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1. Rowe D, Strain L, Lowe C, Jones G: A case of acute myeloid leukemia with inv(16)(p13q22) reveals a novel MYH11 breakpoint and a new CBF beta-MYH11 transcript variant. Haematologica; 2007 Oct;92(10):1433-4
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  • [Title] A case of acute myeloid leukemia with inv(16)(p13q22) reveals a novel MYH11 breakpoint and a new CBF beta-MYH11 transcript variant.
  • We present a case of acute myeloid leukemia (AML) with a cytogenetically typical inv(16)(p13q22), M4 morphology and eosinophilia.
  • However, studies revealed a CBF beta-MYH11 fusion transcript which did not correspond to any of the 10 known variants.
  • Subsequent sequencing revealed a new in-frame transcript variant resulting from a novel MYH11 exon 32 breakpoint and a seven base insertion at the fusion point.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Transcription, Genetic / genetics

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  • (PMID = 18024381.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion
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2. Sun X, Zhang W, Ramdas L, Stivers DN, Jones DM, Kantarjian HM, Estey EH, Vadhan-Raj S, Medeiros LJ, Bueso-Ramos CE: Comparative analysis of genes regulated in acute myelomonocytic leukemia with and without inv(16)(p13q22) using microarray techniques, real-time PCR, immunohistochemistry, and flow cytometry immunophenotyping. Mod Pathol; 2007 Aug;20(8):811-20
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  • [Title] Comparative analysis of genes regulated in acute myelomonocytic leukemia with and without inv(16)(p13q22) using microarray techniques, real-time PCR, immunohistochemistry, and flow cytometry immunophenotyping.
  • Acute myeloid leukemia with inv(16)(p13q22), also known as M4Eo, is a distinct type of leukemia with characteristic clinicopathologic and cytogenetic features.
  • The inv(16)(p13q22) or, less commonly, the t(16;16)(p13;q22) causes fusion of the CBFbeta gene at 16q22 and the MYH11 gene at 16p13, creating the novel chimeric protein CBFbeta-MYH11.
  • Cases of acute myelomonocytic leukemia without CBFbeta-MYH11 (M4) acted as our control.
  • We found that in the gene expression profile of M4Eo, NF-kappaB activators and inhibitors were upregulated and downregulated, respectively, suggesting that the NF-kappaB signaling pathway is activated at a higher level in M4Eo than in acute myelomonocytic leukemia M4.
  • These findings most likely represent the functional consequences of the abnormal chimeric protein CBFbeta-MYH11, which is unique to this disease, and suggest that NF-kappaB is a potential therapeutic target for treating M4Eo patients.
  • [MeSH-major] Chromosomes, Human, Pair 16. Flow Cytometry. Gene Expression Profiling / methods. Immunohistochemistry. Immunophenotyping / methods. Leukemia, Myelomonocytic, Acute / genetics. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction

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  • (PMID = 17571080.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30 CA016672-28
  • [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 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factor RelA
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3. Kim HG, Kojima K, Swindle CS, Cotta CV, Huo Y, Reddy V, Klug CA: FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia. Blood; 2008 Feb 01;111(3):1567-74
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  • [Title] FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.
  • The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML).
  • The inv(16) fuses the core binding factor (CBF) beta subunit with the coiled-coil rod domain of smooth muscle myosin heavy chain (SMMHC).
  • Patient samples with the inv(16) also possess mutually exclusive activating mutations in either N-RAS, K-RAS, or the receptor tyrosine kinases, c-KIT and FLT3, in almost 70% of cases.
  • Compared with animals transplanted with only CBFbeta-SMMHC-expressing cells, FLT3-ITD further restricted early myeloid differentiation and promoted peripheralization of primitive myeloblasts as early as 2.5 weeks after transplantation.
  • These results indicate that FLT3-activating mutations can cooperate with CBFbeta-SMMHC in an animal model of inv(16)-associated AML.
  • [MeSH-major] Chromosome Inversion / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Oncogene Proteins, Fusion / metabolism. fms-Like Tyrosine Kinase 3 / metabolism

