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1. 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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2. 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.
  • Three patients were with refractory AML or relapsed, and two patients died within 10 months.
  • 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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3. Xiao Z, Liu S, Liu X, Yu M, Hao Y: Tetraploidy or near-tetraploidy clones with double 8;21 translocation: a non-random additional anomaly of acute myeloid leukemia with t(8;21)(q22;q22). Haematologica; 2005 Mar;90(3):413-4
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  • [Title] Tetraploidy or near-tetraploidy clones with double 8;21 translocation: a non-random additional anomaly of acute myeloid leukemia with t(8;21)(q22;q22).
  • We report on 6 patients with tetraploidy or near-tetraploidy acute myeloid leukemia (AML) with double t(8;21) (q22;q22) and review the literature on cases with the same cytogenetic abnormalities.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid / genetics. Polyploidy. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Clone Cells. Humans. Prognosis

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  • (PMID = 15749680.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
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4. 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.
  • Although he received allogeneic peripheral blood stem cell transplantation after the first remission, he died 9 months after the initial diagnosis due to relapse of the disease and graft-versus-host disease.
  • 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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5. Slavcheva V, Lukanov T, Balatsenko G, Angelova S, Antonov A, Bogdanov L, Tsvetkov N: Clinical case of acute myeloblastic leukemia with t(8;21)(q22;q22) in a patient with Klinefelter's syndrome. Hematol Rep; 2010 Jan 26;2(1):e11

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical case of acute myeloblastic leukemia with t(8;21)(q22;q22) in a patient with Klinefelter's syndrome.
  • We present the clinical case of a patient diagnosed with acute myelomonoblastic leukemia-M4 Eo (AML- M4), where by means of classic cytogenetics a karyotype was found corresponding to Klinefelter's syndrome.

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  • (PMID = 22184514.001).
  • [ISSN] 2038-8330
  • [Journal-full-title] Hematology reports
  • [ISO-abbreviation] Hematol Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3222265
  • [Keywords] NOTNLM ; Klinefelter's syndrome / genetics / leukemia / remission.
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6. Fortier JM, Payton JE, Cahan P, Ley TJ, Walter MJ, Graubert TA: POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature. Leukemia; 2010 May;24(5):950-7
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  • [Title] POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature.
  • The t(8;21)(q22;q22) translocation, present in approximately 5% of adult acute myeloid leukemia (AML) cases, produces the AML1/ETO (AE) fusion protein.
  • Dysregulation of the Pit/Oct/Unc (POU) domain-containing transcription factor POU4F1 is a recurring abnormality in t(8;21) AML.
  • POU4F1 is neither necessary nor sufficient for these AE-dependent properties, suggesting that it contributes to leukemia through novel mechanisms.
  • This expression signature was significantly enriched in human t(8;21) AML samples and was sufficient to cluster t(8;21) AML samples in an unsupervised hierarchical analysis.
  • Among the most highly differentially expressed genes, half are known AML1/ETO targets, implying that the unique transcriptional signature of t(8;21) AML is, in part, attributable to POU4F1 and not AML1/ETO itself.
  • These genes provide novel candidates for understanding the biology and developing therapeutic approaches for t(8;21) AML.

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  • (PMID = 20376082.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / P01 CA101937-010006; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / P30 CA91842
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / POU4F1 protein, human; 0 / Pou4f1 protein, mouse; 0 / RNA, Messenger; 0 / Transcription Factor Brn-3A
  • [Other-IDs] NLM/ NIHMS183891; NLM/ PMC2868953
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7. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Iyer RR, Parikh EH, Shukla SN, Shah PM, Bakshi SR: A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21). Indian J Hum Genet; 2008 Jan;14(1):20-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21).
  • t(8;21)(q22;q22) is the most frequently observed karyotypic abnormality associated with acute myeloid leukemia (AML), specifically in FAB-M2.
  • Short-term unstimulated bone marrow (BM) and peripheral blood lymphocyte culture showed 47,XX, +4,t(8;21) in all metaphase plates; and interphase and metaphase results of AML-ETO fusion was positive and trisomy of 4 was confirmed with WCP probes.
  • Trisomy 4 in AML with t(8;21) is a rare numerical abnormality.

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  • (PMID = 20300287.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2840780
  • [Keywords] NOTNLM ; Acute myeloid leukemia / cytogenetics / fluorescence in situ hybridization
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8. 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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9. 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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. 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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12. 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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13. 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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14. 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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15. 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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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.
  • 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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17. Kawakami K, Nishii K, Hyou R, Watanabe Y, Nakao M, Mitani H, Murata T, Monma F, Yamamori S, Hosokai N, Miura I: A case of acute myeloblastic leukemia with a novel variant of t(8;21)(q22;q22). Int J Hematol; 2008 Jan;87(1):78-82
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  • [Title] A case of acute myeloblastic leukemia with a novel variant of t(8;21)(q22;q22).
  • We encountered a case of acute myeloblastic leukemia (AML), with extramedullary leukemia (EML) and a masked type of the variant translocation t(8;21)(q22;q22).
  • Morphologically, the AML M2 subtype according to the French-American-British (FAB) classification was present.
  • The initial karyotypic interpretation was t(8;9)(q22;q34) on G-banding.
  • Multiplex-fluorescence in situ hybridization (multiplex-FISH) analysis revealed a three-way translocation involving chromosomes 8, 9, and 21, and identified a masked type of variant t(8;21)q22;q22) translocation.
  • The karyotype was finally determined as 45,X,-Y,der(8)t(8;21)(q22;q22), der(9)(8;9)(q22;q34), and der(21)t(9;21)(q34;q22).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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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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18. Kokate P, Ahmad F, Dalvi R, Das BR, Mandava S: Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype. Cancer Genet Cytogenet; 2008 Jul;184(1):52-6
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  • [Title] Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype.
  • Acute myeloid leukemia (AML) is a clinically and molecularly heterogeneous disease characterized by the aberrant proliferation of myeloid stem cells, reduced apoptosis and blockage in cellular differentiation.
  • The present report describes the results of hematological, cytogenetic, and fluorescence in situ hybridization (FISH) analysis in a 25-year-old man diagnosed with AML-M2.
  • Cytogenetic as well as FISH analysis revealed a complex translocation involving four chromosomes, with the karyotype 45,-Y,der(X)t(X;8)(p21;q22),der(8)t(8;21)(q22;q22),ins(15;21)(q15;q22.2q22.3),der(21)t(8;21)(q22;q22).
  • Using a dual-color FISH test with RUNX1T1 and RUNX1 probes, we demonstrated an RUNX1/RUNX1T1 fusion signal on the derivative chromosome 8, establishing this translocation as a novel complex variant of t(8;21)(q22;q22).
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18558290.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. 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.
  • 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

