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1. Whitman SP, Hackanson B, Liyanarachchi S, Liu S, Rush LJ, Maharry K, Margeson D, Davuluri R, Wen J, Witte T, Yu L, Liu C, Bloomfield CD, Marcucci G, Plass C, Caligiuri MA: DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication. Blood; 2008 Sep 1;112(5):2013-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication.
  • We report that acute myeloid leukemia (AML) with an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-PTD), exhibits increased global DNA methylation versus AML with MLL-wildtype (MLL-WT; P = .02).
  • In MLL-PTD(+) cell lines having SLC5A8 promoter hypermethylation, incubation with decitabine activated SLC5A8 expression.
  • In addition, enhanced cell death was observed in SMCT1-expressing MLL-PTD(+) AML cells treated with valproate.
  • Within the majority of MLL-PTD AML is a mechanism in which DNA hypermethylation silences a TSG that, together with MLL-PTD, can contribute further to aberrant chromatin remodeling and altered gene expression.

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  • (PMID = 18566324.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA101956; United States / NCI NIH HHS / CA / CA016058; United States / NCI NIH HHS / CA / P01 CA101956; United States / NCI NIH HHS / CA / CA089341; United States / NCI NIH HHS / CA / CA089317; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / CA077658; United States / NCI NIH HHS / CA / U24 CA114725; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA114725; United States / NCI NIH HHS / CA / K08 CA089317; United States / NCI NIH HHS / CA / CA096887
  • [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 / Cation Transport Proteins; 0 / DNA, Neoplasm; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / SLC5A8 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 614OI1Z5WI / Valproic Acid; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC2518901
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2. Horton SJ, Walf-Vorderwülbecke V, Chatters SJ, Sebire NJ, de Boer J, Williams O: Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities. Blood; 2009 May 14;113(20):4922-9
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  • [Title] Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities.
  • Chromosomal translocations involving 11q23 are frequent in infant acute leukemia and give rise to the formation of MLL fusion genes.
  • However, the dependence of acute leukemia on MLL fusion activity in vivo and the efficacy of targeting this activity to eliminate disease have not been established.
  • We have developed a model for conditional expression of MLL-ENL in hematopoietic progenitor cells, in which expression of the fusion oncogene is turned off by doxycycline.
  • Conditionally immortalized myeloblast cells derived from these progenitors were found to induce leukemia in vivo.
  • Leukemic cells isolated from primary recipient mice were shown to have acquired additional genetic abnormalities and, when transplanted into secondary recipients, induced leukemia with shortened latencies.
  • However, the leukemic cells remained dependent on MLL-ENL expression in vitro and in vivo, and its ablation resulted in regression of established leukemias.
  • This study demonstrates that even genetically complex leukemias can be reversed on inactivation of the initiating MLL fusion and has important implications for the design of novel leukemia therapies.
  • [MeSH-major] Chromosome Aberrations. Genetic Therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / antagonists & inhibitors

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  • (PMID = 19029444.001).
  • [ISSN] 1528-0020
  • [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 / DNA-Binding Proteins; 0 / Mllt1 protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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3. Tamai H, Inokuchi K: 11q23/MLL acute leukemia : update of clinical aspects. J Clin Exp Hematop; 2010;50(2):91-8
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  • [Title] 11q23/MLL acute leukemia : update of clinical aspects.
  • Rearrangements of the MLL gene located at 11q23 are common chromosomal abnormalities associated with acute leukemia (AL), especially infant and secondary leukemia after previous treatment with DNA topoisomerase II inhibitors.
  • 11q23/MLL abnormalities have been widely recognized as an important prognostic factor in AL.
  • Over 70 chromosome partners of 11q23 have been identified to date, at least 50 of which have been cloned and characterized at the molecular level.
  • Recent studies showed that the prognosis of 11q23/MLL AL varies widely according to the partner gene, the leukemia cell lineage, the age of the patient and the treatment administered.
  • Special strategies are needed to treat 11q23/MLL AL, including allogeneic hematopoietic stem cell transplantation, according to the fusion partner.
  • The development of novel methodologies, including new molecular therapeutic targets, is also needed to improve the prognosis of 11q23/MLL AL.
  • The present article provides an update on the current status of prognosis and treatment of 11q23/MLL AL according to the fusion partner.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 21123966.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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4. Verhaak RG, Wouters BJ, Erpelinck CA, Abbas S, Beverloo HB, Lugthart S, Löwenberg B, Delwel R, Valk PJ: Prediction of molecular subtypes in acute myeloid leukemia based on gene expression profiling. Haematologica; 2009 Jan;94(1):131-4
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  • [Title] Prediction of molecular subtypes in acute myeloid leukemia based on gene expression profiling.
  • We examined the gene expression profiles of two independent cohorts of patients with acute myeloid leukemia [n=247 and n=214 (younger than or equal to 60 years)] to study the applicability of gene expression profiling as a single assay in prediction of acute myeloid leukemia-specific molecular subtypes.
  • The favorable cytogenetic acute myeloid leukemia subtypes, i.e., acute myeloid leukemia with t(8;21), t(15;17) or inv(16), were predicted with maximum accuracy (positive and negative predictive value: 100%).
  • Various other characteristic molecular acute myeloid leukemia subtypes, i.e., mutant FLT3 and RAS, abnormalities involving 11q23, -5/5q-, -7/7q-, abnormalities involving 3q (abn3q) and t(9;22), could not be correctly predicted using gene expression profiling.
  • In conclusion, gene expression profiling allows accurate prediction of certain acute myeloid leukemia subtypes, e.g. those characterized by expression of chimeric transcription factors.
  • However, detection of mutations affecting signaling molecules and numerical abnormalities still requires alternative molecular methods.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18838472.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2625407
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5. Shih LY, Liang DC, Fu JF, Wu JH, Wang PN, Lin TL, Dunn P, Kuo MC, Tang TC, Lin TH, Lai CL: Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement. Leukemia; 2006 Feb;20(2):218-23
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  • [Title] Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement.
  • The fusion transcripts of MLL rearrangement [MLL(+)] in acute myeloid leukemia (AML) and their clinicohematologic correlation have not be well characterized in the previous studies.
  • We used Southern blot analysis to screen MLL(+) in de novo AML.
  • Reverse transcriptase-polymerase chain reaction was used to detect the common MLL fusion transcripts. cDNA panhandle PCR was used to identify infrequent or unknown MLL partner genes.
  • MLL(+) was identified in 114 (98 adults) of 988 AML patients.
  • MLL fusion transcripts comprised of 63 partial tandem duplication of MLL (MLL-PTD), 14 MLL-AF9, 9 MLL-AF10, 9 MLL-ELL, 8 MLL-AF6, 4 MLL-ENL and one each of MLL-AF1, MLL-AF4, MLL-MSF, MLL-LCX, MLL-LARG, MLL-SEPT6 and MLL-CBL.
  • The frequency of MLL-PTD was 7.1% in adults and 0.9% in children (P<0.001).
  • 11q23 abnormalities were detected in 64% of MLL/t11q23 and in none of MLL-PTD by conventional cytogenetics.
  • There were no differences in remission rate, event-free survival and overall survival between adult MLL-PTD and MLL/t11q23 groups.
  • The present study showed that cDNA panhandle PCR can identify all rare or novel MLL partner genes.
  • MLL-PTD was rare in childhood AML.
  • MLL(+) adults had a poor outcome with no difference in survival between MLL-PTD and MLL/t11q23 groups.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child, Preschool. Female. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 16341046.001).
  • [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 / 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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6. Worcester HD, Vasef MA: Therapy-related acute myeloid leukemia with 11q23 abnormality coexisting with refractory metastatic Ewing sarcoma: report of a case and review of the literature. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):50-4
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  • [Title] Therapy-related acute myeloid leukemia with 11q23 abnormality coexisting with refractory metastatic Ewing sarcoma: report of a case and review of the literature.
  • The patient's Ewing sarcoma remained refractory to treatment despite continuous intensified chemotherapy and was complicated by a therapy-related acute myeloid leukemia with 11q23 abnormality.
  • Examination of bone marrow at the last clinical follow up demonstrated both acute myeloid leukemia and residual metastatic Ewing sarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Neoplasms / drug therapy. Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / chemically induced. Lung Neoplasms / drug therapy. Sarcoma, Ewing / drug therapy. Translocation, Genetic


7. Saito M, Mori A, Irie T, Tanaka M, Morioka M: [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer]. Rinsho Ketsueki; 2009 Mar;50(3):192-6
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  • [Title] [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer].
  • Among cases of therapy-related acute myeloid leukemia (t-AML) due to DNA topoisomerase II inhibitors, 11q23 abnormality is often detected.
  • The usefulness of paclitaxel as a key drug in chemotherapy for breast cancer has been demonstrated.
  • In this study, we report a patient who developed t-AML with 11q23 abnormality and bone marrow metastasis after breast cancer treatment with paclitaxel.
  • Bone marrow aspiration suggested AML (M4) with (11;19)(q23;p13) chromosome abnormalities.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Bone Marrow Neoplasms / secondary. Breast Neoplasms / pathology. Chromosome Aberrations / drug effects. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / etiology. Neoplasms, Second Primary. Paclitaxel / adverse effects


8. Reichard KK, Zhang QY, Sanchez L, Hozier J, Viswanatha D, Foucar K: Acute myeloid leukemia of donor origin after allogeneic bone marrow transplantation for precursor T-cell acute lymphoblastic leukemia: case report and review of the literature. Am J Hematol; 2006 Mar;81(3):178-85
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  • [Title] Acute myeloid leukemia of donor origin after allogeneic bone marrow transplantation for precursor T-cell acute lymphoblastic leukemia: case report and review of the literature.
  • We report a case of donor-derived acute myeloid leukemia (AML) occurring in a 33-year-old man after allogeneic bone marrow transplantation (BMT) for precursor T-cell acute lymphoblastic -leukemia (T-ALL).
  • Fluorescence in-situ hybridization (FISH) analysis showed the AML to be of donor origin (i.e., karyotypically female) with an 11q23 (mixed lineage leukemia (MLL) gene) translocation, while the original T-ALL exhibited a male karyotype with abnormalities of chromosomes 6, 8, and a t(10;14)(q24;q11.2).
  • Donor-cell leukemia (DCL) after allogeneic BMT is a rare, yet well-documented, event.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / etiology. Living Donors. Neoplasms, Second Primary / etiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Chimera


9. Mikulásová Z, Ilencíková D, Slamka T, Durovcíková D: [Acute myeloblastic leukaemia with alternations of MLL proto-oncogene protein (11q23/MLL+ AML)]. Klin Onkol; 2010;23(6):401-7
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  • [Title] [Acute myeloblastic leukaemia with alternations of MLL proto-oncogene protein (11q23/MLL+ AML)].
  • [Transliterated title] Akútna myeloblastová leukémia s alteráciami MLL protoonkogénu (11q23/MLL+ AML).
  • One of the most common chromosomal breakpoint regions in acute myeloid leukaemia is the chromosome band 11q23.
  • The analysis of this region led to the discovery of the extremely promiscuous MLL gene, in which more than 60 MLL translocation partner genes have been described.
  • Among the most frequent are t(9;11)(p21-22;q23)/MLL-AF9, t(10; 11)(p13; q23)/MLL-AF10, t(11;19)(q23;p13)/MLL-ELL, ENL and t(6;11)(q27;q23)/MLL-AF6.
  • The presented work provides an overview of the molecular mechanisms by means of which MLL proto-oncogene can be converted into oncogene.
  • Genetic alternations of the MLL Proto-Oncogene Protein besides translocation are also represented by complex chromosomal rearrangements, deletions, insertions, partial tandem duplications, amplifications and gains.
  • Abnormalities of the MLL ProtoOncogene Protein are usually connected with bad prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 11 / genetics. Humans. Translocation, Genetic

