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1. Karran P, Offman J, Bignami M: Human mismatch repair, drug-induced DNA damage, and secondary cancer. Biochimie; 2003 Nov;85(11):1149-60
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  • [Title] Human mismatch repair, drug-induced DNA damage, and secondary cancer.
  • More recently, it has become apparent that MMR defects are common in acute myeloid leukaemia/myelodysplastic syndrome (AML/MDS) that follows successful chemotherapy for a primary malignancy.
  • Therapy-related haematological malignancies are often associated with treatment with alkylating agents.
  • Their frequency is increasing and they now account for at least 10% of all AML cases.
  • There is also evidence for an association between MMR deficient AML/MDS and immunosuppressive treatment with thiopurine drugs.
  • Here we review how MMR interacts with alkylating agent and thiopurine-induced DNA damage and suggest possible ways in which MMR defects may arise in therapy-related AML/MDS.
  • [MeSH-major] Base Pair Mismatch / genetics. DNA Damage / drug effects. DNA Repair / genetics. DNA Repair / physiology. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Humans


2. Clavio M, Gatto S, Beltrami G, Cerri R, Carrara P, Pierri I, Canepa L, Miglino M, Balleari E, Masoudi B, Damasio E, Ghio R, Sessarego M, Gobbi M: First line therapy with fludarabine combinations in 42 patients with either post myelodysplastic syndrome or therapy related acute myeloid leukaemia. Leuk Lymphoma; 2001 Jan;40(3-4):305-13
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  • [Title] First line therapy with fludarabine combinations in 42 patients with either post myelodysplastic syndrome or therapy related acute myeloid leukaemia.
  • Acute myeloid leukaemias (AML) evolving from a myelodysplastic syndrome (MDS) or secondary to chemoradiotherapy frequently display unfavorable biologic characteristics.
  • Recently, the association of Fludarabine with intermediate dose Ara-C has produced interesting results particularly in high risk AML patients.
  • Here, we report on 42 secondary AML patients treated with a combination of Fludarabine, intermediate dose Ara-C, G-CSF with or without an antracycline (FLANG, FLAG-IDA or FLAG).
  • Overall, complete remissions (CR) were documented in 14 patients (33%) and partial responses (PR) in 12 (29%), while 10 patients proved resistant (24%).
  • Taken together, these Fludarabine containing regimens proved to be an effective and tolerable treatment for patients with secondary AML.
  • Patients above 70 years of age may also benefit from this therapy, however the problem of treating patients with adverse chromosomal abnormalities still remains unresolved.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / pathology. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Cohort Studies. Cytarabine / administration & dosage. Cytarabine / toxicity. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / toxicity. Humans. Male. Middle Aged. Neoplasms, Second Primary / complications. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / mortality. Remission Induction. Survival Rate


3. Inaba T: [Radiation-induced and therapy-related AML/MDS]. Nihon Rinsho; 2009 Oct;67(10):1880-3
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  • [Title] [Radiation-induced and therapy-related AML/MDS].
  • Radiation induced acute myeloid leukemia (AML) was recognized a century ago, soon after mankind found radiation.
  • Atomic bomb survivors developed de novo AML with relatively short latency with very high frequency.
  • By contrast, excess occurrence of myelodysplastic syndrome (MDS) as well as solid tumors was found decades late.
  • This difference may be due to etiology that many de novo AML patients harbor chimeric leukemogenic genes caused by chromosomal translocations, while MDS patients rarely carry chimeras.
  • Therapy related leukemia is mainly caused by topoisomerase II inhibitors that cause de novo AML with an 11q23 translocation or by alkyrating agents that induce MDS/AML with an AML1 point mutation and monosomy 7.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Myelodysplastic Syndromes / etiology
  • [MeSH-minor] Alkylating Agents / adverse effects. Chimera / genetics. Enzyme Inhibitors / adverse effects. Epigenesis, Genetic. Humans. Nuclear Weapons. Topoisomerase II Inhibitors. Translocation, Genetic