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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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20. 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.
  • Clinically, this type of AML usually shows some specific characteristics and has a good response to chemotherapy with a high remission rate and a relatively long median survival.
  • 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.
  • 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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21. 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).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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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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22. Ahmad F, Kokate P, Chheda P, Dalvi R, Das BR, Mandava S: Molecular cytogenetic findings in a three-way novel variant of t(1;8;21)(p35;q22;q22): a unique relocation of the AML1/ETO fusion gene 1p35 in AML-M2. Cancer Genet Cytogenet; 2008 Jan 15;180(2):153-7
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  • [Title] Molecular cytogenetic findings in a three-way novel variant of t(1;8;21)(p35;q22;q22): a unique relocation of the AML1/ETO fusion gene 1p35 in AML-M2.
  • Acute myeloid leukemia (AML) is a malignant neoplasm of hematopoietic stem cells characterized by an abnormal proliferation of myeloid precursors, a reduced rate of apoptosis, and an arrest in cellular differentiation.
  • The present report deals with the results of hematologic, immunophenotypic, cytogenetic, fluorescence in situ hybridization (FISH), and molecular analyses of a 53-year-old female patient diagnosed with AML-M2.
  • Cytogenetic and FISH analysis revealed a complex translocation involving three chromosomes showing t(1;8;21)(p35;q22;q22).
  • To the best of our knowledge, this is the first report about the relocation of the AML1/ETO fusion gene to the 1p35 rather than der(8), suggesting the presence of a novel variant of t(8;21)(q22;q22) in the observed patient.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18206543.001).
  • [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 / Oncogene Proteins, Fusion
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23. 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.
  • RUNX1, which regulates a gene for hematopoiesis, is frequently mutated in AML and, in this study, one out of three patients showed the mutation R174Q in RUNX1.
  • 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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24. Tirado CA, Chena W, Valdez FJ, Henderson S, Smart RL, Doolittle J, Garcia R, Patel S, Holdridge S, Chastain C, Auchus M, Collins RH: A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation. J Assoc Genet Technol; 2009;35(3):88-92
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  • [Title] A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation.
  • The t(8;21)/RUNX1-RUNX1T1 is found in ~5 percent of cases of acute myeloid leukemia (AML) and in 10 percent of the prior AML with maturation (M2) category of the French-American-British (FAB) classification.
  • While AML with t(8;21) is considered a distinct entity with a favorable prognosis, the clinical consequence of variant translocations is less well defined.
  • In this report we described a 45 year-old male patient having a diagnosis of AML-M2 with morphologic and immunophenotypic features suggestive of t(8;21).
  • Further fluorescence in situ hybridization (FISH) studies using the AML1/ETO and the p58 probes from Abbott Molecular, demonstrated a three-way translocation between chromosomes 1, 21, and 8, with single fusion of RUNX1-RUNX1T1 on the derivative chromosome 8 [t(1;21;8)(p36.1;q22;q22)].

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  • (PMID = 19738329.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. 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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26. Gong JY, Liu XP, Li CW, Zhao XC, Dai Y, Qin S, Xiao JG, Huang Q, Xu FY, Wang F, Cui W, Liu SH, Wang JX: [Clinical and laboratory study of a complex translocation t (6; 21; 8) (p22; q22; q22) in two patients with acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):314-7
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  • [Title] [Clinical and laboratory study of a complex translocation t (6; 21; 8) (p22; q22; q22) in two patients with acute myeloid leukemia].
  • OBJECTIVE: To investigate the clinical and laboratory characteristics of a complex translocation t (6; 21;.
  • 8) (p22; q22;.
  • q22) in two patients with acute myeloid leukemia.
  • 21) (p22; q22; q22), which was confirmed by interphase and metaphase FISH and AML1/ETO fusion transcript was detected by RT-PCR.
  • Both the two patients were diagnosed as AML-M(2), but with different immunophenotype and therapeutic outcome.
  • CONCLUSION: The t (6; 21;.
  • 8) (p22; q22;.
  • q22) is a rare variant of complex translocation of t (8;.
  • 21) (q22; q22).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16875580.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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27. 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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28. 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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29. Kim J, Park TS, Song J, Lee KA, Hong DJ, Min YH, Cheong JW, Choi JR: Detection of FUS-ERG chimeric transcript in two cases of acute myeloid leukemia with t(16;21)(p11.2;q22) with unusual characteristics. Cancer Genet Cytogenet; 2009 Oct 15;194(2):111-8
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  • [Title] Detection of FUS-ERG chimeric transcript in two cases of acute myeloid leukemia with t(16;21)(p11.2;q22) with unusual characteristics.
  • Reciprocal t(16;21)(p11;q22) is a rare chromosomal abnormality in acute myeloid leukemia (AML).
  • Here we report two cases of AML with t(16;21)(p11.2;q22) showing unusual characteristics, and address the clinical, hematological, and molecular aspects of leukemia with t(16;21), along with a review of the literature.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic

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  • (PMID = 19781443.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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30. Li HY, Yue H, Wei XD, Zhu XH, Zhang YL, Zhang LN, Liu YY, Wang P, Fang BJ, Li YF, Song YP: [The efficacy of high-dose cytarabine for patients with t(8;21) AML and with normal karyotype AML]. Zhonghua Xue Ye Xue Za Zhi; 2008 Feb;29(2):110-2
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  • [Title] [The efficacy of high-dose cytarabine for patients with t(8;21) AML and with normal karyotype AML].
  • OBJECTIVE: To compare the efficacy of high-dose cytarabine (HD-Ara-C) based chemotherapy for post-remission treatment in patients with t(8;21) (q22;q22) AML-M2 and those with normal karyotype AML-M2.
  • METHODS: AML-M2 patients were grouped into with (21 cases) or without (23 cases) t(8;21) (q22;q22) karyotype groups.
  • 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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31. 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).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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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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32. 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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33. Park IJ, Park JE, Kim HJ, Jung HJ, Lee WG, Cho SR: Acute myeloid leukemia with t(16;21)(q24;q22) and eosinophilia: case report and review of the literature. Cancer Genet Cytogenet; 2010 Jan 1;196(1):105-8
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  • [Title] Acute myeloid leukemia with t(16;21)(q24;q22) and eosinophilia: case report and review of the literature.
  • The t(16;21)(q24;q22), a rare chromosomal translocation involving chromosome 21 in de novo and therapy-related acute myeloid leukemia (AML), produces a RUNX1-CBFA2T3 fusion gene (previously AML1-MTG16) fusion gene.
  • The translocation has been reported in 20 patients with AML, with eosinophilia present in 3 cases.
  • Here we report a pediatric case of t(16;21)(q24;q22) in de novo AML with eosinophilia and suggest that eosinophilia is a hematologic characteristic of at least a subpopulation of AML with t(16;21)(q24;q22).
  • A 4-year-old Korean girl was admitted with complaints of pale appearance and dizziness, and was diagnosed with acute myelomonocytic leukemia.
  • The karyotype was 47,XX, + 8,t(16;21)(q24;q22)[18]/46,XX[2].
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Translocation, Genetic
  • [MeSH-minor] Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Myeloid, Acute. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19963144.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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34. 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