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  • (PMID = 21351416.001).
  • [ISSN] 0862-495X
  • [Journal-full-title] Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
  • [ISO-abbreviation] Klin Onkol
  • [Language] slo
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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10. DiMartino JF, Lacayo NJ, Varadi M, Li L, Saraiya C, Ravindranath Y, Yu R, Sikic BI, Raimondi SC, Dahl GV: Low or absent SPARC expression in acute myeloid leukemia with MLL rearrangements is associated with sensitivity to growth inhibition by exogenous SPARC protein. Leukemia; 2006 Mar;20(3):426-32
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  • [Title] Low or absent SPARC expression in acute myeloid leukemia with MLL rearrangements is associated with sensitivity to growth inhibition by exogenous SPARC protein.
  • Although SPARC has been implicated as a tumor suppressor in humans, its function in normal or malignant hematopoiesis has not previously been studied.
  • We found that the leukemic cells of AML patients with MLL gene rearrangements express low to undetectable amounts of SPARC whereas normal hematopoietic progenitors and most AML patients express this gene.
  • SPARC RNA and protein levels were also low or undetectable in AML cell lines with MLL translocations.
  • Consistent with its tumor suppressive effects in various solid tumor models, exogenous SPARC protein selectively reduced the growth of cell lines with MLL rearrangements by inhibiting cell cycle progression from G1 to S phase.
  • The lack of SPARC expression in MLL-rearranged cell lines was associated with dense promoter methylation.
  • Our results suggest that low or absent SPARC expression is a consistent feature of AML cells with MLL rearrangements and that SPARC may function as a tumor suppressor in this subset of patients.
  • A potential role of exogenous SPARC in the therapy of MLL-rearranged AML warrants further investigation.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid / metabolism. Myeloid-Lymphoid Leukemia Protein / genetics. Osteonectin / metabolism
  • [MeSH-minor] Acute Disease. Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16424866.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / K08 CA818818; United States / NCRR NIH HHS / RR / M01 RR 00070; United States / NCI NIH HHS / CA / R01 CA90916; United States / NCI NIH HHS / CA / R01 CA92474
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MLL protein, human; 0 / Osteonectin; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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11. Zhao XC, Li CW, Dai Y, Liu XP, Qin S, Liu SH, Mi YC, Wang JX: [Combination of interphase- and metaphase-fluorescence in situ hybridization to identify 11q23/MLL abnormalities in acute leukemia patients]. Zhonghua Xue Ye Xue Za Zhi; 2006 Oct;27(10):682-6
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  • [Title] [Combination of interphase- and metaphase-fluorescence in situ hybridization to identify 11q23/MLL abnormalities in acute leukemia patients].
  • OBJECTIVE: To explore a rapid, sensitive and effective method for identifying 11 q23/MLL gene rearrangements and investigate the incidence and clinical features of adult acute leukemia (AL) patients with 11 q23/MLL abnormalities.
  • The abnormal signals were screened by interphase- fluorescence in situ hybridization (FISH) with dual-color break-apart 11 q23/MLL-specific probe, and the 11 q23/MLL gene rearrangements were determined by metaphase-FISH.
  • 0%) with 11q23/MLL translocations were revealed by FISH, among which only 4 (3.
  • Three patients were reported by CCA to have del( 11) ( q23) , while by FISH assay two of them were 11 q23/MLL translocation and one was true deletion of I lq23 telomeric terminus.
  • Furthermore by FISH assay II q23/MLL translocations were identified in one each patient with normal karyotype, with 11 q + and without overt 11 q23 abnormality.
  • Eight patients with MLL gene amplification including polysome, homogenous staining region (hsr) and double minute chromosome (dmin) were also disclosed by FISH.
  • AL patients with 11 q23/MLL abnormalities were frequently diagnosed as pro-B acute lymphoblastic leukemia (pro-B ALL) ,acute monocytic leukemia (AMoL) or biphenotypic acute leukemia (BAL).
  • CONCLUSION: FISH with dual-color break-apart I q23/MLL -specific probe is a rapid and sensitive method to detect 11 q23/MLL abnormalities, as compared with CCA.
  • FISH also effectively discloses translocations and amplifications involving 11 q23/MLL,and should be performed in patients diagnosed as pro-B ALL,AMoL or BAL, with CCA normal karyotype.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. In Situ Hybridization, Fluorescence / methods. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Chromosome Deletion. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Interphase / genetics. Male. Metaphase / genetics. Middle Aged. Translocation, Genetic

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  • (PMID = 17343201.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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12. Sierra M, Alonso A, Odero MD, Gonzalez MB, Lahortiga I, Pérez JJ, García JL, Gutiérrez NC, Calasanz MJ, San Miguel JF, Hernández JM: Geographic differences in the incidence of cytogenetic abnormalities of acute myelogenous leukemia (AML) in Spain. Leuk Res; 2006 Aug;30(8):943-8
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  • [Title] Geographic differences in the incidence of cytogenetic abnormalities of acute myelogenous leukemia (AML) in Spain.
  • The incidence of chromosomal abnormalities in acute myeloid leukemia (AML) differs according to geographical regions in Spain.
  • Age ranged between 1 month and 94 years with a median of 61 years.
  • Numerical abnormalities as sole cytogenetic changes were detected in 15% of patients, while structural aberrations were present in 28% of cases, and both abnormalities were found in 22% of patients.
  • Other chromosomal abnormalities, such as inv(16) or 11q23 rearrangements, were found at similar frequencies in the three regions.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Genetics, Population. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16503352.001).
  • [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
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13. Liu LB, Liu L, Wang XB, Xiao J, Zou P: Cytobiological and clinicobiological features of AML with 11q23 chromosome abnormalities. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):932-6

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  • [Title] Cytobiological and clinicobiological features of AML with 11q23 chromosome abnormalities.
  • To investigate the interrelationship among morphology, immunology and clinical features in adult acute myeloid leukemia cases with 11q23 chromosome abnormalities, 210 newly diagnosed AML patients were retrospectively analyzed by cell morphology, immunophenotyping, G-banding or R-bamding analysis and clinical features.
  • The results showed that 13 cases were found with 11q23 rearrangements or deletion (the incidence rate was 6.19%.
  • Immunophenotyping tests indicated that AML cases with 11q23 abnormalities usually expressed the marker molecules of hematopoietic stem or progenitor cells, monocytic lineage cells, such as CD34, CD117, CD14, CD15 and CD11b.
  • The complete remission rate of the cases with 11q23 abnormalities was comparable to that of the cases with normal karyotype (P = 0.075), but the median disease-free survival in the former was significantly lower than that in the latter (P < 0.001).
  • It is concluded that the category AML with 11q23 abnormalities accounts for 6.19% of all the newly diagnosed AML cases, that seems to be closely associated with monocytic differentiation blocking with a dismal prognosis.

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  • (PMID = 16403253.001).
  • [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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14. Shin SY, Koo SH, Kwon KC, Park JW, Song JH, Ko YH, Jo DY: Chromosome 8 pentasomy with partial tandem duplication of 11q23 in a case of de novo acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Oct;194(1):44-7
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  • [Title] Chromosome 8 pentasomy with partial tandem duplication of 11q23 in a case of de novo acute myeloid leukemia.
  • Polysomy 8 is a rare abnormality, one that has been reported as associated with secondary evolution, monocytic differentiation, or poor prognosis in myeloid neoplasm.
  • To date, only three cases of pentasomy 8 accompanied with 11q23 rearrangement have been reported.
  • Reported here is a novel case of pentasomy 8 with partial tandem duplication of 11q23 in de novo acute myeloid leukemia.
  • The findings contribute to understanding of the relation between the two abnormalities, which have their own individual leukemogenic potencies.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Aged. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD15 / blood. Antigens, CD34 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Gene Duplication. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Proto-Oncogene Proteins c-kit / blood. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 19737653.001).
  • [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 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.11.2 / Antigens, CD13
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15. Tamai H, Yamaguchi H, Hamaguchi H, Yagasaki F, Bessho M, Kobayashi T, Akiyama H, Sakamaki H, Takahashi S, Tojo A, Ohmine K, Ozawa K, Okumura H, Nakao S, Arai A, Miura O, Toyota S, Gomi S, Murai Y, Usui N, Miyazawa K, Ohyashiki K, Takahashi N, Sawada K, Kato A, Oshimi K, Inokuchi K, Dan K: Clinical features of adult acute leukemia with 11q23 abnormalities in Japan: a co-operative multicenter study. Int J Hematol; 2008 Mar;87(2):195-202
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  • [Title] Clinical features of adult acute leukemia with 11q23 abnormalities in Japan: a co-operative multicenter study.
  • To clarify the clinical features of adult patients with acute leukemia (AL) with 11q23 abnormalities, we performed a retrospective analysis of data from 58 adult Japanese patients: 51 with acute myeloid leukemia (AML), and 7 with acute lymphoblastic leukemia (ALL).
  • The incidences according to fusion partners in AML were: t(9;11), 31.3%; t(11;19), 27.4%; t(6;11), 21.5%.
  • The incidence of patients with t(11;19) was higher than those in the US and Europe, and the incidence of t(4;11) was lower than that in childhood.
  • The results indicated the poor prognosis of AML with 11q23 abnormalities regardless of the fusion partners.
  • AML patients with 11q23 aged <60 years in the first CR who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) showed a more favorable outcome than those treated without allo-HSCT, although the differences were not statistically significant (P = 0.322 for DFS, P = 0.138 for OS).
  • This result suggests that treatment strategies including allo-HSCT may be considered in the first CR in cases of AML with 11q23 abnormalities.
  • However, further studies involving a large number of cases are required to assess the effect of allo-HSCT on adult AL with 11q23 abnormalities.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • (PMID = 18253706.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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16. Garzon R, Volinia S, Liu CG, Fernandez-Cymering C, Palumbo T, Pichiorri F, Fabbri M, Coombes K, Alder H, Nakamura T, Flomenberg N, Marcucci G, Calin GA, Kornblau SM, Kantarjian H, Bloomfield CD, Andreeff M, Croce CM: MicroRNA signatures associated with cytogenetics and prognosis in acute myeloid leukemia. Blood; 2008 Mar 15;111(6):3183-9
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  • [Title] MicroRNA signatures associated with cytogenetics and prognosis in acute myeloid leukemia.
  • To determine whether miRNAs are associated with cytogenetic abnormalities and clinical features in acute myeloid leukemia (AML), we evaluated the miRNA expression of CD34(+) cells and 122 untreated adult AML cases using a microarray platform.
  • We identified several miRNAs differentially expressed between CD34(+) normal cells and the AML samples. miRNA expression was also closely associated with selected cytogenetic and molecular abnormalities, such as t(11q23), isolated trisomy 8, and FLT3-ITD mutations.