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  • (PMID = 19860183.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 7
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4. Harada H, Harada Y, Tanaka H, Kimura A, Inaba T: Implications of somatic mutations in the AML1 gene in radiation-associated and therapy-related myelodysplastic syndrome/acute myeloid leukemia. Blood; 2003 Jan 15;101(2):673-80
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  • [Title] Implications of somatic mutations in the AML1 gene in radiation-associated and therapy-related myelodysplastic syndrome/acute myeloid leukemia.
  • Somatically acquired point mutations of AML1/RUNX1 gene have been recently identified in rare cases of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Moreover, germ line mutations of AML1 were found in an autosomal dominant disease, familial platelet disorder with predisposition to AML (FPD/AML), suggesting that AML1 mutants, as well as AML1 chimeras, contribute to the transformation of hematopoietic progenitors.
  • In this report, we showed that AML1 point mutations were found in 6 (46%) of 13 MDS patients among atomic bomb (A-bomb) survivors in Hiroshima.
  • Unlike acute or chronic leukemia patients among A-bomb survivors, MDS patients exposed relatively low-dose radiation and developed the disease after a long latency period.
  • AML1 mutations also were found in 5 (38%) of 13 therapy-related AML/MDS patients who were treated with alkylating agents with or without local radiation therapy.
  • In contrast, frequency of AML1 mutation in sporadic MDS patients was 2.7% (2 of 74).
  • Among AML1 mutations identified in this study, truncated-type mutants lost DNA binding potential and trans-activation activity.
  • All missense mutations with one exception (Gly42Arg) lacked DNA binding ability and down-regulated the trans-activation potential of wild-type AML1 in a dominant-negative fashion.
  • The Gly42Arg mutation that was shared by 2 patients bound DNA even more avidly than wild-type AML1 and enhanced the trans-activation potential of normal AML1.
  • These results suggest that AML1 point mutations are related to low-dose radiation or alkylating agents and play a role distinct from that of leukemogenic chimeras as a result of chromosomal translocations caused by sublethal radiation or topoisomerase II inhibitors.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Proto-Oncogene Proteins. Radioactive Fallout / adverse effects. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Case-Control Studies. Core Binding Factor Alpha 2 Subunit. DNA Mutational Analysis. Female. Humans. Japan. Male. Middle Aged. Point Mutation / genetics. Protein Binding / genetics. Radiation Dosage. Transcription Factor AP-2. Transcription, Genetic


5. Voso MT, D'Alò F, Greco M, Fabiani E, Criscuolo M, Migliara G, Pagano L, Fianchi L, Guidi F, Hohaus S, Leone G: Epigenetic changes in therapy-related MDS/AML. Chem Biol Interact; 2010 Mar 19;184(1-2):46-9
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  • [Title] Epigenetic changes in therapy-related MDS/AML.
  • Therapy-related Myelodysplastic Syndromes/Acute Myeloid Leukemias (t-MDS/AML) are one of the most compelling long term adverse events occurring in cancer survivors treated with chemo-radiotherapy regimes.
  • Cytotoxic drugs and radiation have been shown to affect tissue DNA methylation profile.
  • Gene promoter methylation is a common finding in t-MDS/AML and has been associated to a shorter latency period from the treatment of the primary tumor.
  • Among the studied genes, p15 methylation correlated to monosomy/deletion of chromosome 7q, suggesting that it could be a relevant event in alkylating agent-induced leukemogenesis.
  • We found frequent methylation of DAPK in the t-MDS/AML group, especially in patients with a previous lymphoproliferative disease.
  • In patients studied for concurrent methylation of several promoters, t-MDS/AML were significantly more frequently hypermethylated in 2 or more promoter regions than de novo MDS or AML suggesting that promoter hypermethylation of genes involved in cell cycle control, apoptosis and DNA repair pathways is a frequent finding in t-MDS/AML and may contribute to secondary leukemogenesis.
  • [MeSH-major] Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


6. Seiter K, Feldman EJ, Sreekantaiah C, Pozzuoli M, Weisberger J, Liu D, Papageorgio C, Weiss M, Kancherla R, Ahmed T: Secondary acute myelogenous leukemia and myelodysplasia without abnormalities of chromosome 11q23 following treatment of acute leukemia with topoisomerase II-based chemotherapy. Leukemia; 2001 Jun;15(6):963-70
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  • [Title] Secondary acute myelogenous leukemia and myelodysplasia without abnormalities of chromosome 11q23 following treatment of acute leukemia with topoisomerase II-based chemotherapy.
  • Therapy-related MDS and AML are complications of intensive chemotherapy regimens.
  • Traditionally, patients exposed to topoisomerase II inhibitors are reported to develop secondary AML with abnormalities of chromosome 11q23.
  • We evaluated the long-term hematologic toxicity of topoisomerase II-intensive high-dose mitoxantrone-based chemotherapy in 163 newly diagnosed acute leukemia patients treated over an 8 year period.
  • Four patients developed MDS with progression to AML, three patients developed new abnormalities at the time of relapse, and three patients (including one of the former patients) had changes that were not associated with hematologic disease.
  • Despite the use of topoisomerase II-intensive treatment, no patient developed an abnormality involving chromosome 11q23.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / ultrastructure. Enzyme Inhibitors / adverse effects. Leukemia, Myeloid / chemically induced. Mitoxantrone / adverse effects. Myelodysplastic Syndromes / chemically induced. Neoplasm Proteins / antagonists & inhibitors. Neoplasms, Second Primary / chemically induced. Topoisomerase II Inhibitors
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Cytarabine / administration & dosage. Disease Progression. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Incidence. Karyotyping. Life Tables. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Randomized Controlled Trials as Topic. Remission Induction. Retrospective Studies. Treatment Outcome. Tretinoin / administration & dosage