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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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35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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36. De Braekeleer E, Douet-Guilbert N, Le Bris MJ, Morel F, Férec C, De Braekeleer M: RUNX1-MTG16 fusion gene in acute myeloblastic leukemia with t(16;21)(q24;q22): case report and review of the literature. Cancer Genet Cytogenet; 2008 Aug;185(1):47-50
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  • [Title] RUNX1-MTG16 fusion gene in acute myeloblastic leukemia with t(16;21)(q24;q22): case report and review of the literature.
  • A diagnosis of acute myeloid leukemia (AML) type 2 (FAB classification) was made.
  • Banding cytogenetic techniques performed on bone marrow cells showed a 48,XX,+8,+9,del(9)(q22q33)x2 ,t(16;21)(q24;q22)[20]/46,XX[2] karyotype.
  • The t(16;21)(q24;q22) has been described in 16 AML cases, including ours.
  • The significant homology between MGT16 and MTG8 suggests that the RUNX1-MTG16 fusion gene induced by the t(16;21)(q24;q22) is a variant of the RUNX1-MTG8 that shares similar activity.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Phosphoproteins / genetics. Repressor Proteins / genetics. Translocation, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 18656694.001).
  • [ISSN] 1873-4456
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFA2T3 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 22
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37. Moore SD, Offor O, Ferry JA, Amrein PC, Morton CC, Dal Cin P: ELF4 is fused to ERG in a case of acute myeloid leukemia with a t(X;21)(q25-26;q22). Leuk Res; 2006 Aug;30(8):1037-42
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  • [Title] ELF4 is fused to ERG in a case of acute myeloid leukemia with a t(X;21)(q25-26;q22).
  • We report a novel chromosomal translocation in AML, t(X;21)(q25-26;q22), resulting in a fusion transcript between two ETS domain family members, ELF4 (at Xq25) and ERG (at 21q22).
  • ERG has been associated previously with other fusion partners, specifically FUS and EWSR1, and implicated in both AML and Ewing's sarcoma.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, X / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion. Trans-Activators / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Chromosome Mapping / methods. Fatal Outcome. Female. Humans. In Situ Hybridization, Fluorescence / methods. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Translocation, Genetic

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  • (PMID = 16303180.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006516
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ELF4 protein, human; 0 / ERG protein, human; 0 / Oncogene Proteins, Fusion; 0 / Trans-Activators; 0 / Transcription Factors
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38. 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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39. 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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40. Lafiura KM, Bielawski DM, Posecion NC Jr, Ostrea EM Jr, Matherly LH, Taub JW, Ge Y: Association between prenatal pesticide exposures and the generation of leukemia-associated T(8;21). Pediatr Blood Cancer; 2007 Oct 15;49(5):624-8
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  • [Title] Association between prenatal pesticide exposures and the generation of leukemia-associated T(8;21).
  • BACKGROUND: This study was designed to investigate the relationship between prenatal pesticide exposures and the generation of leukemia-associated t(8;21)(q22;q22), one of the most common cytogenetic abnormalities in childhood acute myeloid leukemia (AML).
  • The generation of t(8;21) was determined in the corresponding umbilical cord blood samples by detection of the AML1-ETO fusion transcripts derived from t(8;21) using nested RT-PCR.
  • Levels for the AML1-ETO fusion transcripts were quantitated by real-time RT-PCR in the t(8;21) positive cord blood samples.
  • RESULTS: In the present study using umbilical cord blood samples obtained from infants whose prenatal exposure to the pesticide, propoxur, was determined by meconium analysis, we showed that (i) incidence of t(8;21) in the exposed group was two-fold higher than that in the unexposed group; and (ii) the levels for AML1-ETO fusion transcripts resulting from t(8;21) positively correlated with propoxur concentrations in meconium.
  • Similar heterogeneity in the fusion transcripts was detected in the t(8;21) positive cord blood samples as in our previous study with t(8;21) AML patients.
  • CONCLUSION: These results further confirm the prenatal origin of t(8;21) and establish a significant correlation between prenatal pesticide exposures and the generation of t(8;21).
  • They suggest that prenatal pesticide exposures may be causal factors for the generation of leukemia-associated chromosomal translocations.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia / etiology. Propoxur / analysis. Translocation, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2007 Oct 15;49(5):607-8 [17712841.001]
  • (PMID = 17610268.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA92308; United States / NICHD NIH HHS / HD / HD039428
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pesticides; BFH029TL73 / Propoxur
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41. Yan M, Kanbe E, Peterson LF, Boyapati A, Miao Y, Wang Y, Chen IM, Chen Z, Rowley JD, Willman CL, Zhang DE: A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis. Nat Med; 2006 Aug;12(8):945-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis.
  • The t(8;21)(q22;q22) translocation is one of the most common genetic abnormalities in acute myeloid leukemia (AML), identified in 15% of all cases of AML, including 40-50% of FAB M2 subtype and rare cases of M0, M1 and M4 subtypes.
  • Although alterations of gene expression and hematopoietic cell proliferation have been reported in the presence of AML1-ETO, its expression does not lead to the development of leukemia.
  • Expression of AML1-ETO9a leads to rapid development of leukemia in a mouse retroviral transduction-transplantation model.
  • More importantly, coexpression of AML1-ETO and AML1-ETO9a results in the substantially earlier onset of AML and blocks myeloid cell differentiation at a more immature stage.
  • [MeSH-major] Alternative Splicing. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 16892037.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA096735; United States / NCI NIH HHS / CA / CA104509; United States / NHLBI NIH HHS / HL / F32HL079900
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
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42. 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.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics

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

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  • (PMID = 16876862.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P 30 CA33572-20; United States / NCI NIH HHS / CA / P01 CA030206-24
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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44. Kim H, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ: [A Case of Acute Myeloid Leukemia with Masked t(8;21).]. Korean J Lab Med; 2006 Oct;26(5):338-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A Case of Acute Myeloid Leukemia with Masked t(8;21).].
  • We report a case that revealed the characteristics of acute myeloblastic leukemia with maturation (AML-M2) on the morphology of the bone marrow biopsy and 45,X,-Y in conventional cytogenetic study, but was confirmed to have a typical AML1/ETO translocation by molecular studies using reverse transcriptase polymerase chain reaction and fluorescence in situ hybridization.
  • Insertion of ETO gene on chromosome 8 into chromosome 21 in this patient resulted in the development of the chimeric gene, AML1/ETO, on the long arm of chromosome 21.
  • Our final report on the patient's karyotype: 45,X,-Y.ish ins(21;8)(q22;q22q22)(AML1 +,ETO +;ETO +,AML1-).
  • In case typical morphologic features compatible with recurrent cytogenetic abnormalities are shown, molecular studies in addition to conventional cytogenetic study might be required to confirm the diagnosis.

