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1. 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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  • [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


2. Lu GH: Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia. Beijing Da Xue Xue Bao; 2005 Feb 18;37(1):10-3
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  • [Title] Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia.
  • Therapy-related acute myeloid leukemia (tAML) is one of the two forms of secondary acute myeloid leukemia, with one derived from de novo myelodysplastic syndrome (MDS) and the other from exposure to environmental or therapeutic agents such as radiation and toxins.
  • There has been a marked increase in the number of incidences of therapy-related acute myeloid leukemia.
  • The majority of tAML resulting from the use of cytotoxic agents can be divided into two groups based on the drugs administered to the patient.
  • Due to the unfavorable outcome of the disease and the need for prompt intensive treatment, a timely accurate diagnosis of tAML is critical to patient care.
  • In this study, an interesting case with therapy-related myelodysplastic syndrome and acute myeloid leukemia (tMDS/tAML) will be presented.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / diagnosis. Lymphoma, B-Cell / drug therapy. Neoplasms, Second Primary / diagnosis

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  • (PMID = 15719033.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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3. Offman J, Gascoigne K, Bristow F, Macpherson P, Bignami M, Casorelli I, Leone G, Pagano L, Sica S, Halil O, Cummins D, Banner NR, Karran P: Repeated sequences in CASPASE-5 and FANCD2 but not NF1 are targets for mutation in microsatellite-unstable acute leukemia/myelodysplastic syndrome. Mol Cancer Res; 2005 May;3(5):251-60
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  • [Title] Repeated sequences in CASPASE-5 and FANCD2 but not NF1 are targets for mutation in microsatellite-unstable acute leukemia/myelodysplastic syndrome.
  • It is widespread among some tumor types, such as colorectal or endometrial carcinoma, but is rarely found in leukemia.
  • Therapy-related acute myeloid leukemia/myelodysplastic syndrome (tAML/MDS) is an exception, and MSI is frequent in tAML/MDS following cancer chemotherapy or organ transplantation.
  • We examined established MSI+ cell lines and tAML/MDS cases for frameshift-like mutations of repetitive sequences in several genes that have known, or suspected, relevance to leukemia.
  • CASPASE-5, an acknowledged frameshift target in MSI+ gastrointestinal tract tumors, was frequently mutated in MSI+ cell lines (67%) and in tAML/MDS (29%).
  • Frameshift-like mutations were also observed in the NF1 and FANCD2 genes that are associated with genetic conditions conferring a predisposition to leukemia.
  • FANCD2 mutations were also common in MSI+ tAML/MDS, although NF1 mutations were not observed.
  • [MeSH-major] Caspases / genetics. Leukemia, Myeloid, Acute / genetics. Microsatellite Repeats / genetics. Mutagenesis / genetics. Myelodysplastic Syndromes / genetics


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4. Leone G, Pagano L, Ben-Yehuda D, Voso MT: Therapy-related leukemia and myelodysplasia: susceptibility and incidence. Haematologica; 2007 Oct;92(10):1389-98
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  • [Title] Therapy-related leukemia and myelodysplasia: susceptibility and incidence.
  • Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is an increasingly recognized treatment complication in patients treated with radiotherapy or chemotherapy for previous hematologic malignancies or solid tumors.
  • Distinct clinical entities have been described according to the primary treatment, corresponding to defined genetic lesions.
  • Chromosome 7 and/or 5 losses or deletions are typical of alkylating agent-induced AML, while development of t-AML with balanced translocations involving chromosome bands 11q23 and 21q22 has been related to previous therapy with drugs targeting DNA-topoisomerase II.
  • Their combination may significantly increase the risk of t-MDS/AML.
  • Among patients with hematologic malignancies, long-term survivors of Hodgkin's lymphoma are exposed to an increased risk of t-MDS/AML, particularly when receiving MOPP-based, and escalated BEACOPP regimens, and when alkylators are combined with radiotherapy.
  • Patients with Hodgkin's and non-Hodgkin's lymphoma are at highest risk when total body irradiation followed by autologous stem cell transplantation is used as rescue or consolidation therapy.
  • The addition of granulocyte-colony-stimulating factor and radiotherapy plays a significant role in t-AML following treatment of children with acute lymphoblastic leukemia.
  • In non-hematologic malignancies, treatment for breast cancer and germ-cell tumors has been associated with a 1-5% lifetime risk of both lymphoid as well as myeloid leukemia.
  • In all cases the risk of t-MDS/AML drops sharply by 10 years after treatment.
  • [MeSH-major] Disease Susceptibility. Drug-Related Side Effects and Adverse Reactions. Leukemia / chemically induced. Leukemia / complications. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / complications. Radiotherapy / adverse effects
  • [MeSH-minor] Animals. DNA / genetics. DNA Repair / genetics. DNA Topoisomerases, Type II / metabolism. Humans. Incidence. Polymorphism, Genetic / genetics. Risk Factors. Topoisomerase II Inhibitors


5. Godley LA, Larson RA: Therapy-related myeloid leukemia. Semin Oncol; 2008 Aug;35(4):418-29
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  • [Title] Therapy-related myeloid leukemia.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) are thought to be the direct consequence of mutational events induced by chemotherapy, radiation therapy, immunosuppressive therapy, or a combination of these modalities, given for a pre-existing condition.
  • The outcomes for these patients have been poor historically compared to people who develop de novo AML.
  • The spectrum of cytogenetic abnormalities in t-AML is similar to de novo AML, but the frequency of unfavorable cytogenetics, such as a complex karyotype or deletion or loss of chromosomes 5 and/or 7, is considerably higher in t-AML.
  • Survival varies according to cytogenetic risk group in t-AML patients, with better outcomes being observed in those with favorable-risk karyotypes.
  • Treatment recommendations should be based on performance status and karyotype.
  • A deeper understanding of the factors that predispose patients to the development of therapy-related myeloid leukemia would help clinicians monitor patients more carefully after treatment for a primary condition.
  • Ultimately, this knowledge could influence initial treatment strategies with the goal of decreasing the incidence of this serious complication.

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  • (PMID = 18692692.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA 14599; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / P30 CA014599-30; United States / NCI NIH HHS / CA / CA 40046; United States / NCI NIH HHS / CA / CA014599-30; United States / NCI NIH HHS / CA / P01 CA040046-14; United States / NCI NIH HHS / CA / CA040046-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 51
  • [Other-IDs] NLM/ NIHMS66055; NLM/ PMC2600445
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6. 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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  • [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


7. Abrahamsen AF: [Acute myelogenous leukemia and myelodysplastic syndrome after treatment with cytostatic agents]. Tidsskr Nor Laegeforen; 2000 Sep 10;120(21):2542-5
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  • [Title] [Acute myelogenous leukemia and myelodysplastic syndrome after treatment with cytostatic agents].
  • INTRODUCTION: The introduction of high dose chemotherapy of cancer has been followed by an increased incidence of therapy-related acute myeloid leukaemia and myelodysplastic syndrome.
  • RESULTS: After standard doses of leukaemogenic drugs the incidence of acute myeloid leukaemia and myelodysplastic syndrome is reported to be 0-4%, increasing to 8-10% after high dose therapy.
  • At diagnosis of acute myeloid leukaemia and myelodysplastic syndrome, most of the patients have chromosomal abnormalities.
  • INTERPRETATION: The prognosis of therapy-related acute myeloid leukaemia and myelodysplastic syndrome is poor compared to that in primary acute myeloid leukaemia and myelodysplastic syndrome.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Dose-Response Relationship, Drug. Humans