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  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Cancer Cell. 2006 Jan;9(1):57-68 [16413472.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12822-7 [10536006.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):723-33 [11179217.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Cancer Res. 2002 Apr 15;62(8):2232-5 [11956074.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Nat Struct Biol. 2002 Sep;9(9):674-9 [12172539.001]
  • [Cites] Blood. 2002 Dec 1;100(12):4154-61 [12393674.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):607-19 [12509458.001]
  • [Cites] Curr Opin Genet Dev. 2003 Feb;13(1):48-54 [12573435.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4342-6 [12560221.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 27;94(11):5697-702 [9159135.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11863-8 [9751756.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7432-43 [9819429.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7 Suppl):1789s-1793s [10197598.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):144-6 [10508507.001]
  • [Cites] Br J Haematol. 2005 Jan;128(1):18-34 [15606546.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):523-38 [12899708.001]
  • [Cites] Haematologica. 2004 Jan;89(1):106 [14754614.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4924-9 [15044690.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3200-7 [15070703.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4297-307 [15156186.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1213-25 [1827140.001]
  • [Cites] Virology. 1993 May;194(1):314-31 [8386878.001]
  • [Cites] Mol Cell Biol. 1993 Jun;13(6):3324-39 [8497254.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Blood. 1995 May 1;85(9):2289-302 [7727763.001]
  • [Cites] J Exp Med. 1996 Jan 1;183(1):187-94 [8551222.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1630-5 [8643682.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8508-11 [8710900.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12359-63 [8901586.001]
  • [Cites] Cell. 1996 Nov 15;87(4):687-96 [8929537.001]
  • [Cites] J Biol Chem. 2005 Dec 2;280(48):40097-103 [16199529.001]
  • (PMID = 17967943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK067186; United States / NCI NIH HHS / CA / R01 CA096798; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NCI NIH HHS / CA / R01CA96798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / Smooth Muscle Myosins
  • [Other-IDs] NLM/ PMC2214774
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4. Lee SY, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ, Park IY: [A case of therapy-related acute myeloid leukemia associated with inv(16)]. Korean J Lab Med; 2007 Feb;27(1):19-21
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  • [Title] [A case of therapy-related acute myeloid leukemia associated with inv(16)].
  • The inv(16)(p13q22) is found in de novo AML and is closely associated with the FAB subtype M4eo.
  • The inv(16) is rarely reported in therapy-related AML (t-AML) patients.
  • Herein, we report a case of t-AML with inv(16) after combination chemotherapy using antimitotic agent and alkylating agent (cis-platin-paclitaxel) for ovarian serous cystadenocarcinoma.
  • [MeSH-major] Antimitotic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosome Inversion. Chromosomes, Human, Pair 16 / genetics. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 18094545.001).
  • [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 / Antimitotic Agents; 0 / Taxoids; Q20Q21Q62J / Cisplatin; TP protocol
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5. Helbling D, Mueller BU, Timchenko NA, Schardt J, Eyer M, Betts DR, Jotterand M, Meyer-Monard S, Fey MF, Pabst T: CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16). Blood; 2005 Aug 15;106(4):1369-75
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  • [Title] CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16).
  • The pericentric inversion of chromosome 16, inv(16)(p13q22), is associated with acute myeloid leukemia (AML) subtype M4Eo that is characterized by the presence of myelomonocytic blasts and atypical eosinophils.
  • This rearrangement fuses the CBFB and MYH11 genes, with the latter encoding the smooth muscle myosin heavy chain (SMMHC).
  • The myeloid transcription factor CCAAT/enhancer-binding protein alpha (CEBPA) is crucial for normal granulopoiesis.
  • Here, we found that conditional expression of core-binding factor beta (CBFB)-SMMHC in U937 cells suppresses CEBPA protein expression and binding activity.
  • No differences were detected in CEBPA mRNA levels in patients with inv(16) AML-M4Eo (n = 12) compared to patients with AML with a normal karyotype and M4 subtype (n = 6), whereas CEBPA protein and binding activity were significantly reduced in patients with CBFB-SMMHC.
  • Furthermore, calreticulin, an inhibitor of CEBPA translation, was induced on mRNA and protein level in CBFB-SMMHC patients with AML and after expression of CBFB-SMMHC in the U937-cell system.
  • Our results suggest that modulation of CEBPA by calreticulin represents a novel mechanism involved in the differentiation block in CBFB-SMMHC AML.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Calreticulin / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Cell Differentiation. Female. Humans. Male. Middle Aged. RNA, Neoplasm / analysis. RNA, Small Interfering / pharmacology. Translocation, Genetic

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  • (PMID = 15855281.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Calreticulin; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / inv(16) fusion protein, human
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6. Bowen DT, Frew ME, Hills R, Gale RE, Wheatley K, Groves MJ, Langabeer SE, Kottaridis PD, Moorman AV, Burnett AK, Linch DC: RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years. Blood; 2005 Sep 15;106(6):2113-9
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  • [Title] RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years.
  • The pathogenesis of acute myeloid leukemia (AML) involves the cooperation of mutations promoting proliferation/survival and those impairing differentiation.
  • KRAS mutation was overrepresented in inv(16)(p13q22) (P = .004).
  • Twenty-three percent of KRAS mutations were within the inv(16) subgroup.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. ras Proteins / genetics
  • [MeSH-minor] Acute Disease. Age Factors. Cytogenetic Analysis. DNA Mutational Analysis. Genes, ras. Humans. Middle Aged. Molecular Epidemiology. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Survival Analysis. Treatment Outcome. fms-Like Tyrosine Kinase 3

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  • (PMID = 15951308.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
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7. Zhao W, Claxton DF, Medeiros LJ, Lu D, Vadhan-Raj S, Kantarjian HM, Nguyen MH, Bueso-Ramos CE: Immunohistochemical analysis of CBFbeta-SMMHC protein reveals a unique nuclear localization in acute myeloid leukemia with inv(16)(p13q22). Am J Surg Pathol; 2006 Nov;30(11):1436-44
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  • [Title] Immunohistochemical analysis of CBFbeta-SMMHC protein reveals a unique nuclear localization in acute myeloid leukemia with inv(16)(p13q22).
  • The inv(16)(p13q22) or, less commonly the t(16;16)(p13;q22), is characteristic of acute myeloid leukemia (AML) with abnormal bone marrow eosinophils, also known as AML-M4Eo.
  • This abnormality creates a fusion gene, 5' core binding factor beta (CBF-beta) gene and the 3' MYH11 gene, the latter encoding smooth muscle myosin heavy chain gene (SMMHC).
  • [MeSH-major] Cell Nucleus / metabolism. Chromosome Inversion. Immunohistochemistry. Leukemia, Myelomonocytic, Acute / diagnosis. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Adolescent. Adult. Chromosomes, Human, Pair 16 / genetics. Core Binding Factor beta Subunit / genetics. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myosin Heavy Chains / genetics. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Time Factors