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  • (PMID = 18156748.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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45. Kelly MJ, Meloni-Ehrig AM, Manley PE, Altura RA: Poor outcome in a pediatric patient with acute myeloid leukemia associated with a variant t(8;21) and trisomy 6. Cancer Genet Cytogenet; 2009 Feb;189(1):48-52
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  • [Title] Poor outcome in a pediatric patient with acute myeloid leukemia associated with a variant t(8;21) and trisomy 6.
  • RUNX1T1/RUNX1 (formerly ETO/AML1) is a molecular marker that is usually associated with a favorable outcome in both pediatric and adult patients with acute myeloid leukemia (AML).
  • We describe a 10-year-old girl with AML associated with an RUNX1T1/RUNX1 fusion.
  • 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.
  • As a sole abnormality, it has been associated mainly with myelodysplastic syndrome and AML.
  • 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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46. LaFiura KM, Edwards H, Taub JW, Matherly LH, Fontana JA, Mohamed AN, Ravindranath Y, Ge Y, Children's Oncology Group: Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children's Oncology Group. Oncogene; 2008 Aug 21;27(36):4933-42
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  • [Title] Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children's Oncology Group.
  • t(8;21)(q22;q22) results in the AML1-ETO (A1E) fusion gene and is a common cytogenetic abnormality in acute myeloid leukemia (AML).
  • By RT-PCR amplifications and DNA sequencing, numerous in-frame and out-of-frame AML1b-ETO and AML1c-ETO transcripts were identified in 13 pediatric t(8;21) AMLs, likely resulting from alternate splicing, internal deletions and/or breakpoint region insertions involving both the AML1 (RUNX1) and ETO regions.
  • These structure alterations were found in AML1c-ETO but not AML1b-ETO transcripts in two adult t(8;21) AMLs.
  • Our results demonstrate a remarkable and unprecedented heterogeneity in A1E fusion transcripts in t(8;21) myeloblasts and suggest that synthesis of alternate A1E transcript and protein forms can significantly impact the regulation of AML1 responsive genes.

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  • (PMID = 18469864.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092308; United States / NCI NIH HHS / CA / CA30969; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / R01 CA076641; United States / NCI NIH HHS / CA / CA76641; United States / NCI NIH HHS / CA / P30 CA022453; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA92308
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS505499; NLM/ PMC3763903
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47. 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


48. Albano F, Specchia G, Anelli L, Liso A, Zagaria A, Santoro A, Mirto S, Liso V, Rocchi M: Submicroscopic deletions in an acute myeloid leukemia case with a four-way t(8;11;16;21). Leuk Res; 2005 Jul;29(7):855-8
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  • [Title] Submicroscopic deletions in an acute myeloid leukemia case with a four-way t(8;11;16;21).
  • The t(8;21)(q22;q22) rearrangement is observed in about 15% of acute myelocitic leukemia (AML) cases, while variant t(8;21) translocations are detected in 6-10% of AML patients positive for the 5'RUNX1/3'CBFA2T1 fusion gene.
  • We report a detailed molecular cytogenetic analysis of a four-way variant t(8;11;16;21)(q22;q14;q12;q22) performed by fluorescence in situ hybridization with specific BAC and PAC clones.
  • The study demonstrated the loss of several megabases belonging to chromosomes 11 and 16 whereas no deletion was detected on der(21).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Sequence Deletion. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Bone Marrow Cells / pathology. Humans. In Situ Hybridization, Fluorescence

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  • (PMID = 15927680.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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49. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • CONCLUSION: We report for the first time that mutKIT, and particularly mutKIT17, confer higher relapse risk, and both mutKIT17 and mutKIT8 appear to adversely affect OS in AML with inv(16).
  • We also confirm the adverse impact of mutKIT on relapse risk in t(8;21) AML.
  • We suggest that patients with core-binding factor AML should be screened for mutKIT at diagnosis for both prognostic and therapeutic purposes, given that activated KIT potentially can be targeted with novel tyrosine kinase inhibitors.
  • [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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50. Harrison CJ, Hills RK, Moorman AV, Grimwade DJ, Hann I, Webb DK, Wheatley K, de Graaf SS, van den Berg E, Burnett AK, Gibson BE: Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12. J Clin Oncol; 2010 Jun 1;28(16):2674-81
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  • [Title] Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12.
  • PURPOSE: Karyotype is an independent indicator of prognosis in acute myeloid leukemia (AML) that is widely applied to risk-adapted therapy.
  • Because AML is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.
  • The core binding factor leukemias with the translocations t(8;21)(q22;q22) and inv(16)(p13q22) occurred at incidences of 14% and 7%, respectively, predominantly in older children, and their prognosis was favorable.
  • CONCLUSION: Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with AML, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality


51. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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52. 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).
  • Frequent genetic abnormalities were, loss of a sex chromosome (56/99, 56.5%) and del(9)(q22) (24/99, 24.2%).
  • 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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53. Lasa A, Carricondo MT, Carnicer MJ, Perea G, Aventín A, Nomdedeu JF: A new D816 c-KIT gene mutation in refractory AML1-ETO leukemia. Haematologica; 2006 Sep;91(9):1283-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new D816 c-KIT gene mutation in refractory AML1-ETO leukemia.
  • One of the most common genetic events in acute myeloid leukemia (AML) is the t(8;21) (q22;q22) translocation, which contributes to leukemic transformation.
  • Secondary genetic alterations such as mutations in receptor tyrosine kinases are thus required to induce overt AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit. Leukemia, Myeloid / genetics. Mutation. Oncogene Proteins, Fusion. Proto-Oncogene Proteins c-kit / genetics

