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3. Pullarkat ST, Pullarkat V, Kroft SH, Wilson CS, Ahsanuddin AN, Mann KP, Thein M, Grody WW, Brynes RK: Systemic mastocytosis associated with t(8;21)(q22;q22) acute myeloid leukemia. J Hematop; 2009 Mar;2(1):27-33
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  • [Title] Systemic mastocytosis associated with t(8;21)(q22;q22) acute myeloid leukemia.
  • Although KIT mutations are present in 20-25% of cases of t(8;21)(q22;q22) acute myeloid leukemia (AML), concurrent development of systemic mastocytosis (SM) is exceedingly rare.
  • We examined the clinicopathologic features of SM associated with t(8;21)(q22;q22) AML in ten patients (six from our institutions and four from published literature) with t(8;21) AML and SM.
  • In the majority of these cases, a definitive diagnosis of SM was made after chemotherapy, when the mast cell infiltrates were prominent.
  • Four of the ten patients failed to achieve remission after standard chemotherapy and seven of the ten patients have died of AML.
  • SM associated with t(8;21) AML carries a dismal prognosis; therefore, detection of concurrent SM at diagnosis of t(8;21) AML has important prognostic implications.

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  • (PMID = 19669220.001).
  • [ISSN] 1868-9256
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2713498
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4. Jones D, Yao H, Romans A, Dando C, Pierce S, Borthakur G, Hamilton A, Bueso-Ramos C, Ravandi F, Garcia-Manero G, Kantarjian H: Modeling interactions between leukemia-specific chromosomal changes, somatic mutations, and gene expression patterns during progression of core-binding factor leukemias. Genes Chromosomes Cancer; 2010 Feb;49(2):182-91
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  • [Title] Modeling interactions between leukemia-specific chromosomal changes, somatic mutations, and gene expression patterns during progression of core-binding factor leukemias.
  • We studied genetic changes occurring over time in cancers presenting with a relatively simple karyotype, namely two related core-binding factor (CBF) acute myeloid leukemias (AMLs), to assess how specific chromosomal changes are selected based on tumor subtype and acquired somatic mutations.
  • Expression profiles for DNA replication/repair genes and the mutation status of KRAS, NRAS, FLT3, and KIT were compared with the karyotypic changes at diagnosis and relapse(s) in 94 cases of inv(16)(p13.1q22)-AML and 82 cases of t(8;21)(q22;q22)-AML.
  • The majority of both AML types demonstrated a simple aneuploid pattern of cytogenetic progression, with highly distinctive patterns of chromosome copy number changes, such as +22 and +13 exclusively in inv(16)-AML and -Y and -X in t(8;21)-AML.
  • Selection of certain cytogenetic changes correlated with particular somatic mutations, such as +8 with RAS mutation, and absence of kinase pathway mutations in t(8;21)-AML with localized deletions at chromosome band 9q22.
  • Alterations in transcript levels of mitotic spindle kinases such as CHEK1, AURKA, and AURKB were associated with the aneuploid progression pattern, particularly in t(8;21) cases.
  • Despite the similarity in the initiating genetics of the two CBF AML types, highly tumor-specific patterns of limited aneuploidy are noted that persist and continue to accumulate at relapse.

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  • (PMID = 19908318.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100707; United States / NCI NIH HHS / CA / 1P50CA100707-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factors
  • [Other-IDs] NLM/ NIHMS155604; NLM/ PMC4161977
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5. Schafhausen P, Dierlamm J, Bokemeyer C, Bruemmendorf TH, Bacher U, Zander AR, Schnittger S, Hochhaus A: Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib. Cancer Genet Cytogenet; 2009 Feb;189(1):63-7
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  • [Title] Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Oncogene Proteins, Fusion / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Translocation, Genetic / genetics
  • [MeSH-minor] Benzamides. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Humans. Imatinib Mesylate. Karyotyping. Middle Aged

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  • (PMID = 19167615.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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6. 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.
  • Case 2 accorded with AML-M(2b) in which abnormal increase of myelocytes mainly appeared.
  • 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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7. 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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  • [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