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  • (PMID = 17063086.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 3.6.4.1 / Myosin Heavy Chains
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8. Zhou HF, Li JY, Qian SX, Qiu HR, Zhang SJ, Zhang JF, Wu YJ, Shen RL: [Bulky lymphadenopathy in acute myeloid leukemia with inv (16) (p13q22): a case report]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Oct;14(5):1033-7
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  • [Title] [Bulky lymphadenopathy in acute myeloid leukemia with inv (16) (p13q22): a case report].
  • The study was aimed to investigate the different prognosis of acute myeloid leukemia (AML) with inv (16).
  • The karyotype and inv (16) were detected by conventional cytogeneties and fluorescence in situ hybridization (FISH), respectively, the immunophenotype was detected by flow cytometry.
  • The results showed that conventional cytogenetics and FISH analysis revealed inv (16).
  • It is concluded that bulky lymphadenopathy in AML with inv (16) may be a negative prognostic sign.
  • FISH for inv (16) is specific and constitutes an reliable tool to be used for diagnosis and minimal residual disease (MRD).

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  • (PMID = 17096914.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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9. Merzianu M, Medeiros LJ, Cortes J, Yin C, Lin P, Jones D, Glassman A, Kantarjian H, Huh Y: inv(16)(p13q22) in chronic myelogenous leukemia in blast phase: a clinicopathologic, cytogenetic, and molecular study of five cases. Am J Clin Pathol; 2005 Nov;124(5):807-14
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  • [Title] inv(16)(p13q22) in chronic myelogenous leukemia in blast phase: a clinicopathologic, cytogenetic, and molecular study of five cases.
  • Blast phase (BP) in chronic myelogenous leukemia (CML) frequently is accompanied by cytogenetic abnormalities in addition to t(9;22)(q34;q11.2).
  • We describe 5 patients with CML in blast phase (CML-BP) in which t(9;22) and inv(16)(p13q22) were identified by conventional cytogenetics, with confirmation of BCR-ABL and CBFss-MYH11 by fluorescence in situ hybridization.
  • The morphologic findings at the time of BP resembled de novo acute myeloid leukemia (AML) carrying inv(16)(p13q22), with abnormal eosinophils in the bone marrow and monocytosis in the peripheral blood in all cases.
  • In 1 patient, inv(16)(p13q22) and abnormal eosinophils were detected in the bone marrow 2 months before CML-BP.
  • The clinical course of these patients was similar to patients with CML-BP without evidence of inv(16)(p13q22).
  • These cases illustrate that inv(16)(p13q22) is a form of cytogenetic evolution that rarely occurs in patients with CML at the time of BP.
  • In this setting, unlike de novo AML, inv(16)(p13q22) in CML-BP is not associated with a favorable prognosis.
  • [MeSH-major] Blast Crisis / genetics. Chromosome Inversion. Chromosomes, Human, Pair 16. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

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  • (PMID = 16203287.001).
  • [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] EC 3.6.4.1 / Myosin Heavy Chains
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10. Sakai R, Fujimaki K, Yamazaki E, Sakamoto H, Kanamori H, Miura I, Ishigatsubo Y: Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22). Int J Hematol; 2006 Dec;84(5):417-20
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  • [Title] Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22).
  • inv(16)(p13q22) is associated with de novo acute myelomonocytic leukemia with dysplastic bone marrow eosinophils (AMML Eo), which has a relatively favorable clinical course with a longer remission duration and better survival prospects.
  • On the other hand, t(5; 17)(q13;q11), although relatively rare, has been reported to be a component of complex chromosomal abnormalities in myelodysplastic syndromes and secondary acute myeloid leukemia (AML).
  • We treated a 29-year-old woman with the first reported case of de novo AMML Eo with inv(16)(p13q22) in addition to t(5; 17)(q13;q11).
  • Accordingly, the primary nature of the leukemic cells in this case differs from the findings for core-binding factor AML with inv(16)(p13q22).
  • We believe this report is the first of de novo AMML Eo with t(5; 17)(q13;q11) showing as a secondary chromosomal aberration with inv(16)(p13q22).
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosome Inversion. Chromosomes, Human / genetics. Eosinophils / pathology. Leukemia, Myelomonocytic, Acute. Translocation, Genetic

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  • (PMID = 17189222.001).
  • [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
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11. Tretiak NM, Vakul'chuk OM, Kalinina SIu: [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)]. Lik Sprava; 2008 Jan-Feb;(1-2):89-96
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  • [Title] [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)].
  • 3 patients with secondary acute non-lymphoblastic leucosis have been observed.
  • The cytogenetic analysis revealed pathologic karyotypes: 46, XY,+8, t(8;21), inv 16.