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  • (PMID = 11070993.001).
  • [ISSN] 0029-2001
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] NORWAY
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 38
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8. Au WY, Fung A, Man C, Ma SK, Wan TS, Liang R, Kwong YL: Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations. Br J Haematol; 2003 Mar;120(6):1062-5
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  • [Title] Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations.
  • Seventeen patients with therapy-related myelodysplastic syndrome/acute myeloid leukaemia (t-MDS/AML) were examined for aberrant p15 gene methylation by methylation-specific polymerase chain reaction.
  • Ten patients (58%) showed p15 methylation, which was significantly related to monosomy/deletion of chromosome 7q, but not to antecedent chemotherapy, blast count, leukaemic evolution or survival.
  • In three of six patients with marrow samples obtained prior to the diagnosis of t-MDS/AML, p15 methylation predated disease development by up to 2 years.
  • These results showed that p15 methylation was an early event in the evolution of some t-MDS/AML patients.
  • [MeSH-major] Cell Cycle Proteins. Leukemia, Myeloid / metabolism. Myelodysplastic Syndromes / metabolism. Promoter Regions, Genetic. Transcription Factors / genetics. Tumor Suppressor Proteins
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Transplantation. Cyclin-Dependent Kinase Inhibitor p15. DNA Methylation. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Time Factors

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  • (PMID = 12648079.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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9. Kwong YL: Azathioprine: association with therapy-related myelodysplastic syndrome and acute myeloid leukemia. J Rheumatol; 2010 Mar;37(3):485-90
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  • [Title] Azathioprine: association with therapy-related myelodysplastic syndrome and acute myeloid leukemia.
  • A recognized carcinogen, azathioprine is also associated with the development of therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/AML).
  • METHODS: In 56 reported cases, azathioprine had been administered for a median of 65 months (range 6-192) to a median cumulative dose of 146 g (range 19-750) before t-MDS/AML developed.
  • RESULTS: In 11 patients, repeated episodes of cytopenias developed during azathioprine therapy, ante-dating the development of t-MDS/AML.
  • These changes were cytogenetic hallmarks of MDS/AML secondary to known leukemogenic agents and radiotherapy.
  • It will be prudent to review the need for azathioprine therapy when unexpected cytopenias occur and prescription has been prolonged.
  • [MeSH-major] Azathioprine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Adult. Aged. Autoimmune Diseases / drug therapy. Female. Graft Rejection / prevention & control. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Karyotyping. Male. Middle Aged


10. 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.
  • This may explain the lower remission rate obtained with conventional chemotherapy.
  • 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).
  • At the time of this analysis, after a mean follow-up of 12 months, the mean duration of CR is 16 months (range 3-66) and the mean survival is 11 months (range 1-67).
  • The median time to granulocyte recovery (neutrophils > 0.5 x 10(9)/l) was 20 days (range 12-39) and 50 x 10(9)/l platelets were reached at a median of 26 days (range 9-56).
  • 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

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  • (PMID = 11426552.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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11. Sakugawa M, Kojima K, Kaneda K, Masuda K, Dansako H, Shinagawa K, Ishimaru F, Ikeda K, Niiya K, Harada M, Tanimoto M: Therapy-related myelodysplastic syndrome/acute myeloid leukemia M2 and translocation (8;21). Ann Hematol; 2001 Dec;80(12):763-6
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  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia M2 and translocation (8;21).
  • An 80-year-old woman developed therapy-related myelodysplastic syndrome with translocation (8;21), which was successfully treated with an acute myeloid leukemia oriented chemotherapy.
  • The leukemia cell morphology alerted us to the possibility of the presence of t(8;21) before cytogenetic results were obtained, and AML1/ETO fusion transcript was detected by reverse transcription polymerase chain reaction.
  • Our experience suggests that recognition of typical morphological features for de novo M2 acute myeloid leukemia with t(8;21) would be important in diagnosis of therapy related myelodysplastic syndrome/acute myeloid leukemia with this translocation, which could respond to an intensive chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology. Translocation, Genetic
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Nucleus / pathology. Cytoplasm / pathology. Electrophoresis, Agar Gel. Endometrial Neoplasms / drug therapy. Erythroblasts / pathology. Female. Humans. Immunophenotyping. Megakaryocytes / pathology. Reverse Transcriptase Polymerase Chain Reaction


12. Bolufer P, Collado M, Barragan E, Calasanz MJ, Colomer D, Tormo M, González M, Brunet S, Batlle M, Cervera J, Sanz MA: Profile of polymorphisms of drug-metabolising enzymes and the risk of therapy-related leukaemia. Br J Haematol; 2007 Feb;136(4):590-6
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  • [Title] Profile of polymorphisms of drug-metabolising enzymes and the risk of therapy-related leukaemia.
  • Therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/t-MDS) results from an impaired ability to detoxify chemotherapeutic drugs or repair drug-induced genetic damage caused by genetic polymorphisms in enzymes involved in the metabolism of drugs.
  • We analysed the prevalence of genetic polymorphisms of CYP1A1*2A(T6235C), CYP2E1*5B(C-1019T), CYP3A4*1B(A-290G), del{GSTT1}, del{GSTM1}, NQO1*2(C609T), MTHFR(C677T) and TYMS 2R/3R in 78 t-AML/t-MDS and 458 normal individuals (control group, CG) using real-time and conventional polymerase chain reaction (PCR)-based methods.
  • The incidences of polymorphisms among t-AML/t-MDS patients and CG individuals were similar.
  • However, a polymorphism profile consisting of CYP1A1*2A, del{GSTT1} and NQO1*2 strongly modified the risk of t-AML/t-MDS.
  • The absence of all three polymorphisms decreased the risk of t-AML/t-MDS 18-fold (odds ratio (OR) = 0.054, 95% confidence interval (CI) = 0.005-0.63, P = 0.02), whereas the presence of only NQO1*2 or all three polymorphisms enhanced the risk of t-AML/t-MDS (OR = 2.09, 95% CI = 1.08-4.03, P = 0.03 and OR = 18.42, 95% CI = 1.59-212.76, P = 0.02 respectively).
  • Thus, the profiles of genetic polymorphisms of drug-metabolising enzymes might explain the increased risk to t-AML/t-MDS observed in some patients treated with polychemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytochrome P-450 CYP1A1 / genetics. Female. Genetic Predisposition to Disease. Genotype. Glutathione Transferase / genetics. Humans. Inactivation, Metabolic / genetics. Infant. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / enzymology. Myelodysplastic Syndromes / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasm Proteins / genetics. Retrospective Studies

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  • (PMID = 17367411.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
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13. Díaz Beveridge R, Aparicio Urtasun J: [Therapy-related acute leukaemia and myelodysplastic syndrome]. An Med Interna; 2003 May;20(5):257-68
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  • [Title] [Therapy-related acute leukaemia and myelodysplastic syndrome].
  • [Transliterated title] Leucemias agudas y síndromes mielodisplásicos secundarios al tratamiento oncológico.
  • Secondary hematological malignancies represent a severe complication of cancer treatment.
  • Their real incidence is unknown because of the heterogeneity of primary tumors, their therapies, and their prognosis.
  • The usual presentation is an acute leukemia or myelodysplastic syndrome.
  • Two different diseases have been described with particular clinical and cytogenetic features, namely the one associated with alkylating drugs and that related to epipodophylotoxins.
  • Conventional chemotherapy is mainly palliative, whereas allogenic transplantation allows the cure of a small percentage of cases.
  • Thus, potential curative therapies for solid tumors should be optimized and patients maintained in long-term surveillance programs.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / adverse effects. Leukemia, Myeloid / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Podophyllotoxin / adverse effects
  • [MeSH-minor] Acute Disease. Bone Marrow Transplantation. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Neoplasms / drug therapy. Palliative Care. Prognosis