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  • (PMID = 16956837.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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54. 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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55. 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 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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56. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • 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%).
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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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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57. 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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  • [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.
  • Both cases were thought to represent therapy-related AML because the patients had previously received combination chemotherapy including epipodophyllotoxin, anthracycline, and alkylating agents for the ATL.
  • 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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58. Zhu Q, Hu JP, Jia PM, Wang ZY, Tong JH: [cAMP analogue 8-CPT-cAMP inducing differentiation in the M2b subtype of acute myeloid leukemia cell line Kasumi-1]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Feb;16(1):44-7
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  • [Title] [cAMP analogue 8-CPT-cAMP inducing differentiation in the M2b subtype of acute myeloid leukemia cell line Kasumi-1].
  • This study was aimed to investigate the possible effects of cyclic adenosine monophosphate (cAMP) analogue 8-(4-chlorophenylthio) adenosine 3', 5'-cyclic monophosphate (8-CPT-cAMP) on the M(2b) subtype of acute myeloid leukemia (AML-M(2b)) cells.
  • AML-M(2b) is characterized by the non-random chromosome translocation t (8;.
  • 21) (q22; q22), through which AML1 (acute myeloid leukemia 1) gene on chromosome 21 is fused with ETO (eight twenty-one) gene on chromosome 8, coding correspondent AML1-ETO fusion protein, which plays a crucial role in the leukemogenesis of AML-M(2b).
  • The AML-M(2b) cell line Kasumi-1 cells were used as an in vitro model.
  • This results may provide experimental and theoretical basis for the breakthrough of differentiation-induced therapy extended to another leukemia.

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  • (PMID = 18315898.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Thionucleotides; 41941-66-6 / 8-((4-chlorophenyl)thio)cyclic-3',5'-AMP; E0399OZS9N / Cyclic AMP
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59. 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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60. Poland KS, Shardy DL, Azim M, Naeem R, Krance RA, Dreyer ZE, Neeley ES, Zhang N, Qiu YH, Kornblau SM, Plon SE: Overexpression of ZNF342 by juxtaposition with MPO promoter/enhancer in the novel translocation t(17;19)(q23;q13.32) in pediatric acute myeloid leukemia and analysis of ZNF342 expression in leukemia. Genes Chromosomes Cancer; 2009 Jun;48(6):480-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of ZNF342 by juxtaposition with MPO promoter/enhancer in the novel translocation t(17;19)(q23;q13.32) in pediatric acute myeloid leukemia and analysis of ZNF342 expression in leukemia.
  • We report a novel translocation t(17;19)(q22;q13.32) found in 100% of blast cells from a pediatric acute myeloid leukemia (AML) patient.
  • Fluorescence in situ hybridization and vectorette polymerase chain reaction were used to precisely map the chromosomal breakpoint located on the derivative chromosome 17 at 352 bp 5' of MPO, encoding myeloperoxidase a highly expressed protein in myeloid cells, and 2,085 bp 5' of ZNF342 on 19q, encoding a transcription factor expressed in human stem cells and previously implicated in mouse models of leukemia.
  • Analysis of RNA levels from the patient sample revealed significant overexpression of ZNF342, potentially contributing to AML formation.
  • This is the first report of a translocation in myeloid leukemia occurring only in the promoter/enhancer regions of the two genes involved, similar to translocations commonly found in lymphoid malignancies.
  • Analysis of ZNF342 protein levels in a large dataset of leukemia samples by reverse phase protein array showed that higher levels of ZNF342 expression in acute lymphoblastic leukemia was associated with poorer outcome (P = 0.033).
  • In the myeloid leukemia samples with the highest ZNF342 expression, there was overrepresentation of FLT3 internal tandem duplication (P = 0.0016) and AML subtype M7 (P = 0.0002).
  • Thus, overexpression of ZNF342 by translocation or other mechanisms contributes to leukemia biology in multiple hematopoietic compartments.

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  • (PMID = 19255975.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NHLBI NIH HHS / HL / T32HL066991; United States / NIDDK NIH HHS / DK / T32 DK60445; United States / NIDDK NIH HHS / DK / T32 DK060445; United States / NHLBI NIH HHS / HL / T32 HL066991; United States / NCI NIH HHS / CA / 2P01CA55164-05A1; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors; EC 1.11.1.7 / Peroxidase
  • [Other-IDs] NLM/ NIHMS378346; NLM/ PMC3385932
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61. 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.
  • Furthermore, despite being considered as a more favorable AML risk group, only approximately half of the CBF AML patients are cured with current therapy, indicating the need for improved therapeutic approaches.
  • This review summarizes the most recent laboratory and clinical discoveries relevant to this subset of AML and how they are being applied for in an effort to improve the cure rate in patients with the disease.
  • [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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62. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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.
  • RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.
  • 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

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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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63. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in molecular genetics and treatment of core-binding factor acute myeloid leukemia.
  • PURPOSE OF REVIEW: Core-binding factor (CBF) acute myeloid leukemia (AML) is among the most common cytogenetic subtypes of AML, being detected in approximately 13% of adults with primary disease.
  • Although CBF-AML is associated with a relatively favorable prognosis, only one-half of the patients are cured.
  • Herein we review recent discoveries of genetic and epigenetic alterations in CBF-AML that may represent novel prognostic markers and therapeutic targets and lead to improvement of the still disappointing clinical outcome of these patients.
  • RECENT FINDINGS: Several acquired gene mutations and gene-expression and microRNA-expression changes that occur in addition to t(8;21)(q22;q22) and inv(16)(p13q22)/t(16;16)(p13;q22), the cytogenetic hallmarks of CBF-AML, have been recently reported.
  • Alterations that may represent cooperative events in CBF-AML leukemogenesis include mutations in the KIT, FLT3, JAK2 and RAS genes, haploinsufficiency of the putative tumor suppressor genes TLE1 and TLE4 in t(8;21)-positive patients with del(9q), MN1 overexpression in inv(16) patients, and epigenetic and posttranscriptional silencing of CEBPA.
  • Genome-wide gene-expression and microRNA-expression profiling identifying subgroups of CBF-AML patients with distinct molecular signatures, different clinical outcomes, or both, have also been reported.
  • SUMMARY: Progress has been made in delineating the genetic basis of CBF-AML that will likely result in improved prognostication and development of novel, risk-adapted therapeutic approaches.