12. Al-Quran SZ, Olivares A, Lin P, Stephens TW, Medeiros LJ, Abruzzo LV: Myeloid sarcoma of the urinary bladder and epididymis as a primary manifestation of acute myeloid leukemia with inv(16). Arch Pathol Lab Med; 2006 Jun;130(6):862-6
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  • [Title] Myeloid sarcoma of the urinary bladder and epididymis as a primary manifestation of acute myeloid leukemia with inv(16).
  • Myeloid sarcoma (MS) of the lower urinary tract is rare.
  • Although blood and bone marrow examinations showed no morphologic evidence of leukemia, conventional cytogenetic studies of marrow demonstrated inv(16)(p13q22) in 4 of 20 metaphases; fluorescence in situ hybridization of the bladder neoplasm also showed inv(16).
  • In our literature review, we identified 7 cases of MS involving bladder, only 3 without evidence of an associated myeloid neoplasm in marrow, none with cytogenetic data.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. Genital Neoplasms, Male / pathology. Sarcoma, Myeloid / pathology. Urinary Bladder Neoplasms / pathology

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  • (PMID = 16740041.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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13. Paschka P, Marcucci G, Ruppert AS, Mrózek K, Chen H, Kittles RA, Vukosavljevic T, Perrotti D, Vardiman JW, Carroll AJ, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B: Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study. J Clin Oncol; 2006 Aug 20;24(24):3904-11
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  • [Title] Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study.
  • PURPOSE: To analyze the prognostic impact of mutated KIT (mutKIT) in core-binding factor acute myeloid leukemia (AML) with inv(16)(p13q22) and t(8;21)(q22;q22).
  • PATIENTS AND METHODS: Sixty-one adults with inv(16) and 49 adults with t(8;21), assigned to postremission therapy with repetitive cycles of higher dose cytarabine were analyzed for mutKIT in exon 17 (mutKIT17) and 8 (mutKIT8) by denaturing high-performance liquid chromatography and direct sequencing at diagnosis.
  • RESULTS: Among patients with inv(16), 29.5% had mutKIT (16% with mutKIT17 and 13% with sole mutKIT8).
  • In inv(16), the cumulative incidence of relapse (CIR) was higher for patients with mutKIT (P = .05; 5-year CIR, 56% v 29%) and those with mutKIT17 (P = .002; 5-year CIR, 80% v 29%) compared with wtKIT patients.
  • 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).
  • [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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14. 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.
  • 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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15. Paschka P: Core binding factor acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):410-7
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  • [Title] Core binding factor acute myeloid leukemia.
  • Core binding factor (CBF) acute myeloid leukemia (AML) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult de novo AML cases.
  • Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16) AML, thereby supporting the notion that they represent two distinct biologic and clinical entities.
  • [MeSH-major] Chromosome Inversion. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual / diagnosis. Prognosis

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  • (PMID = 18692691.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors
  • [Number-of-references] 76
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16. 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.
  • 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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17. Xu W, Zhou HF, Fan L, Qian SX, Chen LJ, Qiu HR, Zhang SJ, Li JY: Trisomy 22 as the sole abnormality is an important marker for the diagnosis of acute myeloid leukemia with inversion 16. Onkologie; 2008 Sep;31(8-9):440-4
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  • [Title] Trisomy 22 as the sole abnormality is an important marker for the diagnosis of acute myeloid leukemia with inversion 16.
  • BACKGROUND: The inversion of chromosome 16 (inv(16) (p13q22)) and the related t(16;16)(p13;q22) are chromosomal aberrations observed in approximately 10% of de novo acute myeloid leukemia (AML), mostly classified as M4Eo subtype, and associated with a relatively favorable outcome.
  • Trisomy 22 is an uncommon karyotypic aberration in AML and is often associated with inv(16)(p13q22).
  • The aim of this study was to explore the value of trisomy 22 in the diagnosis of AML with inv(16).
  • RESULTS: R-banding CC did not reveal inv(16) in any of the 19 AML with trisomy 22, but FISH analysis showed inv(16) in 11 cases and del(16)(q22) in 1 case.
  • Among the 11 cases with inv(16), 9 showed trisomy 22 as the sole abnormality, 1 was complicated by trisomy 8, and 1 was del(16)(q22).
  • CONCLUSION: This study further confirmed that trisomy 22 as the sole abnormality can be regarded as an important marker for inv(16) in AML.
  • [MeSH-major] Chromosome Inversion / genetics. Chromosomes, Human, Pair 16 / genetics. Genetic Markers / genetics. Genetic Predisposition to Disease / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Trisomy / diagnosis. Trisomy / genetics