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  • (PMID = 12831302.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; L36H50F353 / Podophyllotoxin
  • [Number-of-references] 83
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14. Aguilera DG, Vaklavas C, Tsimberidou AM, Wen S, Medeiros LJ, Corey SJ: Pediatric therapy-related myelodysplastic syndrome/acute myeloid leukemia: the MD Anderson Cancer Center experience. J Pediatr Hematol Oncol; 2009 Nov;31(11):803-11
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  • [Title] Pediatric therapy-related myelodysplastic syndrome/acute myeloid leukemia: the MD Anderson Cancer Center experience.
  • Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is a long-term complication of pediatric cancer.
  • We retrospectively studied pediatric t-MDS/AML patients treated at MD Anderson from 1975 to 2007.
  • We also compared those patients to pediatric patients with de novo MDS/AML during this time interval.
  • Among 2589 children with cancer treated at MD Anderson, we identified 22 patients with t-MDS/AML.
  • Patients with t-MDS/AML had a median age of 14 years.
  • Group 1 (n=5) underwent stem cell transplantation without induction chemotherapy.
  • Group 2 (n=5) patients received AML-type chemotherapy and a stem cell transplant postremission (n=5).
  • Group 3 (n=4) received a stem cell transplant as salvage therapy.
  • Patients with de novo AML were younger (P=0.001) and higher rates of complete remission (P=0.03), and survival (P<0.0001).
  • Independent factors predicting shorter survival were poor/intermediate-risk cytogenetics (P=0.01), lower hemoglobin level (P=0.0001), and t-MDS/AML (vs. de novo) (P=0.003).
  • Childhood t-MDS/AML has a poor prognosis.
  • Although patients benefited from AML-type induction chemotherapy followed by stem cell transplantation as postremission therapy, effective therapies, and prevention are needed.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / mortality. Neoplasms, Second Primary / mortality
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Hodgkin Disease / mortality. Hodgkin Disease / therapy. Humans. Male. Osteosarcoma / mortality. Osteosarcoma / therapy. Retrospective Studies. Risk Factors. Sex Factors. Stem Cell Transplantation. Survival Rate. Transplantation, Homologous


15. Braun T, Fenaux P: Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia. Br J Haematol; 2008 May;141(5):576-86
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  • [Title] Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia.
  • Novel strategies are required for treatment of acute myeloid leukaemia (AML) and higher risk myelodysplastic syndrome (MDS) patients who are not eligible for intensive chemotherapy and/or allogenic stem cell transplantation.
  • Clinical phase II studies with the oral FTIs tipifarnib and lonafarnib in previously untreated AML, MDS and chronic myelomonocytic leukaemia yielded rather encouraging results while results in relapsed and/or refractory AML were disappointing.
  • Results of a phase III trial in untreated AML in the elderly with tipifarnib were also disappointing.
  • Clinical responses were not related to RAS mutations, suggesting additional actions of FTIs on other molecular targets.
  • The combination of existing FTIs with other treatments, such as chemotherapy (in AML) and hypomethylating agents (in MDS and AML), is under investigation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Farnesyltranstransferase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


16. Campos A, Costa NM, Vaz CP, Carvalhais A, Roncon S, Campilho F, Pimentel P: Secondary malignancies after stem cell transplantation. J Clin Oncol; 2004 Jul 15;22(14_suppl):6651

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  • : 6651 Background: Several reports have suggested that patients who undergo stem cell transplantation (SCT) are at increased risk of developing therapy-related secondary malignancies because of several risk factors, including malignant primary disease, conditioning with radiation and/or chemotherapy, and graft-versus-host disease (GVHD).
  • Twelve post-transplant malignancies were identified in 10 patients (11 after autologous and 1 after allogeneic SCT), 7 male and 4 female, with a median age of 32 years (range: 1-55).
  • RESULTS: At 10 years the actuarial probability of a second neoplasm after SCT was 6.0% (± 2.5%), being 3.2% (± 3.2%) for allogeneic, and 8.0% (± 3.5%) for autologous SCT.
  • The mean follow-up time was 29 months (± 1.3).
  • The median time from SCT to diagnosis of second neoplasm was 10.5 months (range: 2.96-71.5), and overall survival at 10 years was 40% (± 17%).
  • The remaining patient, a man with primary diagnosis of acute myeloid leukaemia M5, underwent allogeneic SCT conditioned with busulfan and cyclophosphamide.
  • He developed a late severe chronic GVHD with mouth involvement, being treated mainly with cyclosporine and prednisone.
  • The follow-up time is necessarily insufficient for allogeneic SCT.
  • There is a trend between autologous SCT for Hodgkin disease and secondary myelodysplastic syndrome.
  • More studies are necessary to define risks factors, mainly for patients with a long expectancy of life after SCT.

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  • (PMID = 28016395.001).
  • [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. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.
  • The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • Using the issues identified in the earlier analysis, the ERG conducted those repairs to the revised model that were feasible within time constraints.
  • The results of these exploratory analyses indicated that: for standard-dose chemotherapy (SDC)-treated patients, of six treatment options available, best supportive care (BSC) was likely the most cost-effective option up to a threshold of 51,000 pounds/quality-adjusted life-year (QALY) [beyond 51,000 pounds/QALY, aza + low-dose chemotherapy (LDC) became cost-effective]; for LDC-treated patients, of four options available, BSC was again the most cost-effective option up to a willingness-to-pay threshold of 51,000 pounds/QALY (aza + LDC became cost-effective after 51,000 pounds/QALY); for BSC-treated patients, aza + BSC became cost-effective relative to BSC at a threshold of about 52,000 pounds/QALY.
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • Given the general paucity of economic modelling work in MDS and the limitations of the submitted industry model there is an evident need for an independent cost-effectiveness analysis of aza in MDS.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


18. Kim SJ, Park TS, Lee ST, Song J, Suh B, Kim SH, Jang SJ, Lee CH, Choi JR: Therapy-related myelodysplastic syndrome/acute myeloid leukemia after treatment with temozolomide in a patient with glioblastoma multiforme. Ann Clin Lab Sci; 2009;39(4):392-8
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  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia after treatment with temozolomide in a patient with glioblastoma multiforme.
  • Therapy-related myelodysplastic syndrome and acute leukemia after treatment with temozolomide have rarely been described in the literature.
  • The cases included anaplastic astrocytoma (4 cases), anaplastic oligodendroglioma (2 cases), low grade astrocytoma (2 cases), low grade oligodendroglioma (1 case), and one case of secondary Philadelphia-positive acute lymphoblastic leukemia in a patient with glioblastoma multiforme.
  • Here we report a novel case of therapy-related myelodysplastic syndrome/acute myeloid leukemia associated with der(1;7)(q10;p10) in a glioblastoma multiforme patient treated with temozolomide.
  • Results of bone marrow morphology, chromosome, and fluorescent in situ hybridization (FISH) analyses, as well as the clinical history, strongly suggest a treatment-related etiology in our case.
  • In past reports, karyotypes in cases of therapy-related myelodysplastic syndrome/acute myeloid leukemia mostly demonstrated abnormalities in chromosomes 5 and 7.
  • However, we report a case of temozolomide-related myelodysplastic syndrome/acute myeloid leukemia with der(1;7)(q10;p10), possibly the first reported case, to the authors' knowledge.
  • [MeSH-major] Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Adult. Aged. Biopsy. Bone Marrow Cells / pathology. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Magnetic Resonance Imaging. Male. Middle Aged. Skin / pathology


19. Lessard M, Hélias C, Struski S, Perrusson N, Uettwiller F, Mozziconacci MJ, Lafage-Pochitaloff M, Dastugue N, Terré C, Brizard F, Cornillet-Lefebvre P, Mugneret F, Barin C, Herry A, Luquet I, Desangles F, Michaux L, Verellen-Dumoulin C, Perrot C, Van den Akker J, Lespinasse J, Eclache V, Berger R, Groupe Francophone de Cytogénétique Hématologique: Fluorescence in situ hybridization analysis of 110 hematopoietic disorders with chromosome 5 abnormalities: do de novo and therapy-related myelodysplastic syndrome-acute myeloid leukemia actually differ? Cancer Genet Cytogenet; 2007 Jul 1;176(1):1-21
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  • [Title] Fluorescence in situ hybridization analysis of 110 hematopoietic disorders with chromosome 5 abnormalities: do de novo and therapy-related myelodysplastic syndrome-acute myeloid leukemia actually differ?
  • A retrospective cytogenetic study of acute myeloid leukemias (AML) and myelodysplastic syndromes (MDS) was conducted by the Groupe Francophone de Cytogénétique Hématologique (GFCH) to evaluate the structural abnormalities of chromosome 5 associated with other chromosomal abnormalities, in particular of chromosome 7, in these pathologies.
  • In all, 110 cases of AML/MDS were recruited based on the presence of chromosome 5 abnormalities under conventional cytogenetics and supplemented by a systematic fluorescence in situ hybridization study of chromosomes 5 and 7.
  • Of the 110 patients, 28 had a hematopoietic disorder secondary to chemotherapy, radiotherapy, or both.
  • Among 82 patients with de novo AML/MDS, 63 were older than 60 years.
  • Systematic investigation of the exposure to mutagens and oncogenes is thus essential to specify the factors potentially involved in MDS/AML with 5q abnormalities.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 7. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Chromosome Deletion. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasms, Radiation-Induced. Translocation, Genetic