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  • (PMID = 18187662.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01 CA076259; United States / NCI NIH HHS / CA / P01CA81534; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / P01 CA055164
  • [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 / Antigens, CD34; 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2265455
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17. Lu Y, Xu W, Chen Z, Lou J, Jin J: [Clinical and cytogenetics studies on acute myeloid leukemia with abnormality of chromosome 11]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Oct;25(5):583-5
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  • [Title] [Clinical and cytogenetics studies on acute myeloid leukemia with abnormality of chromosome 11].
  • OBJECTIVE: To investigate the incidence of chromosome 11 abnormality in acute myeloid leukemia and its relationship with the clinical aspects and prognosis.
  • METHODS: Conventional cytogenetic analysis of R-band was used to detect the abnormalities of chromosome 11 in 356 acute myeloid leukemia patients.
  • RESULTS: Thirty-four out of 356 patients (9.55%) had abnormalities of chromosome 11, of which 20 (58.8%) involved in 11q23, 7 (19.9%) had translocations involving 11p15, 5 (14.7%) had-11, and the rest had other abnormalities such as +11, and t(11;14).
  • The incidence of 11q23 involvement in M4 and M5 was higher than other subtypes of acute myeloid leukemia (AML).
  • Ten cases with 11q23 abnormality had additional cytogenetic aberrations.
  • The CR rate was lower than that of whole cases of acute myeloid leukemia(34.3% versus 64.0%).
  • The CR rate of AML with 11q23 abnormality was lower than that of AML with normal karyotype (25% versus 55.6%).
  • In other 10 patients with additional chromosome aberrations, the CR rate was lower than that of AML with 11q23 alone.
  • Only 2 patients acquired CR in 5 patients with-11.
  • CONCLUSION: 11q23 was a frequent aberration in chromosome 11 anomaly, which was often detected in M4 and M5.
  • It might be associated with the pathogenesis of acute monolytic leukemia.
  • The patients with chromosome 11 anomaly had poorer prognosis.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18841578.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan 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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18. Kuchenbauer F, Kern W, Schoch C, Kohlmann A, Hiddemann W, Haferlach T, Schnittger S: Detailed analysis of FLT3 expression levels in acute myeloid leukemia. Haematologica; 2005 Dec;90(12):1617-25
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  • [Title] Detailed analysis of FLT3 expression levels in acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of acute myeloid leukemia (AML).
  • Independent analysis of FLT3 expression in cytogenetic AML subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive AML.
  • On the molecular level, no differences in FLT3 expression levels were detected between AML with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).
  • Furthermore, no significant difference could be found between the group of t(11q23) and MLL-PTD (p=0.180) or between MLL-PTD positive and MLL negative normal karyotypes (p=0.859).
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Disease-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences

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  • [CommentIn] Haematologica. 2005 Dec;90(12):1586 [16330422.001]
  • (PMID = 16330434.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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19. Gluzman DF, Nadgornaya VA, Sklyarenko LM, Zavelevych MP, Koval SV, Poludnenko LY, Ivanovskaya TS: Study of morphocytochemical and immunophenotypic features of acute leukemia stem cells. Exp Oncol; 2008 Jun;30(2):102-5
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  • [Title] Study of morphocytochemical and immunophenotypic features of acute leukemia stem cells.
  • The results of our studies suggest that the standard panel for classification of acute leukemias should be supplemented with several new markers allowing us to identify more precisely the different forms of the leukemias being of the closely related origin, for example AML M6b and AML M7.
  • We have also found the similarity between blast cells in pro-B-ALL [t (4;11), 11q23] and AML M5a [t (9;11), 11q23].
  • Such similarity of immunophenotype and cytogenetic abnormalities in blast cells in pro-B-ALL and AML M5a may be considered as hint explaining the cases of AML M5a as a recurrence of leukemia in children with originally diagnosed pro-B-ALL.
  • [MeSH-major] Immunophenotyping / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Child. Hematopoietic Stem Cells / cytology. Humans. Leukemia / pathology. Megakaryocytes / metabolism. Mice. Mice, SCID. Neoplastic Stem Cells / cytology. Stem Cells / cytology

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  • (PMID = 18566571.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ukraine
  • [Number-of-references] 25
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20. Balkhi MY, Trivedi AK, Geletu M, Christopeit M, Bohlander SK, Behre HM, Behre G: Proteomics of acute myeloid leukaemia: Cytogenetic risk groups differ specifically in their proteome, interactome and post-translational protein modifications. Oncogene; 2006 Nov 9;25(53):7041-58
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  • [Title] Proteomics of acute myeloid leukaemia: Cytogenetic risk groups differ specifically in their proteome, interactome and post-translational protein modifications.
  • Acute myeloid leukaemia (AML) is characterized by specific cytogenetic aberrations that are strong determinants of prognostic outcome and therapeutic response.
  • Because the pathological outcome of AML patients with cytogenetic abnormalities differs considerably, we hypothesized that their proteome may also differ specifically in their expression pattern, protein interaction pathways and post-translational modifications (PTM).
  • We performed this study using 42 AML patients diagnosed for various cytogenetic abnormalities based on two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time of flight mass spectrometry (MS) and MSMS tandem MS.
  • The interactome analysis based on computational bioinformatics reveals major regulating networks: MAPK8 and MYC for complex aberrant karyotype, TP53 for t(8;21), TP53-MYC-PRKAC for 11q23 and JUN and MYC for Inv(16).
  • Further, we analysed 42 MS spectra representative of hnRNPH1, calreticulin and hnRNPA2/B1 in a peak explorer, which reveals a cytogenetic-specific PTM of beta-O-linked N-acetyl glucosamine (O-GlcNAc) of hnRNPH1 in AML patients with 11q23 translocation, an acetylation of calreticulin in t(8;21) translocation and methylation of hnRNPA2/B1 in patients with translocations of t(8;21) and inv(16).
  • [MeSH-major] Cytogenetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Protein Processing, Post-Translational. Proteome / genetics. Proteome / metabolism


21. Chen W, Wang E, Lu Y, Gaal KK, Huang Q: Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review. Am J Clin Pathol; 2010 Jan;133(1):75-82
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  • [Title] Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) is a rare secondary leukemia following chemotherapy and/or radiotherapy for primary malignancies.
  • Chromosomal 11q23 abnormality, frequently detected in therapy-related acute myeloid leukemia, is the most common cytogenetic alteration in t-ALL.
  • However, t-ALL cases without 11q23 abnormality have been rarely described.
  • We describe 6 adults with secondary t-ALL without 11q23 abnormalities following various treatment regimens for primary malignancies.
  • In the 48 cases, an 11q23 abnormality involving the MLL gene locus was the predominant chromosomal aberration (32 [67%]), followed by t(9;22) (6 [13%]) and a normal karyotype (4 [8%]).
  • Compared with t-ALL cases with an 11q23 abnormality, cases without an 11q23 abnormality had a relatively longer latency period (median, 36 vs 19 months) and a different primary malignancy spectrum.
  • [MeSH-major] Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 20023261.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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22. Tauchi H, Tomizawa D, Eguchi M, Eguchi-Ishimae M, Koh K, Hirayama M, Miyamura N, Kinukawa N, Hayashi Y, Horibe K, Ishii E: Clinical features and outcome of MLL gene rearranged acute lymphoblastic leukemia in infants with additional chromosomal abnormalities other than 11q23 translocation. Leuk Res; 2008 Oct;32(10):1523-9
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  • [Title] Clinical features and outcome of MLL gene rearranged acute lymphoblastic leukemia in infants with additional chromosomal abnormalities other than 11q23 translocation.
  • The treatment outcome for infant acute lymphoblastic leukemia (ALL) with positive MLL gene rearrangements remains poor.
  • We analyzed whether additional chromosomal abnormalities (ACA) other than 11q23 translocation could affect the disease behavior and its prognosis.
  • Eighteen of seventy-four patients with infant acute lymphoblastic leukemia showed ACA, including three-way translocations in four, other novel translocations in four, and complex structural chromosomal changes in four.
  • Only age less than 6 months and positive central nervous system leukemia were significant prognostic factors by multivariate analysis.
  • Genetic alterations induced by additional chromosomal changes may be associated with disease progression and poorer overall survival rates in infants with MLL-rearranged ALL.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Chromosomes, Human, Pair 11. Disease-Free Survival. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Survival Rate. Translocation, Genetic. Treatment Outcome

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  • (PMID = 18448165.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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23. Maitta RW, Cannizzaro LA, Ramesh KH: Association of MLL amplification with poor outcome in acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):40-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of MLL amplification with poor outcome in acute myeloid leukemia.
  • Chromosomal rearrangements and amplification of the MLL gene at 11q23 are common abnormalities found in patients with severe myelodysplastic disorders and lymphoid and acute myeloid leukemias.
  • MLL rearrangements are associated with aggressive disease in both children and adults, with current evidence suggesting that MLL alterations are associated with a poor prognosis.
  • We report the clinical, cytogenetic and histologic findings of a patient who presented with a de novo diagnosis of AML-M4 and who fits the profile of patients presenting with MLL alterations, such as old age at presentation, rapid progression, therapeutic refractoriness, and poor outcome.
  • Two bone marrow specimens taken 1 month apart show the rapid deterioration of the patient's cytogenetic abnormalities at the 11q23 locus, with amplification of MLL that was originally seen as a homogeneously staining region (hsr) on chromosome 11.
  • In the second biopsy the hsr and MLL amplification appears as nonreciprocal translocation of multiple copies in the form of marked amplification of MLL on chromosome 16 in a background of increasing chromosomal aberrations.
  • This case suggests that either the MLL amplification and translocation alone or in conjunction with other flanking oncogenes may have played an important role in poor patient outcome.
  • [MeSH-major] Gene Amplification / physiology. Leukemia, Myeloid, Acute / diagnosis. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19480936.001).
  • [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] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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24. Cerveira N, Correia C, Bizarro S, Pinto C, Lisboa S, Mariz JM, Marques M, Teixeira MR: SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23). Oncogene; 2006 Oct 5;25(45):6147-52
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  • [Title] SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23).
  • We have identified a new mixed lineage leukemia (MLL) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality.
  • Fluorescence in situ hybridization demonstrated a rearrangement of the MLL gene and molecular genetic analyses identified a septin family gene, SEPT2, located on chromosome 2q37, as the fusion partner of MLL.
  • RNA and DNA analyses showed the existence of an in-frame fusion of MLL exon 7 with SEPT2 exon 3, with the genomic breakpoints located in intron 7 and 2 of MLL and SEPT2, respectively.
  • Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in MLL intron 7 and SEPT2 intron 2.
  • SEPT2 is the fifth septin family gene fused with MLL, making this gene family the most frequently involved in MLL-related AML (about 10% of all known fusion partners).
  • Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of MLL-associated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Phosphoric Monoester Hydrolases / genetics. Translocation, Genetic