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18787351.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Genetic Markers
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18. Andreeva SV, Drozdova VD, Kavardakova NV: [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia]. Tsitol Genet; 2010 May-Jun;44(3):41-52
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  • [Title] [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia].
  • Analysis of chromosomal abnormalities in bone marrow cells in 116 children with diagnosis of acute myeloid leukemia (AML) was performed.
  • The high frequency of evolution was established at t(15;17)(q22;q22) and the absence at inv(16)(p13q22).
  • [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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19. Silva PM, Lourenço GJ, Bognone RA, Delamain MT, Pinto-Junior W, Lima CS: Inherited pericentric inversion of chromosome 16 in chronic phase of chronic myeloid leukaemia. Leuk Res; 2006 Jan;30(1):115-7
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  • [Title] Inherited pericentric inversion of chromosome 16 in chronic phase of chronic myeloid leukaemia.
  • The simultaneous occurrence of two specific acquired chromosomal abnormalities in chronic or acute leukaemias is rare.
  • In chronic myeloid leukaemia (CML), characterised by the t(9;22)(q34;q11), the inv(16)(p13q22) has been described associated with the acceleration of disease or onset of blast crisis.
  • We report on a patient with chronic phase of CML and both acquired t(9;22)(q34;q11) and inherited inv(16)(p13q22), who obtained a complete remission of the disease after bone marrow transplant.
  • [MeSH-major] Blast Crisis / pathology. Chromosome Inversion. Chromosomes, Human, Pair 16. Genetic Diseases, Inborn / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 16054690.001).
  • [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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20. Ohsaka A, Otsubo K, Yokota H, Hisa T, Saito H, Kozaki T: Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo. Cancer Genet Cytogenet; 2008 Jul 15;184(2):113-8
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  • [Title] Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo.
  • We report a novel three-way translocation involving inversion 16 and chromosome 12 at bands 16p13, 16q22, and 12q24 in a patient with therapy-related acute myeloid leukemia (AML)-M4eo.
  • Conventional G-banding of bone marrow cells at diagnosis was suggestive of inv(16)(p13q22) and a translocation of chromosomes 12 and 16.
  • The presence of inv(16) was confirmed by reverse-transcription polymerase chain reaction (RT-PCR) analysis, which corresponded to the type A CBFB-MYH11 chimeric transcript.
  • Spectral karyotyping (SKY) analysis clearly identified a reciprocal translocation between chromosomes 12 and 16.
  • In addition, dual-color fluorescence in situ hybridization (FISH) analysis revealed a fusion signal for the CBFB and MYH11 probes and a signal for the MYH11 probe on the der(16) chromosome, as well as a signal for the CBFB probe on the der(12) chromosome.
  • Thus, the karyotype was refined to 46,XX,der(12)t(12;16)(q24;q22),der(16)inv(16)(p13q22)t(12;16).
  • Although we could not establish that this complex chromosomal aberration occurred either as a one-step, three-way event, or a sequential event with inv(16)(p13q22) followed by t(12;16)(q24;q22), SKY in combination with FISH and RT-PCR analyses successfully detected this complex chromosome abnormality in the patient.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics. Spectral Karyotyping. Translocation, Genetic

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  • (PMID = 18617061.001).
  • [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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21. Mrózek K, Bloomfield CD: Chromosome aberrations, gene mutations and expression changes, and prognosis in adult acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2006;:169-77
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  • [Title] Chromosome aberrations, gene mutations and expression changes, and prognosis in adult acute myeloid leukemia.
  • Pretreatment clinical features and prognosis of patients with acute myeloid leukemia (AML) are strongly influenced by acquired genetic alterations in leukemic cells, which include microscopically detectable chromosome aberrations and, increasingly, submicroscopic gene mutations and changes in gene expression.
  • In many instances, patients with specific cytogenetic findings, e.g., those with a normal karyotype or those with either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22) [collectively referred to as core-binding factor (CBF) AML] can be further subdivided into prognostic categories based on the presence or absence of particular gene mutations or changes in gene expression.

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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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22. 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.
  • Using cell lines, we developed and validated a biochip-based assay called the AMLFusionChip that identifies every FT of AML1-ETO, CBFbeta-MYH11 as well as MLL-AF9, MLL-ENL, MLL-AF6, and MLL-AF10.
  • [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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23. Mrózek K, Marcucci G, Paschka P, Bloomfield CD: Advances in molecular genetics and treatment of core-binding factor acute myeloid leukemia. Curr Opin Oncol; 2008 Nov;20(6):711-8
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  • [Title] Advances in molecular genetics and treatment of core-binding factor acute myeloid leukemia.
  • PURPOSE OF REVIEW: Core-binding factor (CBF) acute myeloid leukemia (AML) is among the most common cytogenetic subtypes of AML, being detected in approximately 13% of adults with primary disease.
  • RECENT FINDINGS: Several acquired gene mutations and gene-expression and microRNA-expression changes that occur in addition to t(8;21)(q22;q22) and inv(16)(p13q22)/t(16;16)(p13;q22), the cytogenetic hallmarks of CBF-AML, have been recently reported.
  • Alterations that may represent cooperative events in CBF-AML leukemogenesis include mutations in the KIT, FLT3, JAK2 and RAS genes, haploinsufficiency of the putative tumor suppressor genes TLE1 and TLE4 in t(8;21)-positive patients with del(9q), MN1 overexpression in inv(16) patients, and epigenetic and posttranscriptional silencing of CEBPA.

