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1. 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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  • [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%).
  • Thus, karyotype and age are major determinants of outcome in elderly patients with AML.
  • [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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2. 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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  • [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 platelet count was higher and the rate of myeloperoxidase (MPO)-positive blasts was lower in AML with MLD than in the other WHO categories.
  • 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).
  • Our results confirmed that the cytogenetic profile, MLD phenotype, and MPO-positivity of blasts are associated with survival in patients with AML, and showed that each category had the characteristics of the WHO classification such as incidence, clinical features, and OS.
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries


3. Grimwade D, Hills RK, Moorman AV, Walker H, Chatters S, Goldstone AH, Wheatley K, Harrison CJ, Burnett AK, National Cancer Research Institute Adult Leukaemia Working Group: Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials. Blood; 2010 Jul 22;116(3):354-65
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  • [Title] Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials.
  • Diagnostic karyotype provides the framework for risk-stratification schemes in acute myeloid leukemia (AML); however, the prognostic significance of many rare recurring cytogenetic abnormalities remains uncertain.
  • In multivariable analysis, t(15;17)(q22;q21), t(8;21)(q22;q22), and inv(16)(p13q22)/t(16;16)(p13;q22) were the only abnormalities found to predict a relatively favorable prognosis (P < .001).
  • 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


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4. 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.
  • An independent set of 60 untreated AML patients was used to validate the outcome signatures using real-time polymerase chain reaction.
  • 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.
  • Furthermore, patients with high expression of miR-191 and miR-199a had significantly worse overall and event-free survival than AML patients with low expression (overall survival: miR-191, P = .03; and miR-199a, P = .001, Cox regression).
  • In conclusion, miRNA expression in AML is closely associated with cytogenetics 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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5. 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 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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6. 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).
  • Subsequent molecular short tandem repeat studies confirmed the AML to be of donor origin.
  • 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


7. Chen S, Xue Y, Zhang X, Wu Y, Pan J, Wang Y, Ceng J: A new human acute monocytic leukemia cell line SHI-1 with t(6;11)(q27;q23), p53 gene alterations and high tumorigenicity in nude mice. Haematologica; 2005 Jun;90(6):766-75
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  • [Title] A new human acute monocytic leukemia cell line SHI-1 with t(6;11)(q27;q23), p53 gene alterations and high tumorigenicity in nude mice.
  • BACKGROUND AND OBJECTIVES: Human leukemia cell lines are of great value in leukemia research.
  • Thus far 36 leukemia cell lines carrying the 11q23 translocation and MLL rearrangements, including two cell lines with t(6;11)(q27;q23) and an MLL-AF6 fusion gene have been described.
  • DESIGN AND METHODS: Mononuclear cells isolated from the bone marrow of a patient with acute monocytic leukemia (AML-M5b) at relapse were inoculated and passaged by liquid culture.
  • Karyotypic analysis demonstrated a t(6;11)(q27;q23) translocation accompanied by a deletion of 17p, which are the same abnormalities as were seen in the leukemia cells of this patient in relapse.
  • The MLL-AF6 fusion transcript and the loss of one p53 allele were proven by chromosome painting, FISH and RT-PCR analysis in both SHI-1 cells and the primary leukemia cells.
  • A point mutation of ATC-->ACC at codon 195 of exon 6 in another p53 allele was found by direct sequencing of DNA in SHI-1 cells as well as in the primary leukemia cells.
  • INTERPRETATION AND CONCLUSIONS: SHI-1 is a new monocytic leukemia cell line with the t(6;11) translocation, p53 gene alterations, and high tumorigenicity in nude mice.
  • [MeSH-major] Cell Line, Tumor. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 6. Genes, p53. Leukemia, Monocytic, Acute / genetics. Translocation, Genetic

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  • (PMID = 15951289.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
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8. Xu N, Liu XL, DU QF, Liu Z, Zhong M, Lin R, Song LL, Yi ZS, Meng FY, Zhou SY: [CD56 and CD11b antigen expressions in patients with acute monocytic leukemia and the clinical implications]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Aug;29(8):1605-8