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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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8. Park TS, Choi JR, Yoon SH, Song J, Kim J, Kim SJ, Kwon O, Min YH: Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript. Cancer Genet Cytogenet; 2008 Dec;187(2):61-73
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  • [Title] Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript.
  • Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (AML) that is characterized by peculiar clinical and biologic features, including severe hemorrhagic diathesis, specific recurrent chromosomal aberration, and distinct morphologic features with predominant pathologic promyelocytes.
  • A reciprocal translocation involving chromosomes 15 and 17, t(15;17)(q22;q21), is a characteristic feature of APL that represents approximately 5-8% of AML.
  • In contrast to other AML subtypes, APL is particularly sensitive to treatment with all trans-retinoic acid (ATRA) combined with chemotherapy, converting this once fatal leukemia to a highly curable disease.
  • Nonetheless, therapy-related myelodysplastic syndrome-acute myelogenous leukemia (t-MDS/AML) has been reported as a rare complication of chemotherapy in APL.
  • Of 30 APL cases described as t-MDS/AML in the literature, only 1 case relapsed as acute leukemia with t(3;21)(q26;q22).
  • Here we describe a rare case of APL relapsing as secondary AML with t(3;21)(q26;q22) and clinically characterize this patient using the RUNX1 (previously AML1)-MDS1-EVI1 fusion transcript (with follow-up for 55 months), and review the relevant literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / ultrastructure. Chromosome Painting. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 3 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Female. Humans. Karyotyping. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Proto-Oncogenes / genetics. Sequence Analysis, DNA. Transcription Factors / genetics. Transcription Factors / metabolism. Tretinoin / therapeutic use

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  • (PMID = 19027486.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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9. Zhang J, Liu Z, Shao H, Ma Y, Tong H, Wang Y: Laboratory study of a complex translocation t(2;8;21) (p12;q22;q22) in a patient with acute myelogenous leukemia. Leuk Lymphoma; 2008 Oct;49(10):1925-8
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  • [Title] Laboratory study of a complex translocation t(2;8;21) (p12;q22;q22) in a patient with acute myelogenous leukemia.
  • The t(2;8;21) is a complex translocation of t(8;21), and is very rare.
  • To investigate the laboratory characteristics of a complex translocation t(2;8;21)(p12;q22;q22) in a patient with acute myelogenous leukemia (AML-M2), bone marrow smears were prepared for morphological analysis.
  • 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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10. Lee J, Kern WF, Cain JB, Mulvihill JJ, Li S: A variant t(8;10;21) in a patient with pathological features mimicking atypical chronic myeloid leukemia. Cancer Genet Cytogenet; 2005 May;159(1):79-83
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  • [Title] A variant t(8;10;21) in a patient with pathological features mimicking atypical chronic myeloid leukemia.
  • We report the case of an 11-year-old girl who was initially diagnosed with a chronic myeloproliferative disorder, possibly chronic myelogenous leukemia (CML), based on laboratory and blood and marrow morphological findings.
  • Chromosomal analysis revealed that the patient did not have t(9;22), but a complex t(8;10;21)(q22;q24;q22), a variant of t(8;21).
  • The treatment regime was switched to an acute myeloid leukemia (AML) protocol; the patient responded well and is now in remission.
  • This case demonstrates again that routine clinical cytogenetic analysis plays an important role in the clinical diagnosis, guidance of treatment, and prognostication in hematological disorders.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Genetic Variation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic


