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1. Greco M, D'Alò F, Scardocci A, Criscuolo M, Fabiani E, Guidi F, Di Ruscio A, Migliara G, Pagano L, Fianchi L, Chiusolo P, Hohaus S, Leone G, Voso MT: Promoter methylation of DAPK1, E-cadherin and thrombospondin-1 in de novo and therapy-related myeloid neoplasms. Blood Cells Mol Dis; 2010 Oct 15;45(3):181-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter methylation of DAPK1, E-cadherin and thrombospondin-1 in de novo and therapy-related myeloid neoplasms.
  • DNA methylation is one of the major epigenetic changes in human cancers, leading to silencing of tumor suppressor genes, with a pathogenetic role in tumor development and progression in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
  • Methylation of key promoter regions, induced by cytotoxic therapy together with complex genetic changes, is important in the biology of therapy-related myeloid neoplasms (t-MN).
  • We were interested in the characterization of the methylation pattern of AML and MDS de novo and therapy-related.
  • There were 105 MDS, 208 de novo AML and 72 t-MN (45 MDS and 27 AML).
  • We found no associations between promoter hypermethylation and gender or age at the time of initial diagnosis.
  • In patients with MDS, there were no associations between hypermethylation and clinical characteristics, including IPSS score, WHO classification and cytogenetics.
  • DAPK1 was more frequently methylated in t-MDS/AML when compared to de novo MDS and AML (39% vs 15.3% and 24.4%, p=0.0001), while methylation of CDH1 was similar in t-MDS/AML and AML (51% and 53.4%), but less frequent in de novo MDS (29%) (p=0.003).
  • In the t-MDS/AML group, we found that the methylation pattern appeared to be related to the primary tumor, with DAPK1 more frequently methylated in patients with a previous lymphoproliferative disease (75% vs 32%, p=0.006).
  • TSP1 hypermethylation was rare and not characteristic of t-MDS/AML.
  • In 177 patients studied for concurrent methylation of several promoters, t-MN and AML de novo were significantly more frequently hypermethylated in 2 or more promoter regions than de novo MDS (20% vs 12.4%, p<0.001).
  • Chemotherapy and individual genetic predisposition have a role in t-MDS/AML development, the identification of specific epigenetic modifications may explain complexity and genomic instability of these diseases and give the basis for targeted-therapy.
  • The significant association with previous malignancy subtypes may underlie a likely susceptibility to methylation of specific targets and a role for constitutional epimutations as predisposing factors for the development of therapy-related myeloid neoplasm.
  • [MeSH-major] Apoptosis Regulatory Proteins. Cadherins. Calcium-Calmodulin-Dependent Protein Kinases. DNA Methylation. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Neoplasms, Second Primary / metabolism. Promoter Regions, Genetic. Thrombospondin 1

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20655775.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CDH1 protein, human; 0 / Cadherins; 0 / Thrombospondin 1; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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2. Ogasawara T, Yasuyama M, Kawauchi K: Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). Am J Hematol; 2005 Jun;79(2):136-41
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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 myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
  • We describe a patient who developed myelodysplastic syndrome over 2 years after achieving complete remission of acute myeloid leukemia (AML).
  • The patient was treated in July 1998 with anthracycline, etoposide, and behenoyl cytarabine chemotherapy for AML (French-American-British classification, M2; World Health Organization classification, AML with maturation) and achieved complete remission.
  • The patient was diagnosed with high-grade myelodysplastic syndrome (MDS)/refractory anemia with excess blasts (RAEB) subtype.
  • The pancytopenia progressed rapidly, and he died 2 months after the diagnosis of MDS.
  • Therapy-related MDS and AML (t-MDS/t-AML) developing after treatment for acute leukemia is unusual; the primary leukemia associated with most cases of t-MDS/t-AML is acute promyelocytic leukemia (APL).
  • This unusual case suggests that AML excluding APL should be considered a primary hematologic malignancy for t-MDS/t-AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 5. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / chemically induced. Monosomy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics


3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Nine (5.5%) patients developed new cytogenetic abnormalities.
  • 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


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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • All patients were treated with combination chemotherapy; at writing, four were still alive and one had died during a follow-up period ranging from 1 to 16 months.
  • 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


5. 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


6. Gilliland DG, Gribben JG: Evaluation of the risk of therapy-related MDS/AML after autologous stem cell transplantation. Biol Blood Marrow Transplant; 2002;8(1):9-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the risk of therapy-related MDS/AML after autologous stem cell transplantation.
  • A major complication of autologous stem cell transplantation (ASCT) is the development of therapy-related myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML).
  • This complication likely results from previous exposure of the autologous stem cells to chemotherapy as well as to the high doses of chemotherapy and radiation therapy that are used as part of the conditioning regimen.
  • A number of centers are reporting that, second to disease relapse, therapy-related MDS and AML are among the major causes of morbidity and mortality after ASCT.
  • There is abundant evidence that therapy-related MDS and AML are clonal hemopathies that are consequence of an acquired somatic mutation that confers a proliferative and/or survival advantage to hematopoietic progenitors.
  • However, no single mutation or gene rearrangement is sufficient for the development of therapy-related AML, and the identification of a singlegene rearrangement or point mutation may not necessarily be predictive of the development of therapy-related AML in the post-ASCT setting, a caveat that must be kept in mind when risk is assessed.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Stem Cell Transplantation / adverse effects


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






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