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

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  • (PMID = 18648004.001).
  • [ISSN] 1052-6773
  • [Journal-full-title] Journal of the National Cancer Institute. Monographs
  • [ISO-abbreviation] J. Natl. Cancer Inst. Monographs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors
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65. Mrózek K: Cytogenetic, molecular genetic, and clinical characteristics of acute myeloid leukemia with a complex karyotype. Semin Oncol; 2008 Aug;35(4):365-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic, molecular genetic, and clinical characteristics of acute myeloid leukemia with a complex karyotype.
  • Patients with acute myeloid leukemia (AML) harboring three or more acquired chromosome aberrations in the absence of the prognostically favorable t(8;21)(q22;q22), inv(16)(p13q22)/t(6;16)(p13;q22), and t(15;17)(q22;q21) aberrations form a separate category - AML with a complex karyotype.
  • They constitute 10% to 12% of all AML patents, with the incidence of complex karyotypes increasing with the more advanced age.

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  • (PMID = 18692687.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 77658; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA 16058; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA 101140; United States / NCI NIH HHS / CA / P30 CA016058
  • [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] 83
  • [Other-IDs] NLM/ NIHMS66054; NLM/ PMC3640813
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66. Braoudaki M, Papathanassiou C, Katsibardi K, Tourkadoni N, Karamolegou K, Tzortzatou-Stathopoulou F: The frequency of NPM1 mutations in childhood acute myeloid leukemia. J Hematol Oncol; 2010;3:41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The frequency of NPM1 mutations in childhood acute myeloid leukemia.
  • BACKGROUND: Mutations in the nucleophosmin (NPM1) gene have been solely associated with childhood acute myeloid leukemia (AML).
  • We evaluated the frequency of NPM1 mutations in childhood AML, their relation to clinical and cytogenetic features and the presence of common FLT3 and RAS mutations.
  • FLT3/ITD mutations were observed in 12% of the cases and in one NPM1-mutated case bearing also t(8;21) (q22;q22).
  • The role of different types of NPM1 mutations, either individually or in the presence of other common gene mutations may be essential for childhood AML prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics

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  • (PMID = 20979630.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ PMC2988697
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67. Ahn EY, Yan M, Malakhova OA, Lo MC, Boyapati A, Ommen HB, Hines R, Hokland P, Zhang DE: Disruption of the NHR4 domain structure in AML1-ETO abrogates SON binding and promotes leukemogenesis. Proc Natl Acad Sci U S A; 2008 Nov 4;105(44):17103-8
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  • AML1-ETO is generated from t(8;21)(q22;q22), which is a common form of chromosomal translocation associated with development of acute myeloid leukemia (AML).
  • Although full-length AML1-ETO alone fails to promote leukemia because of its detrimental effects on cell proliferation, an alternatively spliced isoform, AML1-ETO9a, without its C-terminal NHR3/NHR4 domains, strongly induces leukemia.
  • However, full-length AML1-ETO is a major form of fusion product in many t(8;21) AML patients, suggesting additional molecular mechanisms of t(8;21)-related leukemogenesis.
  • Here, we report that disruption of the zinc-chelating structure in the NHR4 domain of AML1-ETO by replacing only one critical amino acid leads to rapid onset of leukemia, demonstrating that the NHR4 domain with the intact structure generates inhibitory effects on leukemogenesis.
  • In t(8;21) AML patient-derived primary leukemic cells and cell lines, abnormal cytoplasmic localization of SON was detected, which may keep cells proliferating in the presence of full-length AML1-ETO.

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  • (PMID = 18952841.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096735; United States / NCI NIH HHS / CA / R01 CA104509; United States / NCI NIH HHS / CA / CA096735; United States / NCI NIH HHS / CA / CA104509
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / SON protein, human
  • [Other-IDs] NLM/ PMC2579385
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68. Osman D, Gobert V, Ponthan F, Heidenreich O, Haenlin M, Waltzer L: A Drosophila model identifies calpains as modulators of the human leukemogenic fusion protein AML1-ETO. Proc Natl Acad Sci U S A; 2009 Jul 21;106(29):12043-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(8:21)(q22;q22) translocation is 1 of the most common chromosomal abnormalities linked to acute myeloid leukemia (AML).
  • This fusion protein acts primarily by interfering with endogenous AML1 function during myeloid differentiation, although relatively few genes are known that participate with AML1-ETO during leukemia progression.
  • Reminiscent of what is observed in AML, AML1-ETO specifically inhibited the differentiation of the blood cell lineage whose development depends on the RUNX factor Lozenge (LZ) and induced increased numbers of LZ(+) progenitors.
  • Remarkably, calpain inhibition triggered AML1-ETO degradation and impaired the clonogenic potential of the human t(8;21) leukemic blood cell line Kasumi-1.
  • Therefore Drosophila provides a promising genetically tractable model to investigate the conserved basis of leukemogenesis and to open avenues in AML therapy.

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  • (PMID = 19581587.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Drosophila Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / lozenge protein, Drosophila; EC 3.4.22.- / CalpB protein, Drosophila; EC 3.4.22.- / Calpain
  • [Other-IDs] NLM/ PMC2715513
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69. 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.
  • Cytogenetic findings separate AML patients into three broad prognostic categories: favorable, intermediate and adverse.
  • In many instances, patients with specific cytogenetic findings, e.g., those with a normal karyotype or those with either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22) [collectively referred to as core-binding factor (CBF) AML] can be further subdivided into prognostic categories based on the presence or absence of particular gene mutations or changes in gene expression.
  • In this article, we briefly review major cytogenetic prognostic categories and discuss molecular genetic findings of prognostic significance in two of the largest cytogenetic groups of patients with AML, namely AML with a normal karyotype and CBF AML.

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  • (PMID = 17124057.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA77658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 48
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70. Fenske TS, Pengue G, Graubert TA: Dominant negative effects of the AML1/ETO fusion oncoprotein. Cell Cycle; 2005 Jan;4(1):33-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(8;21)(q22;q22) translocation, present in 10-15% of acute myeloid leukemia (AML) cases results in the production of the AML1/ETO fusion protein.
  • Expression of AML1/ETO in patients or mouse models is not sufficient to induce AML.
  • Despite convincing evidence that AML1/ETO is directly involved in the pathogenesis of AML, the underlying mechanism is not well understood.
  • Genetic and biochemical experiments suggest that AML1/ETO is a dominant inhibitor of the core binding factor (CBF) transcription complex that includes AML1 (RUNX1), the N-terminal fusion partner in the t(8;21).
  • The dominant negative characteristics of AML1/ETO may be important for AML pathogenesis and may provide a molecular target for therapeutic intervention.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. Leukemia, Myeloid / etiology. Oncogene Proteins, Fusion / physiology
  • [MeSH-minor] Acute Disease. Animals. Ataxin-1. Ataxins. Core Binding Factor alpha Subunits / genetics. Core Binding Factor alpha Subunits / physiology. DNA, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, Dominant. Genes, Neoplasm. Hematopoiesis / genetics. Humans. Mice. Mice, Transgenic. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / physiology. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Translocation, Genetic