7. Dann EJ, Rowe JM: Biology and therapy of secondary leukaemias. Best Pract Res Clin Haematol; 2001 Mar;14(1):119-37
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  • [Title] Biology and therapy of secondary leukaemias.
  • Secondary leukaemias are common, accounting for more than 40% of all patients with acute myeloid leukaemia (AML) or myelodysplastic syndrome (MDS).
  • A clinical history of exposure to haematotoxins or radiation is helpful; however, many older patients are diagnosed with leukaemia with no antecedent history of exposure.
  • These patients' disease show a remarkably similar phenotype to classic therapy-related leukaemia.
  • The specific cytogenetic abnormalities common to MDS, alkylating-agent-related AML and poor-prognosis AML (3q-, -5, 5q-, -7, 7q-, +8, +9, 11q-, 12p-, -18, -19,20q-, +21, t(1;7), t(2;11)), probably reflect a common pathogenesis distinct from that of other de novo AMLs, although the pathogenetic pathway has yet to be elucidated.
  • Typically, these patients are either elderly or have a history of exposure to alkylating agents or environmental exposure 5-7 years prior to diagnosis.
  • Another distinct entity affects the mixed lineage leukaemia (MLL) gene located on 11q23.
  • These account for about 3% of patients with therapy-related leukaemia and have a short latency period from exposure, usually to an inhibitor of topoisomerase II.
  • Other therapy-related patients with t(8:21), inv16 or t(15;17) translocations should be treated as any other de novo AML with similar cytogenetics.
  • In summary, the major prognostic factor is related to the pathogenetic mechanisms of the leukaemia.
  • Patients should receive standard induction therapy.
  • [MeSH-major] Leukemia / chemically induced. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Cytogenetics. Humans. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / etiology. Myelodysplastic Syndromes / therapy. Risk Factors

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  • [Copyright] Copyright 2001 Harcourt Publishers Ltd.
  • (PMID = 11355927.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 102
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8. Side LE, Curtiss NP, Teel K, Kratz C, Wang PW, Larson RA, Le Beau MM, Shannon KM: RAS, FLT3, and TP53 mutations in therapy-related myeloid malignancies with abnormalities of chromosomes 5 and 7. Genes Chromosomes Cancer; 2004 Mar;39(3):217-23
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  • [Title] RAS, FLT3, and TP53 mutations in therapy-related myeloid malignancies with abnormalities of chromosomes 5 and 7.
  • Oncogenic mutations in the KRAS2, NRAS, or FLT3 gene are detected in more than 50% of patients with de novo acute myeloid leukemia (AML).
  • RAS mutations are also prevalent in de novo myelodysplastic syndrome (MDS), especially chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia.
  • However, few studies have examined these genetic lesions in therapy-related myeloid malignancies.
  • Monosomy 7/del(7q) and monosomy 5/del(5q) represent the most common cytogenetic abnormalities in therapy-related MDS and AML (t-MDS/t-AML) and are strongly associated with prior exposure to alkylating agents.
  • Mutational analysis of bone marrow specimens from a well-characterized cohort of 26 t-MDS/t-AML patients with abnormalities of chromosomes 5 and/or 7 revealed 3 with RAS mutations.
  • RAS and FLT3 mutations, which are thought to stimulate the proliferation of leukemia cells, appear to be less common in t-MDS/t-AML than in de novo AML, whereas TP53 mutations are more frequent.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid / genetics. Neoplasms, Second Primary / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins p21(ras) / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. fms-Like Tyrosine Kinase 3