11. Gibson SE, Dong HY, Advani AS, Hsi ED: Expression of the B cell-associated transcription factors PAX5, OCT-2, and BOB.1 in acute myeloid leukemia: associations with B-cell antigen expression and myelomonocytic maturation. Am J Clin Pathol; 2006 Dec;126(6):916-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the B cell-associated transcription factors PAX5, OCT-2, and BOB.1 in acute myeloid leukemia: associations with B-cell antigen expression and myelomonocytic maturation.
  • The aberrant expression of the B-cell transcription factor PAX5 has been described in a subset of acute myeloid leukemia (AML) with t(8;21)(q22;q22) in association with B-cell antigen expression.
  • However, the expression of other B cell-associated transcription factors, particularly OCT-2 and its B cell-specific coactivator BOB.1, has not been described in AML.
  • In this study, expression of PAX5, OCT-2 and BOB.1 was evaluated by immunohistochemical staining of bone marrow samples from 83 cases of AML.
  • The expression patterns were correlated with t(8;21)(q22;q22), B cell-associated antigen expression, and AML subtype.
  • We confirmed the expression of PAX5 in AML with t(8;21)(q22;q22), but also demonstrated its expression in cases that express B-cell antigens but lack this translocation.
  • Although OCT-2 and BOB.1 were not associated with PAX5 expression, we report expression of OCT-2 in AML with myelomonocytic/monocytic maturation and BOB.1 in normal hematopoietic elements.
  • [MeSH-major] Antigens, CD / metabolism. B-Cell-Specific Activator Protein / metabolism. Leukemia, Myeloid / metabolism. Octamer Transcription Factor-2 / metabolism. Trans-Activators / metabolism
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Differentiation. Flow Cytometry. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Monocytes / metabolism. Monocytes / pathology. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Tissue Array Analysis

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  • (PMID = 17074681.001).
  • [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 / Antigens, CD; 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Octamer Transcription Factor-2; 0 / PAX5 protein, human; 0 / POU2AF1 protein, human; 0 / Trans-Activators
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12. 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.
  • The median latency to t-AML onset was 37 months (range, 11-126 months).
  • 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.
  • 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

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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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13. 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.
  • This study was conducted to determine the prognoses and treatment outcomes of patients with AML with this unique cytogenetic change.
  • A total of 22 patients with AML with t(8;21)(q22;q22) were studied.
  • Another 55 patients with AML with a normal karyotype were included for comparison of clinical outcomes.
  • 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.
  • Univariate analysis revealed that a higher platelet count (>15.10(9)/L) at diagnosis, a low white blood cell count (index < or =20), and hematopoietic stem cell transplantation (HSCT) as postremission therapy were associated with improved OS.
  • 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

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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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15. 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;.
  • (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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16. Bacher U, Schnittger S, Kern W, Trenn G, Weisser M, Haferlach T, Schoch C: Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22). Cancer Genet Cytogenet; 2006 Jul 15;168(2):172-4
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  • [Title] Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22).
  • We here report on an 48-year-old male patient with a primary diagnosis of acute myeloid leukemia (AML)-M2 with t(8;21)(q22;q22), who developed complete hematologic and molecular remission after induction chemotherapy.
  • Thirteen months later, he relapsed and showed an AML-M2 with t(3;21)(q26;q22).
  • Retrospectively, polymerase chain reaction (PCR) for AML1-EVI1 and EVI1 overexpression was performed on bone marrow and peripheral blood samples taken at diagnosis and during the first year after the first manifestation of AML to quantify the AML1-EVI1-positive clone.
  • In a bone marrow sample taken 25 days from diagnosis, PCR for AML1-EVI1 was negative, and EVI1 expression, as assessed by quantitative real-time PCR, was within the same range as that of healthy controls.
  • These data suggest that this patient developed a secondary therapy-related AML rather than a relapse.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843110.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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17. Mallo M, Espinet B, Salido M, Ferrer A, Pedro C, Besses C, Pérez-Vila E, Serrano S, Florensa L, Solé F: Gain of multiple copies of the CBFB gene: a new genetic aberration in a case of granulocytic sarcoma. Cancer Genet Cytogenet; 2007 Nov;179(1):62-5

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  • They are often associated with acute myeloid leukemia (AML) with monoblastic or myelomonocytic differentiation, including either AML M2 with t(8;21)(q22;q22) or AML M4Eo with inv(16)(p13q22).
  • We present a case diagnosed with GS associated with AML M4 that presented a normal karyotype with conventional cytogenetic analysis.
  • [MeSH-major] Core Binding Factor beta Subunit / genetics. Gene Dosage. Gene Duplication. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 16. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Middle Aged