20. Buchmann I, Meyer RG, Herr W, Helisch A, Bartenstein P: [Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances]. Nuklearmedizin; 2005;44(3):107-17; quiz N21-2
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  • [Title] [Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances].
  • [Transliterated title] Radioimmuntherapien zur Behandlung der akuten myeloischen Leukämie und des myelodysplastischen Syndroms: Konzeptionelle Chancen.
  • The prognosis of patients with acute myeloid leukaemia (AML) has improved considerably by introduction of aggressive consolidation chemotherapy and haematopoietic stem cell transplantation (SCT).
  • Nevertheless, only 20-30% of patients with AML achieve long-term disease-free survival after SCT.
  • The most common cause of treatment failure is relapse.
  • Additionally, mortality rates are significantly increased by therapy-related causes such as toxicity of chemotherapy and complications of SCT.
  • Including radioimmunotherapies in the treatment of AML and myelodyplastic syndrome (MDS) allows for the achievement of a pronounced antileukaemic effect for the reduction of relapse rates on the one hand.
  • On the other hand, no increase of acute toxicity and later complications should be induced.
  • This paper provides a systematic and critical review of the currently used radionuclides and immunoconjugates for the treatment of AML and MDS and summarizes the literature on primary tumour cell reductive radioimmunotherapies on the one hand and conditioning radioimmunotherapies before SCT on the other hand.
  • [MeSH-major] Leukemia, Myeloid, Acute / radiotherapy. Myelodysplastic Syndromes / radiotherapy. Radioimmunotherapy


21. Roboz GJ, Bennett JM, Coleman M, Ritchie EK, Furman RR, Rossi A, Jhaveri K, Feldman EJ, Leonard JP: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following initial treatment with chemotherapy plus radioimmunotherapy for indolent non-Hodgkin lymphoma. Leuk Res; 2007 Aug;31(8):1141-4
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following initial treatment with chemotherapy plus radioimmunotherapy for indolent non-Hodgkin lymphoma.
  • Patients with indolent non-Hodgkin lymphoma (I-NHL) often receive multiple courses of cytotoxic chemotherapy over several years.
  • Radioimmunotherapy (RIT) has become an important part of treatment for relapsed patients and tositumomab/lodine I-131 tositumomab is a promising regimen currently being incorporated into first-line therapy.
  • While treatment-related myelodysplasia (tMDS) and acute myeloid leukemia (tAML) are well-known, poor-prognosis complications of conventional chemotherapy and radiation therapy, they have not been previously observed as a consequence of initial treatment with RIT-based regimens.
  • We describe four patients with tMDS/tAML who received a sequential chemotherapy and tositumomab/lodine I-131 tositumomab program as their initial and only lymphoma treatment.
  • Our findings suggest that the potential risk of these important complications must be considered in the development of this novel therapeutic strategy in the first-line setting.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Lymphoma, Non-Hodgkin / drug therapy. Myelodysplastic Syndromes / chemically induced. Radioimmunotherapy / adverse effects
  • [MeSH-minor] Adult. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Iodine Radioisotopes. Male. Middle Aged


22. Fern L, Pallis M, Ian Carter G, Seedhouse C, Russell N, Byrne J: Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS. Br J Haematol; 2004 Jul;126(1):63-71
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  • [Title] Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS.
  • The molecular pathogenesis of therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/MDS) remains uncertain.
  • However, clonal haemopoiesis may develop following stem cell transplantation and precede the development of t-AML/MDS.
  • Moreover, accelerated telomere shortening may be induced by replicative stress or oxidative damage, leading to genomic instability, and inactivating polymorphisms of the gene encoding NADPH-quinone oxidoreductase (NQO1) are more frequently observed in patients with t-AML.
  • We studied clonal haemopoiesis, telomere length and NQO1 status in 146 patients receiving conventional chemotherapy for non-myeloid malignancies.
  • Telomere length was reduced in patients following chemotherapy (n = 52) compared with controls (n = 42) (P < 0.001), particularly in those with clonal haemopoiesis (P < 0.002).
  • Whilst there was a trend towards telomere shortening in control subjects polymorphic for NQO1-187Ser (n = 12), chemotherapy-exposed patients polymorphic for the NQO1-187Ser allele (n = 29) had significantly shorter telomeres (P < 0.001).
  • Furthermore, chemotherapy-treated patients with the NQO1-187Ser, polymorphism were more likely to develop clonal haemopoiesis than patients with wild type NQO1 (odds ratio = 7; 1.16-42.6).
  • We conclude that a switch to clonal haemopoiesis may occur after conventional chemotherapy and lead to accelerated telomere shortening.
  • Patients with the NQO1-187Ser polymorphism have an increased risk of developing both clonal haemopoiesis and telomere shortening, which may partly explain the predisposition to t-AML in NQO1-187Ser null individuals.
  • [MeSH-major] Hematopoiesis. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Stem Cell Transplantation / adverse effects. Telomere / ultrastructure

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  • (PMID = 15198733.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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23. Virchis A, Koh M, Rankin P, Mehta A, Potter M, Hoffbrand AV, Prentice HG: Fludarabine, cytosine arabinoside, granulocyte-colony stimulating factor with or without idarubicin in the treatment of high risk acute leukaemia or myelodysplastic syndromes. Br J Haematol; 2004 Jan;124(1):26-32
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  • [Title] Fludarabine, cytosine arabinoside, granulocyte-colony stimulating factor with or without idarubicin in the treatment of high risk acute leukaemia or myelodysplastic syndromes.
  • The combination of fludarabine (FDR), high dose cytarabine and granulocyte colony stimulating factor (FLAG) with or without idarubicin (Ida) was used in the treatment of poor risk acute leukaemia or myelodysplastic syndrome (MDS) in a single centre experience.
  • Such patients proceeded either to further chemotherapy or a haematopoietic stem cell transplant (HSCT).
  • The median time to neutrophil and platelet recovery was 28 and 31 d, respectively.
  • There was a 17% incidence of treatment-related deaths, of which 39% was caused by invasive aspergillus infection.
  • The results show that FLAG +/- Ida is an effective and well-tolerated remission induction regimen for poor risk leukaemia and MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Cytarabine / administration & dosage. Female. Filgrastim. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Idarubicin / administration & dosage. Infusions, Intravenous. Male. Middle Aged. Recombinant Proteins. Stem Cell Transplantation. Survival Analysis. Treatment Outcome

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  • [CommentIn] Br J Haematol. 2004 Oct;127(2):238-9 [15461640.001]
  • (PMID = 14675405.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin; FLAG protocol
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24. Arana-Yi C, Block AW, Sait SN, Ford LA, Barcos M, Baer MR: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine. Leuk Res; 2008 Jul;32(7):1043-8
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) have been reported only rarely following treatment of AML.
  • We report five patients treated for de novo AML who developed t-MDS/t-AML, all with chromosome 7 abnormalities, including -7, del(7)(q22q36) and del(7)(p11.22p22).
  • These cases further document t-MDS/t-AML as a complication of therapy for AML.
  • Presence of chromosome 7 abnormalities in patients with and without prior alkylating agent therapy suggests possible association with the antimetabolite cytarabine.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytarabine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / drug therapy