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  • (PMID = 15611635.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / ATXN1 protein, human; 0 / Ataxin-1; 0 / Ataxins; 0 / Atxn1 protein, mouse; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor alpha Subunits; 0 / DNA, Neoplasm; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion
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71. El-Sissy AH, El-Mashari MA, Bassuni WY, El-Swaayed AF: Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia. J Egypt Natl Canc Inst; 2006 Sep;18(3):244-9
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  • [Title] Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia.
  • BACKGROUND: Immunophenotyping improves both accuracy and reproducibility of acute leukemia classification and is considered particularly useful for identifying aberrant lineage association of acute leukemia, biphenotypic and bilineal acute leukemia, as well as monitoring minimal residual disease.
  • THE AIM OF OUR STUDY: Is to determine aberrant lymphoid antigen expression in Saudi acute myeloid leukemia (AML), correlate them with FAB subtypes, evaluate early surface markers CD7 and CD56, and to investigate the role of cytoplasmic CD79a (a B cell marker that is assigned a high score of 2.0 in the WHO classification).
  • PATIENTS AND METHODS: Thirty four newly diagnosed AML cases were included in this study, 47% showed aberrant lymphoid antigen expression.
  • 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).
  • CONCLUSION: Minimal residual disease in AML is very difficult to trace, detection of aberrant expression of lymphoid antigens will make it easier.
  • [MeSH-major] Antigens, CD56 / analysis. Antigens, CD7 / analysis. Antigens, CD79 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / diagnosis

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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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72. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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).
  • These data allow more reliable prediction of outcome for patients with rarer abnormalities and may facilitate the development of consensus in reporting of karyotypic information in clinical trials involving younger adults with AML.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics


73. Betts DR, Ammann RA, Hirt A, Hengartner H, Beck-Popovic M, Kuhne T, Nobile L, Caflisch U, Wacker P, Niggli FK: The prognostic significance of cytogenetic aberrations in childhood acute myeloid leukaemia. A study of the Swiss Paediatric Oncology Group (SPOG). Eur J Haematol; 2007 Jun;78(6):468-76

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic significance of cytogenetic aberrations in childhood acute myeloid leukaemia. A study of the Swiss Paediatric Oncology Group (SPOG).
  • In childhood-onset acute myeloid leukaemia (AML) the clinical value of karyotypic aberrations is now acknowledged, although there is still debate concerning the prognostic significance of some events.
  • To add to this knowledge, cytogenetic analysis was performed on a consecutive series of 84 childhood AML patients diagnosed in Switzerland.
  • The most frequent aberrations observed were t(11q23) (19% of all patients), t(8;21) (12%) and +8 (11%).
  • It was also noteworthy that patients with the rare aberrations of del(11q) (n = 4) and t(16;21)(p11;q22) (n = 3) had a poor outcome.
  • The results support the importance of cytogenetic analysis in childhood AML, but show that further work is required in the classification of the poor prognosis aberrations.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Incidence. Karyotyping. Male. Prognosis. Remission Induction. Survival Analysis

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  • (PMID = 17419750.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
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74. Agerstam H, Lilljebjörn H, Lassen C, Swedin A, Richter J, Vandenberghe P, Johansson B, Fioretos T: Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome. Genes Chromosomes Cancer; 2007 Jul;46(7):635-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EMS is associated with a high risk of transformation to acute myeloid leukemia (AML), but the mechanisms underlying the disease progression are unknown.
  • In the present study, we have investigated a case of EMS harboring a t(8;22)(p11;q11)/BCR-FGFR1 rearrangement as well as a t(9;21)(q34;q22) at the time of AML transformation.
  • FISH and RT-PCR analyses revealed that the t(9;21) leads to a fusion gene consisting of the 5' part of RUNX1 (exons 1-4) fused to repetitive sequences of a gene with unknown function on chromosome 9, adding 70 amino acids to RUNX1 exon 4.
  • The t(9;21) hence results in a truncation of RUNX1.
  • The most likely functional outcome of the rearrangement was haploinsufficiency of RUNX1, which thus may be one mechanism by which EMS transforms to AML.

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  • (PMID = 17394134.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / RUNX1 protein, human
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75. Liu S, Shen T, Huynh L, Klisovic MI, Rush LJ, Ford JL, Yu J, Becknell B, Li Y, Liu C, Vukosavljevic T, Whitman SP, Chang KS, Byrd JC, Perrotti D, Plass C, Marcucci G: Interplay of RUNX1/MTG8 and DNA methyltransferase 1 in acute myeloid leukemia. Cancer Res; 2005 Feb 15;65(4):1277-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interplay of RUNX1/MTG8 and DNA methyltransferase 1 in acute myeloid leukemia.
  • The translocation t(8;21)(q22;q22) in acute myeloid leukemia (AML) results in the expression of the fusion protein RUNX1/MTG8, which in turn recruits histone deacetylases (HDAC) to silence RUNX1 target genes [e.g., interleukin-3 (IL-3)].
  • By a chromatin immunoprecipitation assay, we identified a RUNX1/MTG8-DNMT1 complex on the IL-3 promoter in Kasumi-1 cells and in primary RUNX1/MTG8-positive AML blasts.
  • These results suggest a novel mechanism for gene silencing mediated by RUNX1/MTG8 and support the combination of HDAC and DNMT inhibitors as a novel therapeutic approach for t(8;21) AML.
  • [MeSH-major] DNA (Cytosine-5-)-Methyltransferase / metabolism. DNA-Binding Proteins / physiology. Leukemia, Myeloid / metabolism. Proto-Oncogene Proteins / physiology. Transcription Factors / physiology
  • [MeSH-minor] Acute Disease. Cell Line. Cell Line, Tumor. Core Binding Factor Alpha 2 Subunit. DNA Methylation. Gene Expression Regulation, Neoplastic / physiology. Gene Silencing. Humans. Interleukin-3 / genetics. Promoter Regions, Genetic. Transcription, Genetic / physiology. Transfection

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  • (PMID = 15735013.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30-CA16058; United States / NCI NIH HHS / CA / R01-CA102031; United States / NCI NIH HHS / CA / R21-CA094552
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Interleukin-3; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1
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76. 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.
  • We analysed gene expression profiles of 83 CBF AML cases with known KIT mutation status in order to gain novel insights in KIT-mutated CBF pathogenesis.
  • [MeSH-major] Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics

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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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77. 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