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  • (PMID = 17981216.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit
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18. Huang L, Abruzzo LV, Valbuena JR, Medeiros LJ, Lin P: Acute myeloid leukemia associated with variant t(8;21) detected by conventional cytogenetic and molecular studies: a report of four cases and review of the literature. Am J Clin Pathol; 2006 Feb;125(2):267-72
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  • [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.
  • 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

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  • (PMID = 16393685.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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19. Giusiano S, Formisano-Tréziny C, Benziane A, Maroc N, Picard C, Hermitte F, Taranger-Charpin C, Gabert J: Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis. Int J Lab Hematol; 2010 Aug 1;32(4):398-409
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  • [Title] Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis.
  • Three major types of rearrangements are involved in acute myeloid leukemias (AML): t(8;21)(q22;q22), inv(16)(p13q22), and 11q23/MLL abnormalities.
  • Their precise identification becomes essential for diagnosis, prognosis, and therapeutic choices.
  • In this study, we propose a biochip-based assay integrated in a global strategy for identification of rare FT in AML, after fluorescence in situ hybridization detection, as described by the World Health Organization classification.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19930410.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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20. Valbuena JR, Medeiros LJ, Rassidakis GZ, Hao S, Wu CD, Chen L, Lin P: Expression of B cell-specific activator protein/PAX5 in acute myeloid leukemia with t(8;21)(q22;q22). Am J Clin Pathol; 2006 Aug;126(2):235-40
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  • [Title] Expression of B cell-specific activator protein/PAX5 in acute myeloid leukemia with t(8;21)(q22;q22).
  • The blasts of acute myeloid leukemia (AML) with t(8;21)(q22;q22) frequently express the B-cell antigen CD19, which is regulated by B cell-specific activator protein (BSAP) encoded by the PAX5 gene, a protein important for B-cell lineage commitment and development.
  • We assessed for BSAP expression in 28 AML cases with t(8;21) and 46 AML cases of other types.
  • CD19 was expressed by 26 (93%) cases of AML with t(8;21) and 1 AML case (2%) without t(8;21).
  • Immunostaining performed on bone marrow biopsy specimens demonstrated BSAP expression in all 28 AML cases with t(8;21): weak, 21; strong, 7.
  • By contrast, BSAP was expressed weakly in only 1 AML case without t(8;21).
  • Oct2 was expressed strongly in 12 of 16 AML cases with t(8;21) and 19 of 46 without t(8;21).
  • These results indicate that silencing of PAX5 is not required for commitment to myeloid differentiation and that BSAP expression in AML is found mainly in cases with t(8;21).
  • [MeSH-major] B-Cell-Specific Activator Protein / metabolism. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / metabolism. Chromosome Banding. Flow Cytometry. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques

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  • (PMID = 16891199.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
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21. 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).
  • After induction therapy, absolute transcript levels (below 10(-3), compared to Kasumi cell line), or a greater than 3 log decrease by comparison to diagnosis levels, were significant predictors of the absence of relapse (P=0.02 and P=0.02, respectively).
  • 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

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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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22. 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.
  • We examined the prognostic utility of serial bone marrow minimal residual disease (MRD) monitoring by RQ-PCR in a cohort of patients with CBF AML with long term clinical follow-up.
  • Twelve relapses occurred at a median of 11 months (range 4 - 17) from diagnosis.
  • RQ-PCR levels at diagnosis, post-induction chemotherapy and post-consolidation were not predictive of outcome.
  • 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).
  • A >or=1 log(10) rise in transcript levels strongly predicts subsequent morphologic relapse in CBF AML and therefore defines molecular relapse.
  • [MeSH-major] Core Binding Factors. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Neoplasm, Residual / diagnosis. Predictive Value of Tests. RNA, Messenger / analysis

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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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