25. 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

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  • (PMID = 14726020.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 98
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26. Carney DA, Westerman DA, Tam CS, Milner A, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Ritchie D, Came N, Seymour JF: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following fludarabine combination chemotherapy. Leukemia; 2010 Dec;24(12):2056-62
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following fludarabine combination chemotherapy.
  • Fludarabine combination chemotherapy achieves high response rates in chronic lymphocytic leukemia (CLL) and indolent lymphoma.
  • The aim of this study was to investigate the incidence and characteristics of treatment-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) after treatment with fludarabine in combination for lymphoproliferative disorders and identify risk factors for its development.
  • In all, 19 cases of t-MDS/AML have been identified for an overall rate of 10.8%.
  • Median overall survival post-t-MDS/AML diagnosis was 11 months.
  • Patients developing t-MDS/AML included 11/54 with follicular lymphoma (FL) (crude rate 20.4%), 5/82 with CLL (6.1%) and 3/24 with Waldenstrom macroglobulinemia or marginal zone lymphoma (12.5%).
  • Most patients had other cytotoxic treatments (median 4, range 0-7) but three with FL had fludarabine combination as their only line of treatment.
  • Of the eleven patients (6.3%) who received mitoxantrone with their first fludarabine combination, four (36.4%) developed t-MDS/AML (P=0.007).
  • There was a trend toward prior cytotoxic therapy increasing the risk for t-MDS/AML (P=0.067).
  • Fludarabine combination chemotherapy is associated with a moderate risk of t-MDS/AML particularly when combined with mitoxantrone.
  • This complication should be considered when evaluating the potential benefit of this treatment in lymphoproliferative disorders.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Vidarabine / analogs & derivatives


27. 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.
  • 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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  • (PMID = 11417484.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Topoisomerase II Inhibitors; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
  • [Number-of-references] 37
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28. Nenoff P, Kliem C, Mittag M, Horn LC, Niederwieser D, Haustein UF: Secondary cutaneous aspergillosis due to Aspergillus flavus in an acute myeloid leukaemia patient following stem cell transplantation. Eur J Dermatol; 2002 Jan-Feb;12(1):93-8
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  • [Title] Secondary cutaneous aspergillosis due to Aspergillus flavus in an acute myeloid leukaemia patient following stem cell transplantation.
  • In a 64-year-old man suffering from hypoblastic myelodysplastic syndrome a secondary acute myeloid leukaemia developed.
  • After induction chemotherapy with resulting partial remission he received an allogenic (related) peripheral blood stem cell transplantation conditioned with 2 Gy total body irradiation.
  • Computer tomography revealed diffuse bilateral infiltrates which were considered to be suspicious for an invasive pulmonary aspergillosis of the left upper lobe.
  • In addition, Aspergillus flavus grew from skin tissue.
  • Despite antifungal treatment the patient died from Aspergillus pneumonia and generalized aspergillosis with dissemination to heart, brain, and skin.
  • [MeSH-major] Aspergillosis / complications. Aspergillus flavus / isolation & purification. Dermatomycoses / etiology. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Lung Diseases, Fungal / complications
  • [MeSH-minor] Acute Disease. Aged. Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Fatal Outcome. Humans. Male

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  • [CommentIn] Eur J Dermatol. 2003 Jan-Feb;13(1):102-3 [12609797.001]
  • (PMID = 11809609.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
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29. Ruutu T, Koivunen E, Nousiainen T, Pelliniemi TT, Almqvist A, Anttila P, Jantunen E, Koistinen P, Koponen A, Mikkola M, Oksanen K, Pulli T, Remes K, Sarkkinen R, Silvennoinen R, Timonen T, Vanhatalo S, Elonen E, Finnish Leukaemia Group: Oral treatment of acute myeloid leukaemia with etoposide, thioguanine, and idarubicin (ETI) in elderly patients: a prospective randomised comparison with intravenous cytarabine, idarubicin, and thioguanine in the second and third treatment cycle. Eur J Haematol; 2004 Jan;72(1):38-44
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  • [Title] Oral treatment of acute myeloid leukaemia with etoposide, thioguanine, and idarubicin (ETI) in elderly patients: a prospective randomised comparison with intravenous cytarabine, idarubicin, and thioguanine in the second and third treatment cycle.
  • A randomised multicentre study was conducted among patients over 65 yr of age with newly diagnosed acute myeloid leukaemia (AML) to compare oral treatment with etoposide 80 mg/m(2) and thioguanine 100 mg/m(2) twice daily on 5 d and idarubicin 15 mg/m(2) on 3 d (ETI) to a mainly i.v. combination of cytarabine 100 mg/m(2) twice daily on 5 d, idarubicin 12 mg/m(2) x 1, and thioguanine (TAI).
  • Sixty-five patients had de novo AML, 21 AML subsequent to myelodysplastic syndrome, and six treatment-related AML.
  • They received at first a 6-d i.v. treatment with cytarabine and idarubicin.
  • After the first treatment, 68 patients were randomised to receive two cycles of ETI (n = 36) or TAI (n = 32) and thereafter maintenance with mercaptopurine and methotrexate.
  • In conclusion, treatment with oral ETI resulted in a similar antileukaemic effect as obtained with mainly i.v.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Administration, Oral. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Injections, Intravenous. Male. Patient Selection. Recurrence. Statistics, Nonparametric. Survival Rate. Thioguanine / administration & dosage. Time Factors

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  • (PMID = 14962261.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Denmark
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; FTK8U1GZNX / Thioguanine; ZRP63D75JW / Idarubicin; ETI protocol
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30. Bergh J, Wiklund T, Erikstein B, Lidbrink E, Lindman H, Malmström P, Kellokumpu-Lehtinen P, Bengtsson NO, Söderlund G, Anker G, Wist E, Ottosson S, Salminen E, Ljungman P, Holte H, Nilsson J, Blomqvist C, Wilking N: Tailored fluorouracil, epirubicin, and cyclophosphamide compared with marrow-supported high-dose chemotherapy as adjuvant treatment for high-risk breast cancer: a randomised trial. Scandinavian Breast Group 9401 study. Lancet; 2000 Oct 21;356(9239):1384-91
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  • [Title] Tailored fluorouracil, epirubicin, and cyclophosphamide compared with marrow-supported high-dose chemotherapy as adjuvant treatment for high-risk breast cancer: a randomised trial. Scandinavian Breast Group 9401 study.
  • BACKGROUND: Chemotherapy drug distribution varies greatly among individual patients.
  • Therefore, we developed an individualised fluorouracil, epirubicin, cyclophosphamide (FEC) regimen to improve outcomes in patients with high-risk early breast cancer.
  • We then did a randomised trial to compare this individually tailored FEC regimen with conventional adjuvant chemotherapy followed by consolidation with high-dose chemotherapy with stem-cell support.
  • METHODS: 525 women younger than 60 years of age with high-risk primary breast cancer were randomised after surgery to receive nine cycles of tailored FEC to haematological equitoxicity with granulocyte colony-stimulating factor (G-CSF) support (n=251), or three cycles of FEC at standard doses followed by high-dose chemotherapy with cyclophosphamide, thiotepa, and carboplatin (CTCb), and peripheral-blood stem-cell or bone-marrow support (n=274).
  • Both groups received locoregional radiation therapy and tamoxifen for 5 years.
  • Patients in the CTCb group experienced more grade 3 or 4 acute toxicity compared with the tailored FEC group (p<0.0001).
  • Two treatment-related deaths (0.7%) occurred in the CTCb group.
  • Six patients in the tailored FEC group developed acute myeloid leukaemia and three developed myelodysplastic syndrome.
  • INTERPRETATION: Tailored FEC with G-CSF support resulted in a significantly improved relapse-free survival and fewer grade 3 and 4 toxicities compared with marrow-supported high-dose chemotherapy with CTCb as adjuvant therapy of women with high-risk primary breast cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Algorithms. Carboplatin / administration & dosage. Carboplatin / adverse effects. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Disease-Free Survival. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Infusions, Intravenous. Leukemia, Myeloid / chemically induced. Lymphatic Metastasis. Mastectomy, Segmental. Middle Aged. Proportional Hazards Models. Sweden. Thiotepa / administration & dosage. Thiotepa / adverse effects