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 14732923.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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9. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML. Leukemia; 2005 Feb;19(2):197-200
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  • [Title] Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.
  • Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%).
  • All three patients were older, had previously received therapy with alkylating agents without topoisomerase II inhibitors, had complex karyotypes including abnormalities of chromosomes 5 or 7, and presented acquired point mutations of the TP53 gene.
  • The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics


10. Herry A, Douet-Guilbert N, Morel F, Le Bris MJ, Morice P, Abgrall JF, Berthou C, De Braekeleer M: Evaluation of chromosome 5 aberrations in complex karyotypes of patients with myeloid disorders reveals their contribution to dicentric and tricentric chromosomes, resulting in the loss of critical 5q regions. Cancer Genet Cytogenet; 2007 Jun;175(2):125-31
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  • [Title] Evaluation of chromosome 5 aberrations in complex karyotypes of patients with myeloid disorders reveals their contribution to dicentric and tricentric chromosomes, resulting in the loss of critical 5q regions.
  • Dicentric chromosomes have often been observed in complex karyotypes in previously reported studies of therapy-related myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
  • Dicentric and tricentric chromosomes were identified in 21 patients (9 MDS and 12 AML) among the 133 consecutive MDS/AML patients (17%) who had a structural or numerical aberration of chromosome 5 using conventional cytogenetic analysis.
  • One third (7/21) of the patients had received alkylating drugs for a previously diagnosed cancer or chronic myeloproliferative disease.
  • Dicentric and tricentric chromosomes involving chromosome 5 are frequently observed in complex karyotypes among patients with de novo or therapy-related MDS/AML.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Deletion. Female. Humans. Karyotyping. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged


11. Lin P, Medeiros LJ, Yin CC, Abruzzo LV: Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Apr 1;166(1):82-5
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  • [Title] Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia.
  • We identified a reciprocal translocation between chromosomes 3 and 8, with breakpoints at bands 3q26 and 8q24, in five patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).
  • In three patients, the AML or MDS developed 36, 52, and 57 months following chemotherapy for soft tissue sarcoma, mantle cell lymphoma, and diffuse large B-cell lymphoma, respectively; in these three patients, the neoplasms were considered to be therapy-related.
  • We conclude that the t(3;8)(q26;q24) is a recurrent translocation associated with therapy-related MDS/AML or de novo AML, and is frequently associated with monosomy 7.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Recurrence, Local / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Humans. Karyotyping. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Male. Middle Aged. Sarcoma / drug therapy. Sarcoma / pathology


12. Andersen MK, Christiansen DH, Kirchhoff M, Pedersen-Bjergaard J: Duplication or amplification of chromosome band 11q23, including the unrearranged MLL gene, is a recurrent abnormality in therapy-related MDS and AML, and is closely related to mutation of the TP53 gene and to previous therapy with alkylating agents. Genes Chromosomes Cancer; 2001 May;31(1):33-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duplication or amplification of chromosome band 11q23, including the unrearranged MLL gene, is a recurrent abnormality in therapy-related MDS and AML, and is closely related to mutation of the TP53 gene and to previous therapy with alkylating agents.
  • Gene amplification is a rare phenomenon in acute leukemia, but recently amplification of specific chromosome bands containing genes rearranged in leukemia-specific balanced chromosome translocations has been reported in a few cases.
  • We detected duplication or amplification of chromosome band 11q23 with 3-7 copies of the MLL gene by fluorescence in situ hybridization in 12 out of 70 unselected patients with therapy-related myelodysplasia or acute myeloid leukemia (17%).
  • Patients with supernumerary copies of MLL were in general older (P = 0.007) and had a shorter survival (P < 0.001) compared to other patients.
  • Duplication or amplification of MLL was significantly associated with a complex karyotype (P = 0.002), with deletion or loss of 5q (P = 0.001), and with prior therapy with alkylating agents.
  • These results support the existence of a specific genetic pathway in t-MDS and t-AML with many previously unidentified chromosome aberrations demonstrated to represent extra copies of parts of 11q, including the unrearranged MLL gene.
  • [MeSH-major] Alkylating Agents / adverse effects. Chromosome Aberrations / genetics. Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53 / genetics. Leukemia, Myeloid / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogenes. Transcription Factors
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Chromosome Banding. Chromosome Disorders. Cytogenetic Analysis / methods. Female. Histone-Lysine N-Methyltransferase. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Nucleic Acid Hybridization / methods. Recurrence