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  • (PMID = 16682951.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
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25. Bumbea H, Serghei L, Vlădăreanu AM, Stefan LM, Casleanu D, Voican I, Begu M: Cryptic genomic abnormalities associated with coexpression of KOR-SA3544 and NG.2 in proB acute lymphoblastic leukemia. Rom J Intern Med; 2007;45(4):387-91
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  • [Title] Cryptic genomic abnormalities associated with coexpression of KOR-SA3544 and NG.2 in proB acute lymphoblastic leukemia.
  • Balanced translocations and chromosomal rearrangements are rare events involved in acute lymphoblastic leukemogenesis, yet little is known about the actual gene anomalies responsible for it.
  • These rearrangements are reflected by the expression of certain surface markers such as KOR-SA3544 for t(9,22) and NG.2 for 11q23 rearrangements and may indicate a poor prognosis.
  • Our purpose was to investigate whether these immunophenotypical and cytogenetical markers also correlate with cytogenetical molecular abnormalities.
  • Initially we have investigated by imunophenotyping 28 patients with acute lymphoblastic leukemia, admitted in the Department of Hematology during the last year.
  • Of those 15 patients, 7 had pro-B acute lymphoblastic leukemia immunophenotype: CD19+CD10+CD34+.
  • In particular, one of them had a complex karyotype, coexpression of myeloid markers (CD33) and a history of breast cancer.
  • [MeSH-major] Antigens / metabolism. Chromosome Aberrations. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteoglycans / metabolism. Receptors, Opioid, kappa / metabolism

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  • (PMID = 18767415.001).
  • [ISSN] 1220-4749
  • [Journal-full-title] Romanian journal of internal medicine = Revue roumaine de médecine interne
  • [ISO-abbreviation] Rom J Intern Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antigens; 0 / OPRK1 protein, human; 0 / Proteoglycans; 0 / Receptors, Opioid, kappa; 0 / chondroitin sulfate proteoglycan 4
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26. Asleson AD, Morgan V, Smith S, Velagaleti GV: Amplification of the RARA gene in acute myeloid leukemia: significant finding or coincidental observation? Cancer Genet Cytogenet; 2010 Oct 1;202(1):33-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification of the RARA gene in acute myeloid leukemia: significant finding or coincidental observation?
  • Oncogene amplification resulting in aberrant expression, although common in solid tumors, is rare in acute myeloid leukemia (AML) and is mostly associated with amplification of MYC, RUNX1, and MLL genes.
  • We present a unique case of a 59-year-old female with a history of breast cancer, now presenting with pancytopenia and bilateral infiltration with effusion in nodules of the right upper lobe of the lung.
  • Chromosome analysis demonstrated a hypodiploid clone with complex numerical/structural abnormalities including 5q deletion, monosomy 7, as well as structurally rearranged chromosome 11 and several marker chromosomes.
  • Fluorescence in situ hybridization (FISH) analysis showed amplification of RARA, loss of 7q, monosomy 7, loss of DEK (6p23), and additional copies of NUP214 (9q34) and MLL (11q23).
  • [MeSH-major] Gene Amplification. Leukemia, Myeloid, Acute / genetics. Receptors, Retinoic Acid / genetics
  • [MeSH-minor] Chromosome Mapping. Chromosomes, Human, Pair 11 / genetics. Female. Flow Cytometry. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Middle Aged

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804918.001).
  • [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 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha
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27. 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).
  • In patients with t(15;17) treated with extended all-trans retinoic acid and anthracycline-based chemotherapy, additional cytogenetic changes did not have an impact on prognosis.
  • Similarly, additional abnormalities did not have a significant adverse effect in t(8;21) AML; whereas in patients with inv(16), the presence of additional changes, particularly +22, predicted a better outcome (P = .004).
  • 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).
  • Patients lacking the aforementioned favorable or adverse aberrations but with 4 or more unrelated abnormalities also exhibited a significantly poorer prognosis (designated "complex" karyotype group).
  • 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


28. 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.
  • Today, the challenge is to propose an individual follow-up for each patient even for those with a rare fusion event.
  • 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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29. Wakui M, Kuriyama K, Miyazaki Y, Hata T, Taniwaki M, Ohtake S, Sakamaki H, Miyawaki S, Naoe T, Ohno R, Tomonaga M: Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol. Int J Hematol; 2008 Mar;87(2):144-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol.
  • We reviewed and categorized 638 of 809 patients who were registered in the Japan Adult Leukemia Study Group acute myeloid leukemia (AML)-97 protocol using morphological means.
  • According to the WHO classification, 171 patients (26.8%) had AML with recurrent genetic abnormalities, 133 (20.8%) had AML with multilineage dysplasia (MLD), 331 (51.9%) had AML not otherwise categorized, and 3 (0.5%) had acute leukemia of ambiguous lineage.
  • The 5-year survival rates for patients with favorable, intermediate, and adverse karyotypes were 63.4, 39.1, and 0.0%, respectively, and 35.5% for those with 11q23 abnormalities (P < 0.0001).
  • Overall survival (OS) did not significantly differ between nine patients with t(9;11) and 23 with other 11q23 abnormalities (P = 0.22).
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries


30. 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.
  • Some immunophenotypes correlate with cytogenetic abnormalities and prognosis.
  • THE AIM OF OUR STUDY: Is to determine aberrant lymphoid antigen expression in Saudi acute myeloid leukemia (AML), correlate them with FAB subtypes, evaluate early surface markers CD7 and CD56, and to investigate the role of cytoplasmic CD79a (a B cell marker that is assigned a high score of 2.0 in the WHO classification).
  • CD9 was the most frequently expressed lymphoid antigen (29.4%) followed by CD7 & CD19 (11.8%), CD4 (8.8%) and CD22 (2.9%).
  • CD9 was expressed in 3/6 (50%) of M3 cases, CD7 was expressed in 11.8% and was mostly confined to FAB M1 and M2 and associated with immature antigens CD34, HLA-DR and TdT.
  • CD56 was also detected in 2 cases with 11q23 rearrangement.
  • CD56 was expressed in 2/7 (28.6%) M2 cases, and was associated with t (8;21) (q22;q22) together with CD19.
  • CD79a was expressed in one case together with CD19, diagnosed as acute biphenotypic leukemia, and was associated with t(8;21) (q22;q22).
  • [MeSH-major] Antigens, CD56 / analysis. Antigens, CD7 / analysis. Antigens, CD79 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / diagnosis

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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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31. 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.
  • Because AML is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.
  • RESULTS: Rearrangements of 11q23 were the most frequent abnormality found in approximately 16% of patients, with 50% of these in infants.
  • The outcome for all patients with 11q23 abnormalities was intermediate; no difference was observed for those with t(9;11)(p21-22;q23).
  • An adverse outcome was observed in patients with monosomy 7, abnormalities of 5q, and t(6;9)(p23;q34).
  • Abnormalities of 3q and complex karyotypes, in the absence of favorable-risk features, have been associated with an adverse outcome in adults, but the results were not significant in this childhood series.
  • However, the presence of 12p abnormalities predicted a poor outcome.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality


32. Pajuelo-Gámez JC, Cervera J, García-Casado Z, Mena-Durán AV, Valencia A, Barragán E, Such E, Bolufer P, Sanz MA: MLL amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Apr 15;174(2):127-31
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  • [Title] MLL amplification in acute myeloid leukemia.
  • The chromosomal alterations at 11q23 that involve the mixed-lineage leukemia gene (MLL, HTRX1, HRX, ALL1) are one of the most common cytogenetic abnormalities in acute leukemia and have been associated with a poor prognosis.
  • Given that not all MLL alterations are seen under conventional cytogenetics or fluorescence in situ hybridization (FISH), it is very important to use molecular techniques to determine the cause of alteration.
  • In this study, we describe two cases of AML in which FISH analysis showed a high-level 11q23 amplification, to confirm if this overexpression may be accompanied by partial tandem duplication of the MLL gene (MLL-PTD).
  • The 11q23 region characterization included conventional cytogenetics, FISH, and comparative genomic hybridization analysis to study the expression patterns of several oncogenes located within the amplified region and detection of partial tandem duplication of the MLL gene by reverse-transcription polymerase chain reaction (RT-PCR) and sequencing.
  • MLL-PTD were detected in the two patients.
  • Moreover, patient 1 showed amplification of the MLL flanking region.
  • Our data suggest that molecular methods such as RT-PCR or sequencing should be used to detect MLL alterations, and that amplification of MLL locus may be extended to its flanking region.
  • [MeSH-major] Gene Amplification. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Acute Disease. Aged. Aneuploidy. Base Sequence. Chromosome Banding. Chromosome Deletion. Female. Genome, Human. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization / methods. Sequence Analysis, DNA

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  • (PMID = 17452254.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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33. Scolnik MP, Aranguren PN, Cuello MT, Palacios MF, Sanjurjo J, Giunta M, Bracco MM, Acevedo S: Biphenotypic acute leukemia with t(15;17). Leuk Lymphoma; 2005 Apr;46(4):607-10
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  • [Title] Biphenotypic acute leukemia with t(15;17).
  • Biphenotypic acute leukemias (BAL) represent 5% of all acute leukemias.
  • The most frequent cytogenetic abnormalities described are Philadelphia chromosome and 11q23 involvement.
  • Immunophenotype revealed the compromise of myeloid and B-lymphoid lineages.
  • This report describes a BAL case with an unfrequent cytogenetic abnormality, and highlights the importance of correlating the results of multiple diagnostic methods in order to establish a correct diagnosis and treatment in BAL patients.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Female. Flow Cytometry / methods. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Trisomy