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  • [ErratumIn] Lancet 2000 Dec 23-30;356(9248):2196
  • (PMID = 11052580.001).
  • [ISSN] 0140-6736
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil; CTCb regimen; FEC protocol
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31. Nivatpumin PJ, Gore SD: Emerging drugs for the treatment of myelodysplastic syndrome. Expert Opin Emerg Drugs; 2005 Aug;10(3):569-90
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  • [Title] Emerging drugs for the treatment of myelodysplastic syndrome.
  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal haematopoietic stem cell disorders characterised by ineffective haematopoiesis and an increased risk of developing acute myeloid leukaemia.
  • However, the majority of patients are not eligible for this therapy, due to excessive treatment-related morbidity and mortality or lack of a suitable donor.
  • As a result, the need for alternative therapies is great.
  • Our improved understanding of the molecular pathogenesis of MDS has resulted in several new promising therapeutic agents.
  • This review will consider the rational development of new agents based on the molecular biology of MDS.
  • [MeSH-major] Drug Industry / trends. Drugs, Investigational / therapeutic use. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 16083330.001).
  • [ISSN] 1744-7623
  • [Journal-full-title] Expert opinion on emerging drugs
  • [ISO-abbreviation] Expert Opin Emerg Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drugs, Investigational
  • [Number-of-references] 185
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32. de Witte T, Oosterveld M, Span B, Muus P, Schattenberg A: Stem cell transplantation for leukemias following myelodysplastic syndromes or secondary to cytotoxic therapy. Rev Clin Exp Hematol; 2002 Mar;6(1):72-85; discussion 86-7
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  • [Title] Stem cell transplantation for leukemias following myelodysplastic syndromes or secondary to cytotoxic therapy.
  • Two main forms of therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/AML) have been recognized.
  • The most frequent type, occurring after treatment with alkylating agents, is characterized by abnormalities of chromosomes 5 and/or 7 and t-MDS/AML following treatment with topoisomerase II inhibitors and is associated with molecular aberrations of MLL (11q23) and AML-1 (21q22).
  • Individuals with certain polymorphisms associated with impaired detoxification of cytotoxic agents have an increased risk of developing MDS or AML after treatment of unrelated cancers.
  • Multidrug chemotherapy is less effective for patients with MDS, or AML following MDS, or t-MDS/AML when compared with primary AML, and results in lower complete remission (CR) rates and lower long-term survival.
  • 21) and inversion 16 are an exception as their treatment outcome is comparable with primary AML patients.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia / therapy. Myelodysplastic Syndromes / complications. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Leukemia, Radiation-Induced / therapy. Risk Factors


33. Anargyrou K, Vaiopoulos G, Terpos E, Tsironi M, Konstantopoulos K, Samarkos M, Meletis J: Low dose melphalan is a treatment option in elderly patients with high risk myelodysplastic syndrome or secondary acute myeloblastic leukaemia. Haematologia (Budap); 2002;32(2):169-73
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  • [Title] Low dose melphalan is a treatment option in elderly patients with high risk myelodysplastic syndrome or secondary acute myeloblastic leukaemia.
  • We present the case of a 71 year-old man with secondary acute myeloblastic leukemia, who was successfully treated with low dose melphalan plus Epo plus G-CSF.
  • We treated the patient with 2 mg of melphalan once a day orally, G-CSF 5 mg/kg 3 times a week and Epo 10.000 ui subcutaneously 3 times a week until the maximum response was obtained.
  • Complete remission was achieved after 16 weeks of continuous treatment.
  • Treatment-related toxicity was not significant.
  • We recommend the use of low dose melphalan in elderly patients with high risk MDS as a treatment option.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Melphalan / administration & dosage. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Aged. Anemia, Refractory, with Excess of Blasts / drug therapy. Drug Therapy, Combination. Erythropoietin / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Remission Induction. Risk Assessment


34. 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.
  • 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


35. 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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  • [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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36. Yakoub-Agha I, de La Salmonière P, Ribaud P, Sutton L, Wattel E, Kuentz M, Jouet JP, Marit G, Milpied N, Deconinck E, Gratecos N, Leporrier M, Chabbert I, Caillot D, Damaj G, Dauriac C, Dreyfus F, François S, Molina L, Tanguy ML, Chevret S, Gluckman E: Allogeneic bone marrow transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia: a long-term study of 70 patients-report of the French society of bone marrow transplantation. J Clin Oncol; 2000 Mar;18(5):963-71
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  • [Title] Allogeneic bone marrow transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia: a long-term study of 70 patients-report of the French society of bone marrow transplantation.
  • PURPOSE: To identify predictive factors of survival, relapse, and transplantation-related mortality (TRM) among patients with therapy-related myelodysplastic syndrome (t-MDS) or acute leukemia (t-AML) who underwent allogeneic bone marrow transplantation (BMT).
  • PATIENTS AND METHODS: From 1980 to 1998, 70 patients underwent allogeneic BMT for t-MDS (n = 31) or t-AML (n = 39) after prior cytotoxic exposure.
  • Thirty-three patients had received induction-type chemotherapy before BMT.
  • At the time of transplantation, there were 24 patients in complete remission (CR) and 46 with active disease.
  • RESULTS: With a median follow-up of 7.9 years (range, 1.1 to 18.8 years) after BMT, 16 patients are alive, whereas 19 died of relapse, 34 of TRM, and one of relapse of the primary disease.
  • CONCLUSION: BMT is an effective treatment for patients with t-MDS or t-AML who have responsive disease and, in particular, who have no poor-risk cytogenetic features.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Megakaryoblastic, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy. Transplantation, Homologous


37. 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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  • [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

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  • (PMID = 11863228.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-30206; United States / NCI NIH HHS / CA / CA-33572
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD34; 0 / Antigens, CD56
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38. Kropff MH, Lang N, Bisping G, Dominé N, Innig G, Hentrich M, Mitterer M, Südhoff T, Fenk R, Straka C, Heinecke A, Koch OM, Ostermann H, Berdel WE, Kienast J: Hyperfractionated cyclophosphamide in combination with pulsed dexamethasone and thalidomide (HyperCDT) in primary refractory or relapsed multiple myeloma. Br J Haematol; 2003 Aug;122(4):607-16
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  • Sixty patients with advanced multiple myeloma received 2-6 monthly treatment courses combining hyperfractionated cyclophosphamide (300 mg/m2 i.v. over 3 h q 12 h x 6, d 1-3) with pulsed dexamethasone (20 mg/m2/d p.o., d 1-4, 9-12, 17-20) and once daily thalidomide at individually escalating doses (100-400 mg/d) depending on tolerability (HyperCDT).
  • During at least one treatment cycle, 67% of patients experienced grade 4 neutropenia resulting in 17% grade 3 and 9% grade 4 infections.
  • Side-effects, presumably related to thalidomide, included neuropathy (40% grade 2, 16% grade 3), constipation (17%), oedema (5%), bradycardia (5%), skin reactions (3%), cerebrovascular events (5%) and deep vein thromboses (8%).
  • Thromboses were not related to known thrombophilic risk factors.
  • Four patients with prior myeloma therapy > 50 months developed myelodysplastic syndrome or secondary acute myeloid leukaemia 2-4 months after study entry.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Brain Ischemia / chemically induced. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Dexamethasone / administration & dosage. Dexamethasone / adverse effects. Disease-Free Survival. Drug Administration Schedule. Female. Follow-Up Studies. Hematologic Diseases / chemically induced. Humans. Leukemia, Myeloid / chemically induced. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Opportunistic Infections / chemically induced. Recurrence. Survival Analysis. Survival Rate. Thalidomide / administration & dosage. Thalidomide / adverse effects. Treatment Outcome. Venous Thrombosis / chemically induced