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  • [Title] [CD56 and CD11b antigen expressions in patients with acute monocytic leukemia and the clinical implications].
  • OBJECTIVE: To investigate the expressions of cell surface differentiation antigen CD56 and CD11b antigen in acute monocytic leukemic (AML-M(5)) cells and their clinical significance.
  • METHODS: A total of 113 cases of de nove adult AML-M(5) were examined genetically and immunologically using G-banding technique, interphase fluorescence in situ hybridization (I-FISH) and flow cytometry immunophenotyping, and the results were analyzed in relation to their clinical data.
  • The incidence of karyotypic abnormalities was 48.57% (55 cases) in these patients, including 25 (22.12%) with 11q23 aberrations.
  • Twenty-five cases were positive for MLL gene abnormalities as found by I-FISH analysis.
  • Compared with the patients positive for both CD56 and CD11b, those negative for both CD56 and CD11b showed increased peripheral blood white blood cell (WBC) count and also increased blast and progenitor cells in the bone marrow (P<0.05); the former patients often had karyotypic abnormalities, commonly involving 11q23 aberrations (P<0.05), whereas the latter patients presented more likely with extramedullary infiltration and refractory leukemia (P<0.01) with lowered complete remission rate and shortened median survival time (P<0.01).
  • CD56-positive patients were more likely to have karyotypic abnormalities and refractory leukemia than CD11b-postive patients (P<0.05), but the peripheral blood WBC counts, bone marrow blast and progenitor cells, extramedullary infiltration, complete remission rate or median survival time showed no significant differences between them (P>0.05).
  • CONCLUSION: AML-M(5) patients with CD56 positivity and high expression of CD11b often have aberrant karyotypes, commonly involving 11q23/MLL gene abnormality.
  • These patients frequently develop extramedullary infiltration and refractory leukemia often with poor prognosis.
  • [MeSH-major] Antigens, CD11b / metabolism. Antigens, CD56 / metabolism. Gene Expression Regulation. Leukemia, Monocytic, Acute / metabolism

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  • (PMID = 19726305.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD56
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9. 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.
  • 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

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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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10. 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.
  • Abnormalities of the MLL ProtoOncogene Protein are usually connected with bad prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myeloid-Lymphoid Leukemia Protein / genetics

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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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11. 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.
  • We analyse 1,271 consecutive patients diagnosed of AML between 1995 and 2002 in three different regions of Spain: northern, central and southern.
  • 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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12. 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.
  • Few studies have reported t-AML due to paclitaxel.
  • 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.
  • Based on the clinical course, t-AML may have developed after paclitaxel therapy.
  • [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


13. 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.
  • 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).
  • Finally, our data suggested that autocrine pathway of VEGF and VEGFRs observed in AML cells with specific chromosomal translocations have contributed to leukemogenesis as activated signaling of receptor tyrosine kinase.
  • [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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14. 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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  • [Title] Impact of trisomy 8 on expression of genes located on chromosome 8 in different AML subgroups.
  • 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.
  • However, no consistent pattern of genes was identified, which shows a higher expression in all AML subtypes with 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.
  • Therefore, trisomy 8 in AML determines no specific disease characteristic but is a disease modulating secondary event.
  • [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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15. Harrison CJ, Hills RK, Moorman AV, Grimwade DJ, Hann I, Webb DK, Wheatley K, de Graaf SS, van den Berg E, Burnett AK, Gibson BE: Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12. J Clin Oncol; 2010 Jun 1;28(16):2674-81
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  • [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.
  • CONCLUSION: Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with AML, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality


16. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

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  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • METHODS: Bone marrow samples were analyzed for chromosomal abnormalities with conventional G-banding techniques and interphase fluorescence in situ hybridization (FISH) using probes to detect BCR/ABL t(9;22)(q34-q11) fusion, cryptic TEL/AML1 t(12:21)(p13-q22) and MLL rearrangement for del 11q23.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.
  • In second case, a 4-year male we observed four copies of AML and two copies of TEL gene in more than 80% of cells.

