784.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 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; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ PMC2649368
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55. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Adult. Aged. Antimetabolites, Antineoplastic / adverse effects. Cytarabine / administration & dosage. Humans. Male. Stem Cell Transplantation. Transplantation, Homologous

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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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