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  • [Cites] Cancer Res. 2008 May 1;68(9):3142-51 [18451139.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1919-28 [18450603.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] Hum Pathol. 2008 Jun;39(6):795-810 [18538168.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3183-8 [18506024.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1177-82 [17377588.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Feb;14(2):187-96 [18215779.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1369-75 [15855281.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1189-98 [15878973.001]
  • [Cites] Int J Hematol. 2005 Jul;82(1):1-8 [16105753.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5705-17 [16110030.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1567-74 [17967943.001]
  • [Cites] Leukemia. 2008 Feb;22(2):303-7 [17960171.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Jul 15;184(2):113-8 [18617061.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):410-7 [18692691.001]
  • [Cites] Int J Hematol. 2008 Sep;88(2):154-8 [18553224.001]
  • [Cites] Br J Haematol. 2008 Sep;142(5):745-53 [18537968.001]
  • [Cites] Oncogene. 2008 Oct 2;27(44):5759-73 [18604246.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3767-75 [10577848.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2482-92 [11331327.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):502-13 [12094236.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10008-13 [12105272.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Mar;36(3):261-72 [12557226.001]
  • [Cites] Curr Opin Genet Dev. 2003 Feb;13(1):48-54 [12573435.001]
  • [Cites] Leukemia. 2003 Feb;17(2):350-8 [12592335.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] Eur J Haematol. 2003 Sep;71(3):143-54 [12930314.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1087-94 [15020610.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3741-50 [15289486.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:80-97 [15561678.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1277-84 [15735013.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1536-42 [16015387.001]
  • [Cites] Am J Clin Pathol. 2006 Feb;125(2):267-72 [16393685.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]
  • [Cites] Oncogene. 2006 Mar 2;25(9):1434-6 [16247455.001]
  • [Cites] Leukemia. 2006 Jan;20(1):87-94 [16281071.001]
  • [Cites] Blood. 2006 May 1;107(9):3463-8 [16384925.001]
  • [Cites] Blood. 2006 May 15;107(10):3847-53 [16434492.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):165-73 [16939487.001]
  • [Cites] Haematologica. 2006 Nov;91(11):1569-70 [17043013.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]
  • [Cites] Leukemia. 2007 Jan;21(1):183-4 [17096014.001]
  • [Cites] Haematologica. 2007 Jan;92(1):137-8 [17229652.001]
  • [Cites] Leuk Res. 2007 Apr;31(4):471-6 [17052753.001]
  • [Cites] Leukemia. 2007 Apr;21(4):725-31 [17287858.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Jun;321(3):953-60 [17389244.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1679-90 [17525718.001]
  • [Cites] Blood. 2007 Aug 1;110(3):799-805 [17412887.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1262-70 [17456725.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1291-300 [17485551.001]
  • [Cites] Br J Haematol. 2007 Sep;138(5):624-31 [17686056.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1639-47 [17494859.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2199-201 [17625612.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6829-37 [17934489.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):457-66 [17996649.001]
  • [Cites] Cytogenet Genome Res. 2007;118(2-4):252-9 [18000378.001]
  • [Cites] Arch Med Res. 2008 Feb;39(2):252-6 [18164974.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Jan 15;180(2):153-7 [18206543.001]
  • [Cites] Leuk Lymphoma. 2008 Mar;49(3):517-23 [18297529.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Apr 1;182(1):56-60 [18328953.001]
  • [Cites] Blood. 2008 Mar 15;111(6):3183-9 [18187662.001]
  • [Cites] Oncogene. 2008 Mar 13;27(12):1767-78 [17891169.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4338-47 [18258796.001]
  • (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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24. 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).
  • 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%.
  • [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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25. Monma F, Nishii K, Shiga J, Sugahara H, Lorenzo F 5th, Watanabe Y, Kawakami K, Hosokai N, Yamamori S, Katayama N, Shiku H: Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients. Leuk Res; 2007 Apr;31(4):471-6
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  • [Title] Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients.
  • The cytogenetic findings in acute myeloid leukemia (AML) are a powerful prognostic indicator.
  • Among these abnormalities, the World Health Organization has classified inv(16)(p13q22), which is closely associated with the M4E classification in the French-American-British system, as indicating a good-risk AML.
  • In this study, we used RT-PCR and FISH analysis to examine 224 Japanese adult de novo AML patients for the presence of the CBFB/MYH11 fusion transcript at the time of diagnosis.
  • The CBFB/MYH11 fusion gene was detected in 17 patients (7.6%): eight patients had the inv(16) chromosome and in all of them it was M4E; nine patients did not have abnormalities in chromosome 16.
  • AML with the CBFB/MYH11 fusion gene but without inv(16) was found in M2, M4, and M5, but not in M4E patients.
  • There were no statistically significant differences in the clinical features of patients with the inv(16) and those with the cryptic inv(16) chromosome.
  • These results indicate that even if eosinophilia is not found, molecular screening for CBFB/MYH11 fusion gene should be performed in all AML patients at the time of diagnosis to help guide disease management.
  • [MeSH-major] Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Chromosome Inversion / genetics. Chromosomes, Human, Pair 16. Humans. In Situ Hybridization, Fluorescence. Incidence. Japan. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17052753.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm
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26. 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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  • [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.