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  • (PMID = 16019491.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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34. Ferguson EC, Talley P, Vora A: Translocation (6;17)(q23;q11.2): a novel cytogenetic abnormality in congenital acute myeloid leukemia? Cancer Genet Cytogenet; 2005 Nov;163(1):71-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (6;17)(q23;q11.2): a novel cytogenetic abnormality in congenital acute myeloid leukemia?
  • Congenital leukemia occurring within 4 weeks of birth is extremely rare and, excluding transient neonatal myeloproliferation associated with Down syndrome, makes up approximately 1% of childhood leukemias.
  • It is usually seen as acute myeloid leukemia (AML), most frequently French-American-British (FAB) types M4 and M5.
  • Recurrent cytogenetic abnormalities have been reported in this group, and in approximately one third of cases the MLL gene at 11q23 is involved.
  • We present a case of congenital leukemia (AML FAB type M1) with an acquired translocation between chromosomes 6 and 17.
  • [MeSH-major] Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 6. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 16271959.001).
  • [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
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35. Gröschel S, Lugthart S, Schlenk RF, Valk PJ, Eiwen K, Goudswaard C, van Putten WJ, Kayser S, Verdonck LF, Lübbert M, Ossenkoppele GJ, Germing U, Schmidt-Wolf I, Schlegelberger B, Krauter J, Ganser A, Döhner H, Löwenberg B, Döhner K, Delwel R: High EVI1 expression predicts outcome in younger adult patients with acute myeloid leukemia and is associated with distinct cytogenetic abnormalities. J Clin Oncol; 2010 Apr 20;28(12):2101-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High EVI1 expression predicts outcome in younger adult patients with acute myeloid leukemia and is associated with distinct cytogenetic abnormalities.
  • PURPOSE The purpose of this study was to investigate frequency and prognostic significance of high EVI1 expression in acute myeloid leukemia (AML).
  • High EVI1 levels (EVI1(+)) were found with similar frequencies in both cohorts combined, with a 10.7% incidence (148 of 1,382).
  • Besides inv(3)/t(3;3), EVI1(+) was significantly associated with chromosome abnormalities monosomy 7 and t(11q23), conferring prognostic impact within these two cytogenetic subsets.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 7. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • (PMID = 20308656.001).
  • [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
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Transcription Factors
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36. de Jesus Marques-Salles T, Liehr T, Mkrtchyan H, Raimondi SC, Tavares de Souza M, de Figueiredo AF, Rouxinol S, Jordy Macedo FC, Abdelhay E, Santos N, Macedo Silva ML: A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):59-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia.
  • Infants diagnosed with acute myelogenous leukemia (AML) are likely to have subtypes M4 or M5 characterized by 11q23 abnormalities like a t(9;11)(p22;q23).
  • Detection of all possible types of chromosomal abnormalities, including mixed lineage leukemia (MLL) gene rearrangements at 11q23, is of importance for the identification of biological subgroups, which might differ in drug resistance and/or clinical outcome.
  • Here, we report the clinical, conventional banding and molecular cytogenetics data of a 6-month-old boy with an AML-M5 presenting with a unique cryptic rearrangement involving the MLL gene: a three-way t(9;19;11)(p11.2;p13.1;q23).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 19167614.001).
  • [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, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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37. Montesinos P, González JD, González J, Rayón C, de Lisa E, Amigo ML, Ossenkoppele GJ, Peñarrubia MJ, Pérez-Encinas M, Bergua J, Debén G, Sayas MJ, de la Serna J, Ribera JM, Bueno J, Milone G, Rivas C, Brunet S, Löwenberg B, Sanz M: Therapy-related myeloid neoplasms in patients with acute promyelocytic leukemia treated with all-trans-retinoic Acid and anthracycline-based chemotherapy. J Clin Oncol; 2010 Aug 20;28(24):3872-9
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myeloid neoplasms in patients with acute promyelocytic leukemia treated with all-trans-retinoic Acid and anthracycline-based chemotherapy.
  • PURPOSE: We analyzed the incidence, risk factors, and outcome of therapy-related myeloid neoplasms (t-MNs) in patients with acute promyelocytic leukemia (APL) in first complete remission (CR).
  • Partial and complete deletions of chromosomes 5 and 7 (nine patients) and 11q23 rearrangements (three patients) were the most common cytogenetic abnormalities.
  • [MeSH-major] Anthracyclines / adverse effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Neoplasms / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / chemically induced. Tretinoin / adverse effects

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  • (PMID = 20625122.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 5688UTC01R / Tretinoin
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38. Jarosova M, Takacova S, Holzerova M, Priwitzerova M, Divoka M, Lakoma I, Mihal V, Indrak K, Divoky V: Cryptic MLL-AF10 fusion caused by insertion of duplicated 5' part of MLL into 10p12 in acute leukemia: a case report. Cancer Genet Cytogenet; 2005 Oct 15;162(2):179-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cryptic MLL-AF10 fusion caused by insertion of duplicated 5' part of MLL into 10p12 in acute leukemia: a case report.
  • Chromosomal translocations involving the mixed lineage leukemia gene (MLL) located at 11q23 belong to common chromosomal abnormalities in both acute lymphoblastic (ALL) and acute myeloid leukemias (AML).
  • It has been suggested that the mechanism of MLL leukemogenesis might be a result of a gain-of-function effect of the MLL fusion gene and simultaneous loss of function of one of the MLL alleles (haploinsufficiency).
  • One of the recurrent translocations in AML-M5 involves chromosomal locus 10p12 and results in the MLL-AF10 fusion gene.
  • Several mechanisms leading to MLL-AF10 fusion have been reported, and they have involved rearrangement of the 11q23 region.
  • We present a detailed structural analysis of an AML case with an extra copy of the 5' part of MLL region and its insertion into the short arm of chromosome 10, resulting in an MLL-AF10 fusion without rearrangement of the MLL alleles on both chromosomes 11.
  • Our observation supports a role for a simple MLL gain-of-function in leukemogenesis.
  • [MeSH-major] Chromosomes, Human, Pair 10. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16213369.001).
  • [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 / MLL protein, human; 0 / MLL-AF10 fusion 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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39. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • However, the incidence and type of MLL rearrangements have not been determined in common ALL (cALL) and CD10+ or CD10- pre-B ALL.
  • EXPERIMENTAL DESIGN: To address this question, we analyzed 29 patients with pro-B ALL, 11 patients with CD10- pre-B ALL, 23 pre-B, and 26 cALL patients with CD10 on 20% to 80%, as well as 136 pre-B and 143 cALL patients with CD10 > or = 80% of blasts.
  • Conventional cytogenetics were done to detect 11q23 abnormalities and in parallel the potential involvement of the MLL gene was evaluated with a split apart fluorescence in situ hybridization probe set.
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • However, no 11q23/MLL translocation was identified among the CD10+ pre-B and cALL patients.
  • MLL-rearranged pro-B and CD10- pre-B ALL cases had similar clinical and immunophenotypic (coexpression of CDw65 and CD15) features at initial diagnosis.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16707593.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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40. Spector LG, Xie Y, Robison LL, Heerema NA, Hilden JM, Lange B, Felix CA, Davies SM, Slavin J, Potter JD, Blair CK, Reaman GH, Ross JA: Maternal diet and infant leukemia: the DNA topoisomerase II inhibitor hypothesis: a report from the children's oncology group. Cancer Epidemiol Biomarkers Prev; 2005 Mar;14(3):651-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maternal diet and infant leukemia: the DNA topoisomerase II inhibitor hypothesis: a report from the children's oncology group.
  • BACKGROUND: The MLL 11q23 translocation arises in utero and is present in 75% of infant leukemias.
  • That MLL+ acute myeloid leukemia (AML) can arise following chemotherapy with DNA topoisomerase II (DNAt2) inhibitors suggests that these substances, which also occur naturally in foods, may contribute toward infant leukemia.
  • We hypothesized that maternal consumption of dietary DNAt2 inhibitors during pregnancy would increase the risk of infant leukemia, particularly AML(MLL+).
  • METHODS: This Children's Oncology Group case-control study consisted of 240 incident cases of infant acute leukemia [AML and acute lymphoblastic leukemia (ALL)] diagnosed during 1996 to 2002 and 255 random digit dialed controls.
  • RESULTS: There was little evidence of an association between the specific DNAt2 index and leukemia overall and by subtype.
  • An exception was AML(MLL+); odds ratios (95% confidence intervals) comparing the second to fourth quartiles to the first were 1.9 (0.5-7.0), 2.1 (0.6-7.7), and 3.2 (0.9-11.9), respectively (P for trend = 0.10).
  • For the vegetable and fruit index, there were significant or near-significant inverse linear trends for all leukemias combined, ALL(MLL+), and AML(MLL-).
  • CONCLUSION: Overall, maternal consumption of fresh vegetables and fruits during pregnancy was associated with a decreased risk of infant leukemia, particularly MLL+.
  • However, for AML(MLL+) cases, maternal consumption of specific DNAt2 inhibitors seemed to increase risk.
  • Although based on small numbers, these data provide some support for distinct etiologic pathways in infant leukemia.

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  • (PMID = 15767345.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA079940; United States / NCI NIH HHS / CA / CA79940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
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41. Andersson A, Edén P, Olofsson T, Fioretos T: Gene expression signatures in childhood acute leukemias are largely unique and distinct from those of normal tissues and other malignancies. BMC Med Genomics; 2010;3:6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression signatures in childhood acute leukemias are largely unique and distinct from those of normal tissues and other malignancies.
  • BACKGROUND: Childhood leukemia is characterized by the presence of balanced chromosomal translocations or by other structural or numerical chromosomal changes.
  • It is well know that leukemias with specific molecular abnormalities display profoundly different global gene expression profiles.
  • METHODS: Using gene set enrichment analysis, we systematically explored whether the transcriptional programs in childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML) were significantly similar to those in different flow-sorted subpopulations of normal hematopoietic cells (n = 8), normal non-hematopoietic tissues (n = 22) or human cancer tissues (n = 13).
  • Moreover, the 11q23/MLL subtype of ALL showed similarities with non-hematopoietic tissues.
  • CONCLUSIONS: This study demonstrates, for the first time, that the expression profiles of childhood leukemia are largely unique, with limited similarities to transcriptional programs active in normal hematopoietic cells, non-hematopoietic normal tissues or the most common forms of human cancer.
  • In addition to providing important pathogenetic insights, these findings should facilitate the identification of candidate genes or transcriptional programs that can be used as unique targets in leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20211010.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2845086
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42. Fröhling S, Schlenk RF, Kayser S, Morhardt M, Benner A, Döhner K, Döhner H, German-Austrian AML Study Group: Cytogenetics and age are major determinants of outcome in intensively treated acute myeloid leukemia patients older than 60 years: results from AMLSG trial AML HD98-B. Blood; 2006 Nov 15;108(10):3280-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics and age are major determinants of outcome in intensively treated acute myeloid leukemia patients older than 60 years: results from AMLSG trial AML HD98-B.
  • To assess the prognostic impact of cytogenetics in elderly patients with acute myeloid leukemia (AML) receiving intensive induction and consolidation treatment according to a single protocol specifically designed for patients above age 60, pretreatment samples from 361 patients registered for the AML HD98-B trial of the German-Austrian AML Study Group were analyzed by chromosome banding and fluorescence in situ hybridization, and cytogenetic findings were correlated with outcome.
  • Using a proportional hazards model with backward selection, 3 prognostic subgroups were identified based on the influence of cytogenetic abnormalities on overall survival (OS): low-risk, t(15;17), and inv(16) in 25 of 361 patients (7%); standard-risk, normal karyotype, t(8;21), t(11q23), +8 within a noncomplex karyotype, and +11 within a noncomplex karyotype in 208 of 361 patients (58%); high-risk, all other aberrations in 128 of 361 patients (35%).
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Aged, 80 and over. Cytogenetic Analysis / methods. Female. Humans. Male. Middle Aged. Prognosis. Proportional Hazards Models. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 16840728.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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43. Weir EG, Ali Ansari-Lari M, Batista DA, Griffin CA, Fuller S, Smith BD, Borowitz MJ: Acute bilineal leukemia: a rare disease with poor outcome. Leukemia; 2007 Nov;21(11):2264-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute bilineal leukemia: a rare disease with poor outcome.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • A subset of these, referred to as acute bilineal leukemias (aBLLs), is characterized by the presence of more than one population of blasts, each comprising a single lineage.
  • We identified 19 cases of aBLL, including 10 mixed T and myeloid (T-My) and nine mixed B and myeloid (B-My); no mixed B and T cases were identified.
  • Three of seven patients with B-My had a t(9;22)(q34q11.2), two had 11q23 translocations and one had del(9).
  • Two of nine patients with T-My had 2p13 translocations; five had other unrelated abnormalities.
  • Of 16 patients with outcome data, only six achieved complete remission and only two remain free of disease 2.5 and 4.5 years after chemotherapy or stem cell transplantation. aBLL is a rare disease that combines B or T and myeloid blasts.
  • Cytogenetic abnormalities of t(9;22) and 11q23 are common in, and may be restricted to, B-My cases, while T-My cases have frequent but generally non-recurring abnormalities.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 17611554.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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44. Matsuda K, Hidaka E, Ishida F, Yamauchi K, Makishima H, Ito T, Suzuki T, Imagawa E, Sano K, Katsuyama T, Ota H: A case of acute myelogenous leukemia with MLL-AF10 fusion caused by insertion of 5' MLL into 10p12, with concurrent 3' MLL deletion. Cancer Genet Cytogenet; 2006 Nov;171(1):24-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myelogenous leukemia with MLL-AF10 fusion caused by insertion of 5' MLL into 10p12, with concurrent 3' MLL deletion.
  • Structural abnormalities involving the mixed-lineage leukemia (MLL) gene on 11q23 have been associated with hematological malignancies.
  • The rearrangement of MLL occurs during translocations and insertions involving a variety of genes on the partner chromosome.
  • We report a rare case of acute myelogenous leukemia (AML-M2) with 11q23 abnormalities.
  • Fluorescence in situ hybridization (FISH) using a commercial dual-color MLL probe detected an atypical signal pattern: one fusion signal, two green signals smaller than those usually detected, and no orange signals.
  • Spectral karyotyping (SKY) analysis indicated that one green signal was detected on the short arm of derivative chromosome 10, and the other green signal on the long arm of a derivative chromosome 11, on which no orange signal was detected.
  • A long-distance inverse polymerase chain reaction (LDI-PCR) identified the fusion partner gene, in which intron 6 of MLL was fused with intron 8 of AF10 on 10p12 in the 5' to 3' direction.
  • Our observations indicated that the MLL-AF10 fusion gene resulted from the insertion of part of the region that included the 5' MLL insertion into 10p12; this was concurrent with the deletion of 3' MLL.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Gene Deletion. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Amino Acid Sequence. Base Sequence. Chromosome Aberrations. Chromosome Banding. Chromosome Breakage. Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Male. Mutagenesis, Insertional / genetics. Sequence Analysis, DNA. Spectral Karyotyping / methods. Transcription Factors / genetics