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  • (PMID = 12899716.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; hyperCDT protocol
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39. Andersen MK, Larson RA, Mauritzson N, Schnittger S, Jhanwar SC, Pedersen-Bjergaard J: Balanced chromosome abnormalities inv(16) and t(15;17) in therapy-related myelodysplastic syndromes and acute leukemia: report from an international workshop. Genes Chromosomes Cancer; 2002 Apr;33(4):395-400
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  • [Title] Balanced chromosome abnormalities inv(16) and t(15;17) in therapy-related myelodysplastic syndromes and acute leukemia: report from an international workshop.
  • The Workshop identified 48 unselected patients with therapy-related myelodysplastic syndrome or acute myeloid leukemia (t-MDS/t-AML) and inv(16), and 41 patients with t(15;17) after chemotherapy (CT) and/or radiotherapy (RT) for a malignant or nonmalignant disease.
  • The general type of previous therapy was RT only in 10 patients with an inv(16) and in 12 patients with a t(15;17), alkylating agents plus topoisomerase II inhibitors in 24 patients with an inv(16) and in 18 patients with a t(15;17), topoisomerase II inhibitors only in 5 patients with an inv(16) and in 2 patients with a t(15;17), alkylating agents only in 6 patients in each subgroup, and other types of chemotherapy in 3 patients in each subgroup.
  • The latency period to development of t-MDS/t-AML was short: a median of 22 months in patients with inv(16) and 29 months in patients with t(15;17).
  • Twenty-six patients (54%) with an inv(16) and 17 patients (41%) with a t(15;17) had additional cytogenetic abnormalities, which were unrelated to age and survival in both subgroups.
  • The disease was overt t-AML in 38/48 patients (79%) with an inv(16) and in 38/41 patients (93%) with a t(15;17).
  • Thirty-three of 39 intensively treated patients (85%) with an inv(16) obtained a complete remission, whereas 24 of 35 intensively treated patients (69%) with a t(15;17) obtained a complete remission.
  • The study supports the observation that t-MDS/t-AML with inv(16) and t(15;17) is often associated with prior therapy with topoisomerase II inhibitors; however, a notable finding was the high frequency of treatment with only radiotherapy, 29% of t(15;17) and 21% of inv(16).
  • Response rates to intensive chemotherapy in this study were comparable to those of de novo disease.
  • [MeSH-major] Chromosome Aberrations / chemically induced. Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Translocation, Genetic / genetics


40. Ostgård LS, Kjeldsen E, Holm MS, Brown Pde N, Pedersen BB, Bendix K, Johansen P, Kristensen JS, Nørgaard JM: Reasons for treating secondary AML as de novo AML. Eur J Haematol; 2010 Sep;85(3):217-26
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  • [Title] Reasons for treating secondary AML as de novo AML.
  • In a Danish bi-regional registry-based study, we conducted an analysis of the incidence and clinical importance of secondary acute myeloid leukaemia (AML).
  • In a total of 630 cases of AML, we found 157 (25%) cases of secondary AML.
  • The secondary leukaemia arose from MDS (myelodysplastic syndrome) in 77 cases (49%), CMPD (chronic myeloproliferative disorder) in 43 cases (27%) and was therapy-related AML (t-AML) in 37 cases (24%).
  • Median age at diagnosis of AML was 69 yr in secondary cases when compared to 66 yr in de novo cases (P = 0.006).
  • In univariate analyses, secondary AML was associated with an inferior complete remission (CR) rate (P = 0.008) and poorer overall survival (OS, P = 0.003) whereas in complete remitters, disease-free survival (DFS) of secondary cases was equal to that of de novo cases.
  • Interestingly, in all further analyses of CR-rates, OS and DFS, when correcting for the influence of age, cytogenetic abnormalities, performance status and leucocyte count (WBC), presence of secondary AML completely lost prognostic significance.
  • We conclude that the presence of secondary AML does not per se convey an unfavourable prognosis and that patients with secondary AML should be offered the chance of benefiting from treatment according to current frontline AML protocols.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cohort Studies. Cytogenetic Analysis. Disease-Free Survival. Female. Humans. Male. Middle Aged. Registries. Young Adult


41. Leleu X, Terriou L, Duhamel A, Moreau AS, Andrieux J, Dupire S, Coiteux V, Berthon C, Micol JB, Guieze R, Facon T, Bauters F: Long-term outcome in acquired aplastic anemia treated with an intensified dose schedule of horse antilymphocyte globulin in combination with androgens. Ann Hematol; 2006 Oct;85(10):711-6
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  • ALG gives about 60% overall survival rate (OS) after 5 years, a 30% of persistent complete remission and a 20% early death rate related to failure.
  • ALG has been incriminated in the emergence of 10 to 20% therapy-related AML/MDS (t-AML/MDS) with the usual doses.
  • Questions remain whether higher doses of ALG could improve the response and OS rates and whether the combination with androgens is able to protect patients from t-AML/MDS.
  • At diagnosis, 6% of AA had an abnormal karyotype using conventional cytogenetic not related to any time-to-event.
  • Two patients displayed a cytogenetic conversion related to the occurrence of secondary malignancies.
  • The incidence of t-AML/MDS was 2.3% with an estimated 10-year cumulative incidence of 3.1.
  • Our results show that higher doses of ALG combined to androgens are feasible and give results close to those recently describe with the immunosuppressive treatments including ALG associated to cyclosporine, with a low SMD/AML incidence rate.
  • [MeSH-major] Androgens / administration & dosage. Anemia, Aplastic / drug therapy. Antilymphocyte Serum / administration & dosage. Immunosuppressive Agents / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Chromosome Aberrations. Disease-Free Survival. Female. Follow-Up Studies. Horses. Humans. Incidence. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Survival Rate. Time Factors

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  • (PMID = 16830141.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgens; 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents
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42. Qian Z, Joslin JM, Tennant TR, Reshmi SC, Young DJ, Stoddart A, Larson RA, Le Beau MM: Cytogenetic and genetic pathways in therapy-related acute myeloid leukemia. Chem Biol Interact; 2010 Mar 19;184(1-2):50-7
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  • [Title] Cytogenetic and genetic pathways in therapy-related acute myeloid leukemia.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) are late complications of cytotoxic therapy used in the treatment of malignant diseases.
  • The most common subtype of t-AML ( approximately 75% of cases) develops after exposure to alkylating agents, and is characterized by loss or deletion of chromosome 5 and/or 7 [-5/del(5q), -7/del(7q)], and a poor outcome (median survival 8 months).
  • In the University of Chicago's series of 386 patients with t-MDS/t-AML, 79 (20%) patients had abnormalities of chromosome 5, 95 (25%) patients had abnormalities of chromosome 7, and 85 (22%) patients had abnormalities of both chromosomes 5 and 7. t-MDS/t-AML with a -5/del(5q) is associated with a complex karyotype, characterized by trisomy 8, as well as loss of 12p, 13q, 16q22, 17p (TP53 locus), chromosome 18, and 20q.
  • In addition, this subtype of t-AML is characterized by a unique expression profile (higher expression of genes) involved in cell cycle control (CCNA2, CCNE2, CDC2), checkpoints (BUB1), or growth (MYC), loss of expression of IRF8, and overexpression of FHL2.
  • Haploinsufficiency of the RPS14, EGR1, APC, NPM1, and CTNNA1 genes on 5q has been implicated in the pathogenesis of MDS/AML.
  • In previous studies, we determined that Egr1 acts by haploinsufficiency and cooperates with mutations induced by alkylating agents to induce myeloid leukemias in the mouse.
  • Identifying the genetic pathways leading to t-AML will provide new insights into the underlying biology of this disease, and may facilitate the identification of new therapeutic targets.