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  • [Cites] J Clin Oncol. 2007 Mar 20;25(9):1151-2; author reply 1152-3 [17369586.001]
  • [Cites] J Clin Invest. 2007 Apr;117(4):1037-48 [17347684.001]
  • [Cites] Eur J Haematol. 2007 Jun;78(6):468-76 [17419750.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Jun;175(2):125-31 [17556068.001]
  • [Cites] Blood. 2007 Jul 1;110(1):409-17 [17374741.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3337-43 [17577018.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3884-91 [17679729.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4603-9 [18559876.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2113-9 [15951308.001]
  • [Cites] Hematol Oncol. 2005 Mar;23(1):18-25 [16142824.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Nat Med. 2006 Jan;12(1):114-21 [16369543.001]
  • [Cites] J Natl Compr Canc Netw. 2006 Jan;4(1):37-50 [16403403.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]
  • [Cites] Hum Mol Genet. 2006 Mar 15;15(6):933-42 [16452126.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Blood. 2006 Jul 1;108(1):63-73 [16522815.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Jul 15;168(2):133-45 [16843103.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Sep;45(9):798-807 [16736498.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3280-8 [16840728.001]
  • [Cites] Leuk Res. 2007 Jan;31(1):39-47 [16687173.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:169-77 [17124057.001]
  • [Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]
  • [Cites] Nat Med. 2007 Jan;13(1):78-83 [17159988.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Aug;153(1):16-25 [15325089.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3741-50 [15289486.001]
  • [Cites] Haematologica. 2004 Sep;89(9):1072-81 [15377468.001]
  • [Cites] Lancet. 1985 Nov 9;2(8463):1035-9 [2865517.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Apr;42(4):358-71 [15645489.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Jul;43(3):227-38 [15846790.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Sep;161(2):125-9 [16102582.001]
  • [Cites] Blood. 1991 Oct 1;78(7):1652-7 [1912553.001]
  • [Cites] Leukemia. 1995 Mar;9(3):370-81 [7885035.001]
  • [Cites] Leuk Res. 1995 Dec;19(12):905-13 [8632659.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):17-31 [9045301.001]
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3158-68 [9738588.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Blood. 1999 Feb 1;93(3):1025-31 [9920852.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Sep;26(1):13-9 [10441000.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Oct;26(2):166-70 [10469455.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Apr;27(4):380-6 [10719368.001]
  • [Cites] Leukemia. 2000 Jun;14(6):1031-8 [10865969.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Sep;29(1):40-7 [10918392.001]
  • [Cites] Leukemia. 2000 Nov;14(11):1885-91 [11069023.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Jan;30(1):15-24 [11107171.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Int J Hematol. 2000 Oct;72(3):261-71 [11185980.001]
  • [Cites] Br J Haematol. 2000 Dec;111(3):801-6 [11122141.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):118-26 [11167792.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Jan 1;124(1):1-6 [11165314.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Jan 1;124(1):7-11 [11165315.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1405-13 [11230485.001]
  • [Cites] Br J Haematol. 2001 May;113(2):305-17 [11380393.001]
  • [Cites] Leukemia. 2001 Jun;15(6):903-9 [11417475.001]
  • [Cites] Leukemia. 2001 Jul;15(7):1133-6 [11455985.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] Haematologica. 2001 Nov;86(11):1158-64 [11694401.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jan;33(1):60-72 [11746988.001]
  • [Cites] Genes Chromosomes Cancer. 2002 May;34(1):42-7 [11921281.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jun;34(2):137-53 [11979548.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Sep;35(1):20-9 [12203786.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):406-12 [12619165.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Nov;38(3):249-52 [14506699.001]
  • [Cites] Leukemia. 2004 Jan;18(1):120-5 [14586477.001]
  • [Cites] Blood. 2004 Jan 1;103(1):229-35 [12946992.001]
  • [Cites] Leuk Lymphoma. 2003 Nov;44(11):1843-53 [14738135.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]
  • [Cites] Haematologica. 2004 Apr;89(4):408-18 [15075074.001]
  • [Cites] Br J Haematol. 2004 Aug;126(3):320-37 [15257704.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5675-87 [16110027.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5705-17 [16110030.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Br J Haematol. 2007 Jan;136(1):96-105 [17129222.001]
  • (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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27. Valencia A, Cervera J, Such E, Ibañez M, Barragán E, Fuster O, Bolufer P, Moscardó F, Sanz MA: A new reliable fluorescence in situ hybridization method for identifying multiple specific cytogenetic abnormalities in acute myeloid leukemia. Leuk Lymphoma; 2010 Apr;51(4):680-5
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  • [Title] A new reliable fluorescence in situ hybridization method for identifying multiple specific cytogenetic abnormalities in acute myeloid leukemia.
  • The usefulness of the new Chromoprobe Multiprobe AML Panel was evaluated in 80 patients with acute myeloid leukemia (AML) in parallel with conventional cytogenetics.
  • We observed a high concordance using both methods, but the panel was very useful in the detection of an inv(16)(p13q22), a cryptic t(15;17)(q22;q21), and a cryptic deletion of the CBFbeta allele not detected with cytogenetics.
  • Moreover, in six of nine patients (67%) without metaphases or with non-evaluable chromosomes, the panel identified three MLL rearrangements, two monosomy 7, one of them also with del(5q), and one inv(16)(p13q22).
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Chromosome Inversion. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 7. DNA Mutational Analysis / methods. Female. Histone-Lysine N-Methyltransferase. Humans. Male. Models, Biological. Monosomy. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. Reproducibility of Results. Substrate Specificity / genetics

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  • (PMID = 20233056.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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28. Grimwade D, Hills RK, Moorman AV, Walker H, Chatters S, Goldstone AH, Wheatley K, Harrison CJ, Burnett AK, National Cancer Research Institute Adult Leukaemia Working Group: Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials. Blood; 2010 Jul 22;116(3):354-65
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  • [Title] Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials.
  • Diagnostic karyotype provides the framework for risk-stratification schemes in acute myeloid leukemia (AML); however, the prognostic significance of many rare recurring cytogenetic abnormalities remains uncertain.
  • We studied the outcomes of 5876 patients (16-59 years of age) who were classified into 54 cytogenetic subgroups and treated in the Medical Research Council trials.
  • 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).
  • In multivariable analyses, various abnormalities predicted a significantly poorer outcome, namely abn(3q) (excluding t(3;5)(q25;q34)), inv(3)(q21q26)/t(3;3)(q21;q26), add(5q)/del(5q), -5, -7, add(7q)/del(7q), t(6;11)(q27;q23), t(10;11)(p11 approximately 13;q23), other t(11q23) (excluding t(9;11)(p21 approximately 22;q23) and t(11;19)(q23;p13)), t(9;22)(q34;q11), -17, and abn(17p).
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics