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  • (PMID = 17074587.001).
  • [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 / MLL protein, human; 0 / MLL-AF10 fusion protein, human; 0 / MLLT10 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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45. Beyer V, Mühlematter D, Parlier V, Cabrol C, Bougeon-Mamin S, Solenthaler M, Tobler A, Pugin P, Gregor M, Hitz F, Hess U, Chapuis B, Laurencet F, Schanz U, Schmidt PM, van Melle G, Jotterand M: Polysomy 8 defines a clinico-cytogenetic entity representing a subset of myeloid hematologic malignancies associated with a poor prognosis: report on a cohort of 12 patients and review of 105 published cases. Cancer Genet Cytogenet; 2005 Jul 15;160(2):97-119
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] Polysomy 8 defines a clinico-cytogenetic entity representing a subset of myeloid hematologic malignancies associated with a poor prognosis: report on a cohort of 12 patients and review of 105 published cases.
  • Here we report on a series of 12 patients with acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), or myeloproliferative disorder (MPD) associated with polysomy 8 as detected by conventional cytogenetics and fluorescence in situ hybridization (FISH).
  • In 60.7% of patients, polysomy 8 occurred as part of complex changes (16.2% with 11q23 rearrangements).
  • No cryptic MLL rearrangements were found in cases in which polysomy 8 was the only karyotypic change.
  • Age significantly reduced median survival, but associated cytogenetic abnormalities did not modify it.
  • Cytogenetic results further demonstrate an in vitro preferential growth of the cells with a high level of aneuploidy suggesting a selective advantage for polysomy 8 cells.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Prognosis. Survival Rate

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  • (PMID = 15993266.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 140
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46. Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B: [Biphenotypic and bilineal acute leukemias]. Acta Med Croatica; 2008 Oct;62(4):387-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biphenotypic and bilineal acute leukemias].
  • Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
  • However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).
  • In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.
  • In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).
  • In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.
  • Chromosome abnormalities are frequent in both entities with a relatively high incidence of Philadelphia chromosome and rearrangements involving 11q23, especially in cases with B- and myeloid involvement.
  • Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19209464.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 30
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47. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16912588.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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48. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
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  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • The various aberrations observed were t(8;21)(q22;q22) (5.2%); t(15;17) (q22;q11-21) (9%); t(9;22)(q34;q11)(1.7%); t(14;17)(q32;q11.2)(0.5%); inv(16)(p13;q22)(1.7%); 11q23 rearrangements (4%); monosomy 7 (2.2%) and 22 (1.1%); deletion of 9q (q22q34) (5.1%), 5q (q13q33) (0.5%) and 13q (q13q31) (0.5%); common trisomies like +8 (5.6%), +16 (1.7%), +22 (1.1%), +21 (0.5%), +13 (0.5%), +11 (0.5%), +3 (0.5%); hyperdiploidy (3.4%); hypodiploidy (1.1%); complex karyotype (4%); and other structural abnormalities (4.5%).
  • Apart from these, three novel chromosomal abnormalities viz. t(8;18), t(7;14), t(13;15) were observed in the current study population.
  • CONCLUSION: This study confirms that the incidence of chromosomal abnormalities varies considerably.
  • Similarly, the frequency of other recurrent FAB associated abnormalities viz.
  • [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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49. Emerenciano M, Agudelo Arias DP, Coser VM, de Brito GD, Macedo Silva ML, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: Molecular cytogenetic findings of acute leukemia included in the Brazilian Collaborative Study Group of Infant acute leukemia. Pediatr Blood Cancer; 2006 Oct 15;47(5):549-54
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  • [Title] Molecular cytogenetic findings of acute leukemia included in the Brazilian Collaborative Study Group of Infant acute leukemia.
  • BACKGROUND: Chromosome abnormalities often occur prenatally in childhood leukemia, characterizing an early event in leukemogenesis.
  • The majority of the abnormalities occurring in infants involve the MLL gene on chromosome band 11q23.
  • We describe the molecular cytogenetic findings of 207 infant acute leukemia (IAL) cases included in the Brazilian Collaborative Study Group of Infant acute leukemia.
  • PROCEDURE: The diagnosis of Acute Lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML) was made according to morphology and immunophenotyping classification, followed by conventional karyotyping.
  • FISH assay for MLL rearrangements was performed only in cases with negative or inconclusive cytogenetic or PCR results.
  • A statistically significant association was observed between pro-B ALL cases and MLL+ve (P=0.0001) cases and the age group 0-3 months with MLL+ve (P=0.008) cases.
  • Two rare cases of pro-T ALL with MLL+ve were found.
  • Other than MLL rearrangements, various other molecular aberrations were detected including TEL/AML1+ve (n=9), E2A/PBX1+ve (n=4), PML/RARA+ve (n=4), and AML1/ETO+ve (n=2).
  • Cytogenetic analysis revealed hyperdiploidy (n=6), del(7) in two cases and del(11)(q23) in seven cases.
  • CONCLUSIONS: Our results show that not only MLL rearrangements, but also other molecular abnormalities occur before birth and may contribute to leukemogenesis.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16261608.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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50. Ramkumar B, Chadha MK, Barcos M, Sait SN, Heyman MR, Baer MR: Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis. Cancer Genet Cytogenet; 2008 Apr 15;182(2):126-9
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  • [Title] Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis.
  • Mitoxantrone is a DNA-topoisomerase 2 inhibitor used as a single agent for treatment of relapsing-remitting or progressive multiple sclerosis (MS).
  • We present here two patients treated with mitoxantrone for MS who subsequently developed acute promyelocytic leukemia (APL).
  • Topoisomerase 2 inhibitors are associated with therapy-related acute myeloid leukemia (t-AML) with 11q23 abnormalities, but therapy-related APL (t-APL) is less common, and documentation of nine cases of t-APL after mitoxantrone therapy for MS suggests a specific association.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / chemically induced. Mitoxantrone / adverse effects. Multiple Sclerosis / drug therapy
  • [MeSH-minor] Chromosomes, Human, Pair 11 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Remission Induction. Translocation, Genetic

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  • [ErratumIn] Cancer Genet Cytogenet. 2008 Oct 15;186(2):130
  • (PMID = 18406875.001).
  • [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 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone
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51. Olde Nordkamp L, Mellink C, van der Schoot E, van den Berg H: Karyotyping, FISH, and PCR in acute lymphoblastic leukemia: competing or complementary diagnostics? J Pediatr Hematol Oncol; 2009 Dec;31(12):930-5
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  • [Title] Karyotyping, FISH, and PCR in acute lymphoblastic leukemia: competing or complementary diagnostics?
  • BACKGROUND: Chromosomal abnormalities, such as t(9;22)(q34;q11) (ABL/BCR), t(12;21)(p13;q22) (TEL/AML1), and t(11q23) (MLL) are independent prognostic indicators in childhood acute lymphoblastic leukemia resulting in risk adapted therapy.
  • Accurate and rapid detection of these abnormalities is mandatory, which is achieved by karyotyping, fluorescence in situ hybridization, and real time quantitative reverse transcriptase polymerase chain reaction (RQ-PCR).
  • All consecutive patients under 18 years with acute lymphoblastic leukaemia were included.
  • However, the sensitivity of karyotyping for detecting the TEL-AML1 fusion gene and the sensitivity of RQ-PCR for detecting MLL-rearrangements was rather low.
  • CONCLUSIONS: Diagnostic accuracy of tests for detecting t(9;22), t(12;21), and t(11q23) is generally high, although sensitivity is not optimal for all anomalies.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Rearrangement. Humans. Infant. Infant, Newborn. Karyotyping. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Retrospective Studies. Translocation, Genetic / genetics

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  • (PMID = 19875970.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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52. Alvarez S, Cigudosa JC: Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel. Hematol Oncol; 2005 Mar;23(1):18-25
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  • [Title] Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel.
  • Therefore, a large number of genetic studies using cytogenetic molecular techniques have been performed to better define the chromosomal abnormalities in this poor-prognosis group.
  • Overrepresented chromosomal material from 8q, 11q23, 21q and 22q was found recurrently and in several cases this was due to the amplification of the MLL (located at 11q23) and AML1/RUNX1 (located at 22q22) genes.
  • As a result of these findings, the presence of MLL copy gain/amplifications or losses of the short arm of chromosome 17, in association with 5/5q, have been found to be indicators of an extremely poor prognosis.
  • [MeSH-major] Chromosomes, Human / genetics. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosome Segregation / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA Repair / genetics. Gene Amplification / genetics. Gene Expression Profiling / methods. Genome, Human / genetics. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm, Residual / genetics. Neoplasm, Residual / metabolism. Neoplasm, Residual / therapy. Risk Factors