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11284033.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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13. Arber DA, Slovak ML, Popplewell L, Bedell V, Ikle D, Rowley JD, International Workshop on Leukemia Karyotype and Prior Therapy: Therapy-related acute myeloid leukemia/myelodysplasia with balanced 21q22 translocations. Am J Clin Pathol; 2002 Feb;117(2):306-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myeloid leukemia/myelodysplasia with balanced 21q22 translocations.
  • The morphologic and immunophenotypic findings of 36 cases of 21q22 acute myeloid leukemia (AML) and myelodysplasia (MDS) were compared, including 14 de novo t(8;21) AMLs, 11 t(8;21) therapy-related AML/MDS cases, and 11 therapy-related AML/MDS cases with other 21q22 balanced translocations [t(n;21)].
  • Cases of de novo and therapy-related t(8;21) disease shared common morphologic features of chunky cytoplasmic granules, perinuclear hofs, and promyelocyte increases that were not seen consistently in the t(n;21) group of t-AML/MDS cases.
  • De novo and therapy-related t(8;21) disease, however, differed by the frequent presence of associated dysplasia in both t-AML/MDS groups, which was infrequent in the de novo t(8;21) group.
  • Therapy-related AMI/MDS with t(8;21) shares characteristic morphologic and immunophenotypic features with de novo t(8;21) AML, but frequently also occurs with associated myelodysplastic changes, similar to other therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Drug-Related Side Effects and Adverse Reactions. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Translocation, Genetic / genetics


14. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Centromeric breakage and highly rearranged chromosome derivatives associated with mutations of TP53 are common in therapy-related MDS and AML after therapy with alkylating agents: an M-FISH study. Genes Chromosomes Cancer; 2005 Apr;42(4):358-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Centromeric breakage and highly rearranged chromosome derivatives associated with mutations of TP53 are common in therapy-related MDS and AML after therapy with alkylating agents: an M-FISH study.
  • Multicolor fluorescence in situ hybridization (M-FISH) was performed on bone marrow cells of 116 unselected cases of therapy-related myelodysplasia (t-MDS) or acute myeloid leukemia (t-AML), and the results were compared with those of previously performed with G-banding.
  • A clustering of breakpoints was observed in the centromeric or pericentromeric region of chromosomes 1, 5, 7, 13, 17, 21, and 22 in 48 of 98 patients with t-MDS and t-AML and an abnormal karyotype, and was related to previous therapy with alkylating agents.
  • M-FISH had little impact on the prognostic classification of t-MDS and t-AML, as only three patients changed prognostic groups as a result of M-FISH.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Centromere. Chromosome Aberrations. Genes, p53. Leukemia, Myeloid / genetics. Mutation. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Translocation, Genetic

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15645489.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
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15. Andersen MK, Pedersen-Bjergaard J: Increased frequency of dicentric chromosomes in therapy-related MDS and AML compared to de novo disease is significantly related to previous treatment with alkylating agents and suggests a specific susceptibility to chromosome breakage at the centromere. Leukemia; 2000 Jan;14(1):105-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased frequency of dicentric chromosomes in therapy-related MDS and AML compared to de novo disease is significantly related to previous treatment with alkylating agents and suggests a specific susceptibility to chromosome breakage at the centromere.
  • Dicentric chromosomes are observed in many malignant diseases including myelodysplasia (MDS) and acute myeloid leukemia (AML) and have often been observed in a subset of these diseases, namely therapy-related MDS (t-MDS) and AML (t-AML).
  • Using fluorescence in situ hybridization (FISH) with centromere-specific probes, we investigated the frequency and type of dicentric chromosomes in 180 consecutive patients with t-MDS and t-AML and in 231 consecutive patients with de novo MDS and AML, whose karyotypes had been studied previously by conventional G-banding.
  • Twenty-seven out of 180 patients with t-MDS or t-AML presented dicentric chromosomes compared to only seven out of 231 patients with de novo disease (P = 0.00003).
  • Patients with dicentric chromosomes presented significantly more often as t-MDS compared to patients without dicentrics (P = 0.046), and the presence of a dicentric chromosome was significantly related to previous therapy with alkylating agents (P = 0.026).
  • Thus, only one out of 27 patients with a dicentric chromosome had not previously received an alkylating agent.
  • A specific susceptibility to breakage at the centromere after exposure to alkylating agents is suggested and may explain the frequent loss of whole chromosomes, in particular chromosomes 5 and 7 in t-MDS and t-AML, if the breaks are not followed by rejoining.
  • Leukemia (2000) 14, 105-111.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Centromere. Chromosome Aberrations. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics

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  • (PMID = 10637484.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
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