29. 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 01;28(16):2674-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • RESULTS: Rearrangements of 11q23 were the most frequent abnormality found in approximately 16% of patients, with 50% of these in infants.
  • 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.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality


30. Lane S, Saal R, Mollee P, Jones M, Grigg A, Taylor K, Seymour J, Kennedy G, Williams B, Grimmett K, Griffiths V, Gill D, Hourigan M, Marlton P: A &gt;or=1 log rise in RQ-PCR transcript levels defines molecular relapse in core binding factor acute myeloid leukemia and predicts subsequent morphologic relapse. Leuk Lymphoma; 2008 Mar;49(3):517-23
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  • [Title] A >or=1 log rise in RQ-PCR transcript levels defines molecular relapse in core binding factor acute myeloid leukemia and predicts subsequent morphologic relapse.
  • Core binding factor acute myeloid leukemia (CBF AML), with t(8;21)(q22;q22), inv(16)(p13q22) or t(16;16)(p13;q22) and the associated fusion gene transcripts AML1/ETO or CBFbeta/MYH11, has a favourable clinical prognosis although significant numbers of patients still suffer relapse.
  • However, a >or=1 log(10) rise at any stage in transcript level relative to the level from a remission bone marrow sample correlated with inferior leukemia free survival (LFS) and imminent morphologic relapse (hazard ratio 8.6).
  • [MeSH-major] Core Binding Factors. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Neoplasm, Residual / diagnosis. Predictive Value of Tests. RNA, Messenger / analysis

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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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31. Chang ST, Hsieh YC, Lee LP, Tzeng CC, Chuang SS: Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up. Chang Gung Med J; 2006 Sep-Oct;29(5):532-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
  • Acute myeloid leukemia (AML) with recurrent genetic abnormalities often carries a favorable prognosis.
  • AML with inv(16)(p13q22) occurs predominantly in younger patients and usually shows granulocytic and monocytic differentiation with abnormal eosinophils.
  • It is referred to as acute myelomonocytic leukemia with abnormal eosinophils (AMML Eo).
  • Chromosomal analysis reveled a karyotype of 46, XY, inv(16)(p13q22).
  • [MeSH-major] Eosinophils / pathology. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 17214400.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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32. 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.
  • [Title] Gain of multiple copies of the CBFB gene: a new genetic aberration in a case of granulocytic sarcoma.
  • Granulocytic sarcomas (GS) are tumor masses of immature myeloid cells presenting at an extramedullary site, mainly the skin, bone, and lymph node.
  • 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).
  • Although the myeloblasts did not show the inv(16)(p13q22) (CBFB/MYH11), a gain of multiple copies of the CBFB gene was detected with fluorescence in situ hybridization 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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33. Manfredi R, Sabbatani S, Chiodo F: Advanced acute myelogenous leukaemia (AML) during HAART-treated HIV disease, manifesting initially as a thyroid mass. Scand J Infect Dis; 2005;37(10):781-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advanced acute myelogenous leukaemia (AML) during HAART-treated HIV disease, manifesting initially as a thyroid mass.
  • A rare case report of acute myelogenous 46 XY, inv(16)(p13q22) leukaemia occurring in a patient with his HIV infection controlled by highly active antiretroviral therapy is reported, in the context of a review of the available literature evidences.
  • A such favourable clinical response to acute, advanced myelogenous leukaemia with an insidious recognition is considered infrequent, especially in the setting of HIV disease.
  • [MeSH-major] Antiretroviral Therapy, Highly Active. HIV Infections / complications. HIV Infections / drug therapy. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 16191903.001).
  • [ISSN] 0036-5548
  • [Journal-full-title] Scandinavian journal of infectious diseases
  • [ISO-abbreviation] Scand. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
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34. Shimada A, Ichikawa H, Taki T, Kubota C, Hongo T, Sako M, Morimoto A, Tawa A, Tsukimoto I, Hayashi Y: Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group. Int J Hematol; 2007 Oct;86(3):289-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group.
  • [MeSH-major] Chromosome Inversion. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics


35. Hiwatari M, Taki T, Tsuchida M, Hanada R, Hongo T, Sako M, Hayashi Y: Novel missense mutations in the tyrosine kinase domain of the platelet-derived growth factor receptor alpha(PDGFRA) gene in childhood acute myeloid leukemia with t(8;21)(q22;q22) or inv(16)(p13q22). Leukemia; 2005 Mar;19(3):476-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel missense mutations in the tyrosine kinase domain of the platelet-derived growth factor receptor alpha(PDGFRA) gene in childhood acute myeloid leukemia with t(8;21)(q22;q22) or inv(16)(p13q22).
  • [MeSH-major] Chromosome Inversion. Leukemia, Myeloid, Acute / genetics. Mutation, Missense. Protein-Tyrosine Kinases / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics
  • [MeSH-minor] Amino Acid Sequence. Child. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Molecular Sequence Data






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