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  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd.
  • (PMID = 16142824.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 53
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53. Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR: A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia. BMC Cancer; 2010;10:518
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  • [Title] A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
  • BACKGROUND: Abnormalities of 11q23 involving the MLL gene are found in approximately 10% of human leukemias.
  • To date, nearly 100 different chromosome bands have been described in rearrangements involving 11q23 and 64 fusion genes have been cloned and characterized at the molecular level.
  • In this work we present the identification of a novel MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric acute leukemia.
  • RESULTS: Fluorescence in situ hybridization of bone marrow G-banded metaphases demonstrated a cryptic insertion of 11q23 in Xq26.3 involving the MLL gene.
  • Breakpoint fusion analysis revealed that a DNA fragment of 653 kb from 11q23, containing MLL exons 1-9 in addition to 16 other 11q23 genes, was inserted into the upstream region of the CT45A2 gene located at Xq26.3.
  • RNA analysis revealed the presence of a novel MLL-CT45A2 fusion transcript in which the first 9 exons of the MLL gene were fused in-frame to exon 2 of the CT45A2 gene, resulting in a spliced MLL fusion transcript with an intact open reading frame.
  • The resulting chimeric transcript predicts a fusion protein where the N-terminus of MLL is fused to the entire open reading frame of CT45A2.
  • CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia, as a result of a cryptic insertion of 11q23 in Xq26.3.
  • Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in acute leukemia, future studies addressing its biologic relevance for leukemogenesis are warranted.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Child. Chromosome Banding. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, X / ultrastructure. Exons. Fatal Outcome. Gene Deletion. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Open Reading Frames

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  • (PMID = 20920256.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CT45A1 protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2956734
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54. Sait SN, Claydon MA, Conroy JM, Nowak NJ, Barcos M, Baer MR: Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):143-6
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  • [Title] Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia.
  • Reciprocal chromosomal translocations involving the MLL gene at chromosome region 11q23 are recurring cytogenetic abnormalities in both de novo and therapy-related acute myeloid leukemia (AML) and in acute lymphoblastic leukemia.
  • We report a t(4;11)(p12;q23) with rearrangement of MLL and FRYL (also known as AF4p12), a human homolog to the furry gene of Drosophila, in an adult patient with therapy-related AML after fludarabine and rituximab therapy for small lymphocytic lymphoma and radiation therapy for breast carcinoma.
  • To our knowledge, t(4;11)(p12;q23) has been reported in two previous patients, and MLL and FRYL rearrangement was demonstrated in one of them.
  • Thus, t(4;11)(p12;q23) with MLL and FRYL involvement represents a new recurring 11q23 translocation, to date seen only in therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Middle Aged. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17854671.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; 4F4X42SYQ6 / Rituximab; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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55. Imai N, Miwa H, Shikami M, Suganuma K, Gotoh M, Hiramatsu A, Wakabayashi M, Watarai M, Hanamura I, Imamura A, Mihara H, Shitara K, Shibuya M, Nitta M: Growth inhibition of AML cells with specific chromosome abnormalities by monoclonal antibodies to receptors for vascular endothelial growth factor. Leuk Res; 2009 Dec;33(12):1650-7
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  • [Title] Growth inhibition of AML cells with specific chromosome abnormalities by monoclonal antibodies to receptors for vascular endothelial growth factor.
  • By using neutralizing monoclonal antibodies to vascular endothelial growth factor receptor type 1 (VEGFR1) and VEGFR2, we have shown that acute myelogenous leukemia (AML) cells with specific chromosome abnormalities are dependent on VEGF/VEGFR system.
  • AML with t(8;21) is the most dependent subtype on VEGF with both VEGFR1 and VEGFR2. t(15;17)AML cells depend on VEGF with VEGFR1.
  • AML cells with 11q23 abnormalities showed variable dependence on VEGF.
  • The growth of t(11;19)AML cells are most extensively inhibited by anti-VEGFR1 antibody.
  • Then, the growth of Kasumi-1, a t(8;21) cell line was suppressed by either anti-VEGFR1 antibody (p=0.0022) or anti-VEGFR2 antibody (p=0.0029) in a dose-dependent manner.
  • The growth of NB4, a t(15;17) cell line was more potently suppressed by anti-VEGFR1 antibody (p=0.0111) than by anti-VEGFR2 antibody (p=0.0477).
  • These results are quite concordant with the results of clinical samples with t(8;21) or t(15;17).
  • As for downstream signals, we have shown that VEGFR2 transduce growth and survival signals through phosphorylation of Akt and MEK in leukemia cells (Kasumi-1).
  • [MeSH-major] Antibodies, Monoclonal / immunology. Cell Division / immunology. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Receptors, Vascular Endothelial Growth Factor / immunology

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  • (PMID = 19342098.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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56. Schoch C, Kohlmann A, Dugas M, Kern W, Schnittger S, Haferlach T: Impact of trisomy 8 on expression of genes located on chromosome 8 in different AML subgroups. Genes Chromosomes Cancer; 2006 Dec;45(12):1164-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Trisomy 8 is the most frequently observed trisomy in acute myeloid leukemia (AML) occurring as a sole karyotype abnormality or in addition to other chromosome aberrations.
  • It was the aim of this study to analyze the impact of trisomy 8 on the expression of genes located on chromosome 8 in distinct AML subgroups characterized by different chromosome abnormalities in addition to trisomy 8.
  • Gene expression analyses were performed on a total of 567 AML cases comprising the following subgroups: +8 sole, +8 within a complex aberrant karyotype, +8 in addition to t(15;17), inv(16), t(8;21), 11q23/MLL, or other abnormalities, AML with normal karyotype and the before mentioned subgroups without trisomy 8.
  • These data suggest that trisomy 8 rather provides a platform for a higher expression of chromosome 8 genes which are individually up-regulated by the respective primary genetic abnormalities.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Trisomy
  • [MeSH-minor] Acute Disease. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Up-Regulation

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17001623.001).
  • [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
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57. Chen SH, Yang CP, Hung IJ, Jaing TH, Shih LY, Tsai MH: Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan. Pediatr Blood Cancer; 2010 Dec 15;55(7):1264-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan.
  • BACKGROUND: Infant leukemia is rare and quite distinct from other childhood leukemias.
  • Differentiating between leukemia and transient myeloproliferative disorder (TMD) in phenotypically normal infants is sometimes difficult.
  • The clinical features and molecular analyses for the fusion transcripts of mixed lineage leukemia (MLL) gene rearrangement in infant leukemia have not been well documented in the Chinese population.
  • PROCEDURE: Forty-five consecutive infants diagnosed with leukemia between 1995 and 2007 in a tertiary medical center in Taiwan were studied.
  • Acute lymphoblastic leukemia (ALL) was diagnosed in 23 infants, acute myeloid leukemia (AML) in 21 (including TMD in 4), and juvenile myelomonocytic leukemia (JMML) in 1.
  • Chromosome 11q23/MLL abnormalities were present in 77% of ALL and 31% of AML.
  • CONCLUSIONS: The molecular assessments and prognostic factors of infant leukemia in Taiwan mirror those in developed Western countries.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Gene Rearrangement. Humans. Infant. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Leukemia, Myelomonocytic, Juvenile / diagnosis. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / therapy. Leukocyte Count. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloproliferative Disorders / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis. Taiwan. Treatment Outcome

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  • [CommentIn] Pediatr Blood Cancer. 2010 Dec 15;55(7):1247-9 [20981686.001]
  • (PMID = 20979094.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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58. Robinson BW, Felix CA: Panhandle PCR approaches to cloning MLL genomic breakpoint junctions and fusion transcript sequences. Methods Mol Biol; 2009;538:85-114
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Panhandle PCR approaches to cloning MLL genomic breakpoint junctions and fusion transcript sequences.
  • Translocations and other rearrangements of the MLL gene at chromosome band 11q23 are biologically and clinically important molecular abnormalities in infant acute leukemias, leukemias associated with chemotherapeutic topoisomerase II poisons and, less often, acute leukemias in adults or myelodysplastic syndrome.
  • Depending on the disease and the regimen, MLL-rearranged leukemias may be associated with inferior prognosis, and MLL rearrangements with some of the more than 60 known MLL-partner genes confer especially adverse effects as response to treatment (Blood 108:441-451, 2006).
  • MLL rearrangements are usually evident as overt balanced chromosomal translocations by conventional cytogenetic analysis but up to one-third are cryptic rearrangements and occur in leukemias with del(11)(q23), a normal karyotype, or trisomy 11, the latter two of which sometimes are associated with partial tandem duplications of MLL itself (Proc Natl Acad Sci USA 97:2814-2819, 2000; Proc Natl Acad Sci USA 94:3899-3902, 1997).
  • In addition, subsets of MLL rearrangements are complex at a cytogenetic level and/or molecular level, and fuse MLL with two different partner genes.
  • Rapid and accurate methods to identify and characterize genomic breakpoint junctions and fusion transcripts resulting from the many types of MLL rearrangements are essential for risk group stratification, treatment protocol assignments, new partner gene discovery, understanding leukemia etiology and pathogenesis, and elucidating the impact of less common MLL-partner genes on biology and prognosis.
  • Due to the vast heterogeneity in partner genes, typical gene-specific PCR based methods are not practical, especially when cytogenetics are normal or do not suggest involvement of a known partner gene of MLL.
  • We have advanced seven different panhandle PCR based methods for cloning 5'-MLL-partner gene-3' and 5'-partner gene-MLL-3' genomic breakpoint junctions and identifying 5'-MLL-partner gene-3' fusion transcripts, all of which employ a stem-loop template shaped schematically like a pan with a handle and amplify the template without knowledge of the unknown partner sequence using primers all derived from MLL alone.
  • [MeSH-major] Chromosome Breakage. Cloning, Molecular / methods. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods
  • [MeSH-minor] Alternative Splicing / genetics. Chromosomes, Human, Pair 11 / genetics. Exons / genetics. Histone-Lysine N-Methyltransferase. Humans

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  • (PMID = 19277575.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77683; United States / NCI NIH HHS / CA / CA80175; United States / NCI NIH HHS / CA / CA85469
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [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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59. Braham-Jmili N, Sendi-Senana H, Labiadh S, Ben Abdelali R, Ben Abdelaziz A, Khelif A, Saad A, Kortas M: [Haematological characteristics, FAB and WHO classification of 153 cases of myeloid acute leukaemia in Tunisia]. Ann Biol Clin (Paris); 2006 Sep-Oct;64(5):457-65

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Haematological characteristics, FAB and WHO classification of 153 cases of myeloid acute leukaemia in Tunisia].
  • [Transliterated title] Caractéristiques hématologiques et classification FAB et OMS de 153 cas de leucémies aiguës myéloïdes en Tunisie.
  • A complete blood analysis with a careful morphologic examination of peripheral blood and bone morrow smears completed by cytochemical reaction will help to classify the most acute myeloid leukaemia (AML).
  • The morphologic conclusion was difficult in 12% cases.
  • Our results showed cloned chromosomal abnormalities in 57% of cases (t(8;21): 12%, t(15;17) : 10%, Inv16: 1,3%, 11q23: 2,6% et complex karyotype: 14,3%).
  • 3 cases of LAM were noted at patients treated for breast cancer with chirurgic chemotherapy and radiotherapy 3, 4 et 5 years after treatment (LAM3 with t(15;17), LAM4 with genetic abnormalities of chromosomes 3, 5, 7, 8, 9, 14 et 16 et LAM 6 with genetic abnormalities of chromosomes 4, 7, 12, 14, 19 et 21).
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Child. Child, Preschool. Chromosome Aberrations. Diagnosis, Differential. Female. Humans. Infant. Karyotyping. Leukemia, Erythroblastic, Acute / blood. Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Myelomonocytic, Acute / blood. Leukemia, Myelomonocytic, Acute / diagnosis. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / blood. Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. Retrospective Studies. Tunisia. World Health Organization

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  • (PMID = 17040877.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
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60. Jiang F, Ai J, Xiao W, Wang Z: FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity. Cancer Lett; 2007 Aug 18;253(2):265-72
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity.
  • U19/EAF2 has also been identified as ELL-associated factor 2 (EAF2) based on its binding to ELL, a fusion partner of MLL in acute myeloid leukemia.
  • U19/EAF2 is a putative transcription factor with a transactivation domain and capability of sequence-specific DNA binding.
  • RESULTS: FB1, an E2A fusion partner in childhood leukemia, was identified as a binding-partner of U19/EAF2.