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  • (PMID = 27960689.001).
  • [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
  • [Publication-country] United States
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17. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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18. 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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  • [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).
  • PATIENTS AND METHODS A diagnostic assay detecting multiple EVI1 splice variants was developed to determine the relative EVI1 expression by single real-time quantitative polymerase chain reaction in 1,382 newly diagnosed adult patients with AML younger than 60 years.
  • Patients were treated on four Dutch-Belgian HOVON (n = 458) and two German-Austrian AML Study Group protocols (n = 924).
  • This adverse prognostic impact was more pronounced in the intermediate cytogenetic risk group (EFS; HR, 1.64; P < .001; and RFS; HR, 1.55; P = .02), and was also apparent in cytogenetically normal AML (EFS; HR, 1.67; P = .008).
  • 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.
  • EVI1(+) was virtually absent in favorable-risk AML and AML with NPM1 mutations.
  • Patients with EVI1(+) AML (n = 28) who received allogeneic stem cell transplantation in first CR had significantly better 5-year RFS (33% +/- 10% v 0%).
  • CONCLUSION EVI1 expression in AML is unequally distributed in cytogenetic subtypes.
  • It predicts poor outcome, particularly among intermediate cytogenetic risk AML.
  • Patients with EVI1(+) AML may benefit from allogeneic transplantation in first CR.
  • [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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19. 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.
  • 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.
  • [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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20. 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.
  • MLL(+) was identified in 114 (98 adults) of 988 AML patients.
  • 11q23 abnormalities were detected in 64% of MLL/t11q23 and in none of MLL-PTD by conventional cytogenetics.
  • MLL-PTD was rare in childhood AML.
  • [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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21. 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.
  • 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.
  • [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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22. 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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  • [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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23. 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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  • [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.
  • We report a rare case of acute myelogenous leukemia (AML-M2) with 11q23 abnormalities.
  • [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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24. 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
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  • 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).
  • Our study demonstrates the existence of a polysomy 8 syndrome, which represents a subtype of AML, MDS, and MPD characterized by a high incidence of secondary diseases, myelomonocytic or monocytic involvement in AML and poor overall survival (6 months).
  • Age significantly reduced median survival, but associated cytogenetic abnormalities did not modify it.
  • [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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25. 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.
  • The common bipotent LSC in AML M7 of low grade and AML M6b may exist analogous to precursor cell common for megakaryocytopoiesis and erythropoiesis.
  • 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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26. 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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  • [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.
  • RESULTS: The median white count at diagnosis was higher in ALL than in AML (154.4 × 10(9)/l vs. 58.3 × 10(9)/l, P = 0.05).
  • Chromosome 11q23/MLL abnormalities were present in 77% of ALL and 31% of AML.
  • The 5-year event-free survival (EFS) in infant ALL and AML showed no difference (18% vs. 12%, respectively).
  • However, no factor was associated with an adverse outcome for infants with 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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27. 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.
  • 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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28. 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).
  • This report may lead to a new thinking about AML pathogenesis, as differences at PTM level could be used to distinguish different subtypes of AML.
  • [MeSH-major] Cytogenetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Protein Processing, Post-Translational. Proteome / genetics. Proteome / metabolism