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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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78. Hasle H, Alonzo TA, Auvrignon A, Behar C, Chang M, Creutzig U, Fischer A, Forestier E, Fynn A, Haas OA, Harbott J, Harrison CJ, Heerema NA, van den Heuvel-Eibrink MM, Kaspers GJ, Locatelli F, Noellke P, Polychronopoulou S, Ravindranath Y, Razzouk B, Reinhardt D, Savva NN, Stark B, Suciu S, Tsukimoto I, Webb DK, Wojcik D, Woods WG, Zimmermann M, Niemeyer CM, Raimondi SC: Monosomy 7 and deletion 7q in children and adolescents with acute myeloid leukemia: an international retrospective study. Blood; 2007 Jun 1;109(11):4641-7
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  • [Title] Monosomy 7 and deletion 7q in children and adolescents with acute myeloid leukemia: an international retrospective study.
  • Monosomy 7 (-7) and deletion 7q del(7q)] are rare in childhood acute myeloid leukemia (AML).
  • We retrospectively collected data on 258 children with AML or refractory anemia with excess blasts in transformation (RAEB-T) and -7 or del(7q) with or without other cytogenetic aberrations +/- other].
  • Karyotypes included -7 (n = 90), -7 other (n = 82), del(7q) (n = 21), and del(7q) other (n = 65).
  • Cytogenetic aberrations considered favorable in AML (8;21)(q22;q22), inv(16)(p13q22), t(15;17)(q22;q21), t(9;11)(p22;q23)] (n = 24) were strongly associated with del(7q) and a higher 5-year survival rate compared with del(7q) without favorable cytogenetics (75% versus 46%, P = .03).
  • Patients with -7 and inv(3),-5/del(5q), or + 21 had a 5-year survival rate of 5%.
  • Childhood AML with chromosome 7 aberrations represents a heterogeneous group of disorders with additional cytogenetic aberrations having a major prognostic impact which should be reflected in future risk-group stratification.
  • [MeSH-major] Chromosomes, Human, Pair 7. Gene Deletion. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Monosomy

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  • (PMID = 17299091.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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79. Andreeva SV, Drozdova VD, Kavardakova NV: [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia]. Tsitol Genet; 2010 May-Jun;44(3):41-52
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  • [Title] [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia].
  • Analysis of chromosomal abnormalities in bone marrow cells in 116 children with diagnosis of acute myeloid leukemia (AML) was performed.
  • Frequency of evolution of clonal chromosome abnormalities in AML constituted 42,3%.
  • The most abundant among them were numerical abnormalities of chromosomes 8, 9, and 21 as well as secondary structural abnormalities in region 12p12, 9p22, 9q22, 9q34, 11q14-23, and 16q22.
  • The high frequency of evolution was established at t(15;17)(q22;q22) and the absence at inv(16)(p13q22).
  • Identity of abnormal chromosome structure at diagnosis and relapse of disease can be an evidence of the influence of chemical agent on establishment of some types of evolution of chromosome abnormalities in leukemic cells in AML in children.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20608159.001).
  • [ISSN] 0564-3783
  • [Journal-full-title] T︠S︡itologii︠a︡ i genetika
  • [ISO-abbreviation] Tsitol. Genet.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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80. 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


81. Suela J, Alvarez S, Cigudosa JC: DNA profiling by arrayCGH in acute myeloid leukemia and myelodysplastic syndromes. Cytogenet Genome Res; 2007;118(2-4):304-9
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  • [Title] DNA profiling by arrayCGH in acute myeloid leukemia and myelodysplastic syndromes.
  • Acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) represent two distinct but related myeloid haematological neoplasms.
  • At diagnosis, a substantial proportion of cases show cytogenetic and molecular genetic markers whose range of specificity is highly variable.
  • Most specific reciprocal translocations, as t(8;21)(q21;q21) or t(15;17)(q22;q21), have been extensively studied and are currently introduced in clinical diagnosis.
  • Recently, single- nucleotide-polymorphism based arrays have been used in AML showing that loss of heterozygosity (LOH) is a common feature in normal karyotype leukemia.
  • [MeSH-major] DNA, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Nucleic Acid Hybridization


82. Zhang LJ, Lu XL, He J, Li Y: [Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia]. Zhonghua Yi Xue Za Zhi; 2006 Aug 29;86(32):2256-60
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  • [Title] [Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia].
  • OBJECTIVE: To study the frequency of mixed lineage leukemia (MLL) gene rearrangements in patients with acute myeloid leukemia (AML) and to determine the significance thereof.
  • METHODS: Conventional cytogenetics (CC) and karyotype analysis were conducted on the bone marrow cells from 58 patients with acute myelocytic leukemia (AML), 47 adults (aged 15 approximately 67) and 11 children (aged 1 approximately 14).
  • Fluorescence in situ hybridization (FISH) using the whole chromosome painting (WCP) probes of the chromosomes 1, 5, 11, 16, 17, and 21 was performed.
  • Forty-seven of these patients with AML were adults and the remaining were children.
  • 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;.
  • CONCLUSION: MLL gene rearrangement is relatively common in AML patients.
  • 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

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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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83. Kamineni P, Baptiste A, Hassan M, Dawkins FW, Zaidi S, Tefferi A, Lindsey M, Taddesse-Heath L: Case of chronic eosinophilic leukemia with deletion of chromosome 16 and hepatitis C. J Natl Med Assoc; 2006 Aug;98(8):1356-60
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  • [Title] Case of chronic eosinophilic leukemia with deletion of chromosome 16 and hepatitis C.
  • Chronic eosinophilic leukemia is a rare entity, characterized by eosinophilia of >1.5 x 10(9)/L, persisting for >6 months after exclusion of other reactive and neoplastic causes of eosinophilia, and occurring in association with a clonal cytogenetic abnormality.
  • Various chromosomal abnormalities have been associated with chronic eosinophilic leukemia.
  • Partial deletion of the long arm of chromosome 16 is a cytogenetic abnormality first reported 20 years ago in patients with acute myeloid leukemia associated with bone marrow eosinophilia (AML-M4Eo).
  • To our knowledge, this is the first case report of isolated del (16) (q22), a cytogenetic abnormality associated with AML-M4Eo, occurring in chronic eosinophilic leukemia.
  • Whether this cytogenetic abnormality might represent a prodromal phase of AML-M4Eo is not known.
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 16916138.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2569582
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84. Retraction. 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 Jul;192(1):54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retraction. Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).

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  • [RetractionOf] Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z. Cancer Genet Cytogenet. 2009 Jan 15;188(2):95-8 [19100512.001]
  • (PMID = 19489159.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Retraction of Publication
  • [Publication-country] United States
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