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  • (PMID = 17395368.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK051193; United States / NIDDK NIH HHS / DK / R37 DK051193-12; United States / NIDDK NIH HHS / DK / R37 DK051193; United States / NCI NIH HHS / CA / CA090386-020002; United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / P50 CA090386-020002; United States / NCI NIH HHS / CA / P50 CA90386; United States / NIDDK NIH HHS / DK / R01 DK51193; United States / NIDDK NIH HHS / DK / DK051193-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / EAF1 protein, human; 0 / EAF2 protein, human; 0 / ELL protein, human; 0 / TFPT protein, human; 0 / Transcription Factors; 0 / Transcriptional Elongation Factors
  • [Other-IDs] NLM/ NIHMS27735; NLM/ PMC1989770
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61. Andreeva SV, Drozdova VD, Emel'ianenko LA: [Chromosome 11 rearrangements in the different haematological neoplasias]. Tsitol Genet; 2007 Mar-Apr;41(2):42-8
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chromosome 11 rearrangements in the different haematological neoplasias].
  • The cases of chromosome 11 abnormalities in leukemic bone marrow cells have constituted 14.0% in acute lymphoblastic leukemia (ALL), 18.7% in acute myeloid leukemia (AML), and 16.7% in refractory anemia (RA).
  • The bands of the short arms 11p13, 11p14, llp15 and the long arms 11q14, 11q21, 11q23 were involved in chromosome rearrangements.
  • The rearrangements of the band 11q23 were detected more often.
  • The results have showed the poor prognosis of the abnormalities not only of 11q21, 11q23 in acute leukemia (AL), but of 11p13, 11p15 in AML as well, while not enough data on this subject is availalbe in the literature.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosome Banding. Female. Humans. Infant. Karyotyping. Male

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  • (PMID = 17494343.001).
  • [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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62. Harper DP, Aplan PD: Chromosomal rearrangements leading to MLL gene fusions: clinical and biological aspects. Cancer Res; 2008 Dec 15;68(24):10024-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal rearrangements leading to MLL gene fusions: clinical and biological aspects.
  • Rearrangements of the MLL gene located at 11q23 are common chromosomal abnormalities associated with acute leukemia, especially infant and therapy-related leukemias.
  • A variety of chimeric oncoproteins resulting from these rearrangements has been described; all of these include the NH(2)-terminal region of MLL implicated in protein-protein interactions and transcriptional repression.
  • Although the molecular basis for the oncogenic activity of MLL chimeric proteins is incompletely understood, it seems to be derived, at least in part, through activation of clustered homeobox (HOX) genes.
  • Here, we survey MLL gene rearrangements that are associated with acute leukemia and discuss molecular pathways leading to these rearrangements.
  • [MeSH-major] Gene Fusion. Gene Rearrangement. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Histone-Lysine N-Methyltransferase. Humans. Infant. Leukemia, Myeloid, Acute / genetics. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19074864.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC010379-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 20
  • [Other-IDs] NLM/ NIHMS69778; NLM/ PMC2614694
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63. Whitman SP, Ruppert AS, Marcucci G, Mrózek K, Paschka P, Langer C, Baldus CD, Wen J, Vukosavljevic T, Powell BL, Carroll AJ, Kolitz JE, Larson RA, Caligiuri MA, Bloomfield CD: Long-term disease-free survivors with cytogenetically normal acute myeloid leukemia and MLL partial tandem duplication: a Cancer and Leukemia Group B study. Blood; 2007 Jun 15;109(12):5164-7
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term disease-free survivors with cytogenetically normal acute myeloid leukemia and MLL partial tandem duplication: a Cancer and Leukemia Group B study.
  • The clinical impact of MLL partial tandem duplication (MLL-PTD) was evaluated in 238 adults aged 18 to 59 years with cytogenetically normal (CN) de novo acute myeloid leukemia (AML) who were treated intensively on similar Cancer and Leukemia Group B protocols 9621 and 19808.
  • Twenty-four (10.1%) patients harbored an MLL-PTD.
  • Of those, 92% achieved complete remission (CR) compared with 83% of patients without MLL-PTD (P=.39).
  • Thirteen MLL-PTD(+) patients relapsed within 1.4 years of achieving CR.
  • MLL-PTD(+) patients who relapsed more often had other adverse CN-AML-associated molecular markers.
  • In contrast with previously reported studies, 9 (41%) MLL-PTD(+) patients continue in long-term first remission (CR1; range, 2.5-7.7 years).
  • Intensive consolidation therapy that included autologous peripheral stem-cell transplantation during CR1 may have contributed to the better outcome of this historically poor-prognosis group of CN-AML patients with MLL-PTD.

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  • (PMID = 17341662.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA098933; United States / NCI NIH HHS / CA / CA089341; United States / NCI NIH HHS / CA / CA41287; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / U10 CA041287; United States / NCI NIH HHS / CA / R01 CA098933; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA096887
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1890839
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64. Daser A, Rabbitts TH: The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis. Semin Cancer Biol; 2005 Jun;15(3):175-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis.
  • The marked association of abnormalities of chromosome 11 long arm, band q23, with human leukaemia led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1).
  • MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual leukaemias, leading to either acute myeloid or lymphoid tumours (hence the name MLL for mixed lineage leukaemia).
  • The unusual finding that a single protein could be involved in both myeloid and lymphoid malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis.
  • These studies have defined MLL-fusion proteins as regulators of gene expression, controlling such elements as HOX genes, and have indicated a variety of mechanisms by which MLL-fusion proteins contribute to leukaemogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism

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  • (PMID = 15826832.001).
  • [ISSN] 1044-579X
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 123
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65. Frey NV, Leid CE, Nowell PC, Tomczak E, Strauser HT, Kasner M, Goldstein S, Loren A, Stadtmauer E, Luger S, Hexner E, Hinkle J, Porter DL: Trisomy 8 in an allogeneic stem cell transplant recipient representative of a donor-derived constitutional abnormality. Am J Hematol; 2008 Nov;83(11):846-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trisomy 8 in an allogeneic stem cell transplant recipient representative of a donor-derived constitutional abnormality.
  • Trisomy 8 is a common cytogenetic abnormality in myeloid malignancies.
  • It can also be present constitutionally and is associated with a wide range of phenotypes.
  • We report a case of a 20-year-old woman with acute myelogenous leukemia associated with the 11q23/MLL translocation who underwent allogeneic hematopoietic stem cell transplantation (HSCT) from a healthy, unrelated 26-year-old female.
  • Fluorescent in situ hybridization (FISH) for the original 11q23/MLL translocation was negative.
  • This represents the first reported case of a person with constitutional trisomy 8 mosaicism serving as a stem cell donor.
  • The case illustrates the importance of identifying donor-derived constitutional abnormalities to avoid the assumption that these cytogenetic abnormalities after HSCT are representative of malignant disease.

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
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  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA117879-03; United States / NCI NIH HHS / CA / K24 CA117879; United States / NCI NIH HHS / CA / K24 CA117879-03; United States / NCI NIH HHS / CA / K24 CA11787901
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  • [Other-IDs] NLM/ NIHMS74574; NLM/ PMC2610424
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66. Ono R, Ihara M, Nakajima H, Ozaki K, Kataoka-Fujiwara Y, Taki T, Nagata K, Inagaki M, Yoshida N, Kitamura T, Hayashi Y, Kinoshita M, Nosaka T: Disruption of Sept6, a fusion partner gene of MLL, does not affect ontogeny, leukemogenesis induced by MLL-SEPT6, or phenotype induced by the loss of Sept4. Mol Cell Biol; 2005 Dec;25(24):10965-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of Sept6, a fusion partner gene of MLL, does not affect ontogeny, leukemogenesis induced by MLL-SEPT6, or phenotype induced by the loss of Sept4.
  • SEPT6 is ubiquitously expressed in tissues and one of the fusion partner genes of MLL in the 11q23 translocations implicated in acute leukemia.
  • We have developed Sept6-deficient mice that exhibited neither gross abnormalities, changes in cytokinesis, nor spontaneous malignancy.
  • Furthermore, a loss of Sept6 did not alter the phenotype of myeloproliferative disease induced by MLL-SEPT6, thus suggesting that Sept6 does not function as a tumor suppressor.
  • To our knowledge, this is the first report demonstrating that a disruption of the translocation partner gene of MLL in 11q23 translocation does not contribute to leukemogenesis by the MLL fusion gene.
  • [MeSH-major] GTP-Binding Proteins / physiology. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 16314519.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / MLL-SEPT6 fusion protein, mouse; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse; EC 3.6.1.- / GTP Phosphohydrolases; EC 3.6.1.- / GTP-Binding Proteins; EC 3.6.1.- / Sept4 protein, mouse; EC 3.6.1.- / Sept6 protein, mouse; EC 3.6.1.- / Septins
  • [Other-IDs] NLM/ PMC1316963
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67. Quentmeier H, Tonelli R, Geffers R, Pession A, Uphoff CC, Drexler HG: Expression of BEX1 in acute myeloid leukemia with MLL rearrangements. Leukemia; 2005 Aug;19(8):1488-9
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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 BEX1 in acute myeloid leukemia with MLL rearrangements.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Nerve Tissue Proteins / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15920485.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BEX1 protein, human; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nerve Tissue Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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68. Konuma T, Ooi J, Takahashi S, Tomonari A, Tsukada N, Kato S, Kasahara S, Uchimaru K, Iseki T, Tojo A, Asano S: Myeloablative unrelated cord blood transplantation for adult acute myeloid leukemia patients with 11q23 abnormalities. Eur J Haematol; 2008 Jun;80(6):545-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloablative unrelated cord blood transplantation for adult acute myeloid leukemia patients with 11q23 abnormalities.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery. Transplantation Conditioning


69. Tamai H: [Prognosis and therapy of adult acute leukemia with 11q23 abnormalities]. Rinsho Ketsueki; 2008 Mar;49(3):193-200
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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 therapy of adult acute leukemia with 11q23 abnormalities].
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia / genetics. Leukemia / therapy. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols. Combined Modality Therapy. Hematopoietic Stem Cell Transplantation. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Prognosis. Proto-Oncogene Proteins c-bcr

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  • (PMID = 18421960.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
  • [Number-of-references] 48
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70. Nigro LL, Sainati L, Leszl A, Mirabile E, Spinelli M, Consarino C, Di Cataldo A, Magro S, Felix CA, Basso G: Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation. Leukemia; 2007 Feb;21(2):360-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation.
  • [MeSH-major] Dendritic Cells / pathology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / immunology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antigens, CD / genetics. Antigens, CD / immunology. Cell Differentiation. Child. Histone-Lysine N-Methyltransferase. Humans

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  • (PMID = 17205059.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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