29. 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

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  • [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).
  • 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.
  • [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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30. 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.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • The various aberrations observed were t(8;21)(q22;q22) (5.2%); t(15;17) (q22;q11-21) (9%); t(9;22)(q34;q11)(1.7%); t(14;17)(q32;q11.2)(0.5%); inv(16)(p13;q22)(1.7%); 11q23 rearrangements (4%); monosomy 7 (2.2%) and 22 (1.1%); deletion of 9q (q22q34) (5.1%), 5q (q13q33) (0.5%) and 13q (q13q31) (0.5%); common trisomies like +8 (5.6%), +16 (1.7%), +22 (1.1%), +21 (0.5%), +13 (0.5%), +11 (0.5%), +3 (0.5%); hyperdiploidy (3.4%); hypodiploidy (1.1%); complex karyotype (4%); and other structural abnormalities (4.5%).
  • 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.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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31. Andreeva SV, Drozdova VD, Emel'ianenko LA: [Chromosome 11 rearrangements in the different haematological neoplasias]. Tsitol Genet; 2007 Mar-Apr;41(2):42-8
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  • 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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32. 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).
  • RESULTS: This study revealed that e.g., the t(12;21) [ETV6-RUNX1] subtype of ALL and the t(15;17) [PML-RARA] subtype of AML had transcriptional programs similar to those in normal Pro-B cells and promyelocytes, respectively.
  • 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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33. 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).
  • DESIGN AND METHODS: To further evaluate the role of FLT3 in AML we investigated FLT3 expression levels in 207 adult AML patients and 8 healthy donors by real-time polymerase chain reaction (PCR).
  • 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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34. 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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  • Complex karyotypes are seen in approximately 15% of de novo MDS/AML and in up to 50% of therapy-related MDS/AML.
  • 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.
  • On the basis of the available data from several studies of AML with complex karyotypes, similar findings on recurrent breakpoints and frequently lost and gained chromosomal regions have been observed.
  • 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.
  • Interestingly, this non-random pattern of DNA gains and losses, that characterizes AML cases with complex karyotypes, affects the gene expression pattern, and a specific expression profile, characterized by the upregulation of genes involved in the DNA repair and chromosome segregation pathways, has been recently reported.
  • Therefore, a comprehensive genome-wide analysis of patients with AML or MDS with complex karyotypes has led to a better characterization of chromosomal aberrations.
  • [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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35. Giusiano S, Formisano-Tréziny C, Benziane A, Maroc N, Picard C, Hermitte F, Taranger-Charpin C, Gabert J: Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis. Int J Lab Hematol; 2010 Aug 1;32(4):398-409
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  • [Title] Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis.
  • Three major types of rearrangements are involved in acute myeloid leukemias (AML): t(8;21)(q22;q22), inv(16)(p13q22), and 11q23/MLL abnormalities.
  • Their precise identification becomes essential for diagnosis, prognosis, and therapeutic choices.
  • In this study, we propose a biochip-based assay integrated in a global strategy for identification of rare FT in AML, after fluorescence in situ hybridization detection, as described by the World Health Organization classification.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19930410.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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36. 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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37. 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.
  • Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML.
  • She was diagnosed with AML-M5.
  • 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

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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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38. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • [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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39. El-Sissy AH, El-Mashari MA, Bassuni WY, El-Swaayed AF: Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia. J Egypt Natl Canc Inst; 2006 Sep;18(3):244-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia.
  • BACKGROUND: Immunophenotyping improves both accuracy and reproducibility of acute leukemia classification and is considered particularly useful for identifying aberrant lineage association of acute leukemia, biphenotypic and bilineal acute leukemia, as well as monitoring minimal residual disease.
  • 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).
  • PATIENTS AND METHODS: Thirty four newly diagnosed AML cases were included in this study, 47% showed aberrant lymphoid antigen expression.
  • CD56 was also detected in 2 cases with 11q23 rearrangement.
  • CD79a was expressed in one case together with CD19, diagnosed as acute biphenotypic leukemia, and was associated with t(8;21) (q22;q22).
  • CONCLUSION: Minimal residual disease in AML is very difficult to trace, detection of aberrant expression of lymphoid antigens will make it easier.
  • [MeSH-major] Antigens, CD56 / analysis. Antigens, CD7 / analysis. Antigens, CD79 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / diagnosis

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  • (PMID = 17671534.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Antigens, CD79; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
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40. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • RESULTS: The characteristics of children with IAL were as follows: 115 boys and 92 girls, age range 0-23 months, mean age 12 months, 145 ALL, and 62 AML.
  • 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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41. 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].
  • 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).
  • Actually, the study of other cytogenetis and immunophenotypic markers are now necessary to confirm diagnosis.
  • 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).
  • In WHO classification, cytology is essential in diagnosis of LAM even if the karytype have an important prognostic value.
  • [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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