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19958752.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / R01 CA140979; United States / NCI NIH HHS / CA / CA14599
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Ireland
  • [Number-of-references] 38
  • [Other-IDs] NLM/ NIHMS167239; NLM/ PMC4642715
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43. Bolufer P, Barragan E, Collado M, Cervera J, López JA, Sanz MA: Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression. Leuk Res; 2006 Dec;30(12):1471-91
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  • [Title] Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression.
  • BACKGROUND: Recent studies have provided evidence that common genetic variations with low penetrance could account for a proportion of leukemia and could also influence disease outcome, although the results obtained are still controversial.
  • MATERIAL AND METHODS: We reviewed 54 recent reports focused on the contribution of genetic polymorphisms to the risk of developing leukemia and to disease progression.
  • The polymorphisms of genes encoding drug-metabolising enzymes (CYP family, NQO1, GSTT1, GSTM1, GSTP1), enzymes involved in folate metabolism (MTHFR, TYMS, SHMT1, MTRR), and DNA repair enzymes (XPD, XPG, RAD51, XRCC1, XRCC3, CHEK2, ATM) were considered in the review.
  • RESULTS: There was a good agreement on the influence of NQO1*2 polymorphism and those of the enzymes involved in DNA repair with the increased risk of therapy-related leukemia/myelodysplastic syndrome.
  • Most studies found a strong association between the polymorphisms MTHFR, C677T or A1298C, and NQO1*2 or *3 and the risk of acute lymphoblastic leukemia (ALL).
  • In addition, most of the studies reported an association between GSTT1 deletions and an increased risk of de novo acute myeloid leukemia.
  • CONCLUSION: The reports reviewed support the hypothesis that several low-penetrance genes with multiplicative effects together with dietary effects, ambient exposition, and individual immune system responses, may account for the risk of leukaemia.
  • [MeSH-major] Enzymes / genetics. Leukemia / genetics. Polymorphism, Genetic

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  • [CommentIn] Leuk Res. 2007 Apr;31(4):569-70 [17118446.001]
  • (PMID = 17023046.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzymes; 935E97BOY8 / Folic Acid
  • [Number-of-references] 112
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44. Kondo H, Kasahara Y, Mori A: Remission induction of refractory anaemia with excess blasts in transformation by sole treatment with granulocyte colony-stimulating factor with persistent chromosomal abnormality. Acta Haematol; 2002;107(3):177-81
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  • [Title] Remission induction of refractory anaemia with excess blasts in transformation by sole treatment with granulocyte colony-stimulating factor with persistent chromosomal abnormality.
  • We report a patient with myelodysplastic syndrome (MDS), refractory anaemia with excess blasts in transformation, in whom complete remission (CR) was achieved with the administration of granulocyte colony-stimulating factor (G-CSF).
  • The 76-year-old patient was admitted to our hospital with a fever and a productive cough; a diagnosis of pneumonia was thus made.
  • Following treatment with antibiotics, the patient's condition improved, and MDS was diagnosed from peripheral blood and bone marrow examinations after the patient recovered from the infection.
  • The patient achieved a sustained haematological CR that was confirmed by morphological and flow cytometric examination after treatment with G-CSF alone, although chromosomal abnormalities persisted.
  • According to the literature, in almost all patients with acute myeloid leukaemia or MDS who were reported to achieve CR by G-CSF, the course was associated with infection, although our case did not have this complication during the course of G-CSF therapy.
  • We suggest that patients with G-CSF alone without infection can achieve CR and that this may be related to a differentiation effect of G-CSF based on persistent chromosomal abnormality in this case.
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / drug therapy. Anemia, Refractory, with Excess of Blasts / genetics. Chromosome Aberrations. Granulocyte Colony-Stimulating Factor / therapeutic use. Remission Induction

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  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 11978940.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.1.3.48 / Antigens, CD45
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45. Leone G, Fianchi L, Pagano L, Voso MT: Incidence and susceptibility to therapy-related myeloid neoplasms. Chem Biol Interact; 2010 Mar 19;184(1-2):39-45
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  • [Title] Incidence and susceptibility to therapy-related myeloid neoplasms.
  • Therapy-related myeloid neoplasms (t-MN) include acute myeloid leukemias and myelodysplastic syndromes arising in patients who have been treated with chemotherapy, radiation therapy, immunosuppressive agents or after documented exposure to environmental carcinogen. t-MN are defined according to the primary treatment and the corresponding genetic and molecular lesions.
  • Chromosome(s) 7 and/or 5 monosomies or deletions are typical of alkylating agent-induced AML, while balanced translocations involving chromosome bands 11q23 and 21q22 are associated to preceeding therapy with DNA-topoisomerase II inhibitors.
  • Combination of polymorphisms impairing detoxification and DNA repair may significantly increase therapy-related myeloid neoplasm risk.
  • The addition of granulocyte-colony stimulating factor (G-CSF) and radiotherapy plays a significant role in t-MN following treatment of childhood acute lymphoblastic leukemia.
  • In solid tumors, treatment for breast cancer and germ-cell tumors has been associated with a 1-5% lifetime risk of t-MN.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / etiology. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / etiology

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20026017.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Topoisomerase II Inhibitors; J64922108F / Benzene
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46. Shim H, Chi HS, Jang S, Seo EJ, Park CJ, Lee JH, Lee JH, Lee KH: Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor. Korean J Hematol; 2010 Sep;45(3):177-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.
  • BACKGROUND: Therapy-related myeloid neoplasm (t-MN) is a distinct class of acute myeloid leukemia (AML) in the World Health Organization (WHO) classification.
  • Both AML and acute lymphoblastic leukemia (ALL) may develop after treatment for primary cancer.
  • Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related acute leukemias (t-AL).
  • METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed acute leukemia.
  • RESULTS: Fourteen patients (0.2%) developed t-AL after treatment for breast cancer.
  • Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related AML (t-AML) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).
  • The median interval between completion of chemotherapy for breast cancer and occurrence of t-AL was 25 months.
  • CONCLUSION: The incidence rate of t-AL after treatment for breast cancer was 0.2% in a tertiary hospital in Korea.
  • Translocation involving the MLL gene was frequently found in t-AL caused by a topoisomerase inhibitor and was related to poor prognosis.

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  • (PMID = 21120206.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983048
  • [Keywords] NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors
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47. Blanco JG, Edick MJ, Hancock ML, Winick NJ, Dervieux T, Amylon MD, Bash RO, Behm FG, Camitta BM, Pui CH, Raimondi SC, Relling MV: Genetic polymorphisms in CYP3A5, CYP3A4 and NQO1 in children who developed therapy-related myeloid malignancies. Pharmacogenetics; 2002 Nov;12(8):605-11
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in CYP3A5, CYP3A4 and NQO1 in children who developed therapy-related myeloid malignancies.
  • Therapy-related acute myeloid leukemia and myelodysplastic syndrome (t-ML) are serious complications that affect some patients after acute lymphoblastic leukemia (ALL) treatment.
  • A polymorphism in CYP3A5 (CYP3A5*3) affects CYP3A activity and the wild-type allele (CYP3A5*1) is in partial linkage with the CYP3A4*1B allele.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytochrome P-450 Enzyme System / genetics. Leukemia, Myeloid / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasms, Second Primary / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Base Sequence. Child. Child, Preschool. Cytochrome P-450 CYP3A. DNA Primers. Female. Humans. Infant. Infant, Newborn. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 12439220.001).
  • [ISSN] 0960-314X
  • [Journal-full-title] Pharmacogenetics
  • [ISO-abbreviation] Pharmacogenetics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA13959; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA29139; United States / NCI NIH HHS / CA / CA30969; United States / NCI NIH HHS / CA / CA31566; United States / NCI NIH HHS / CA / CA32053; United States / NCI NIH HHS / CA / CA33606; United States / NCI NIH HHS / CA / CA33625; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / CA51001; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NIGMS NIH HHS / GM / U01GM61374
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Primers; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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48. Niparuck P, Kanoksil W, Chuncharunee S, Boonsakan P, Ungkanont A, Angchaisuksiri P, Karntisaviwat K, Apilugsanachit A, Rerkamnuatchoke B, Jootar S, Nitiyanant P, Atichartakarn V: Therapy-related myelodysplastic syndrome/acute myeloid leukemia following fludarabine therapy for non-Hodgkin lymphoma and chronic lymphocytic leukemia in Thai patients. Leuk Lymphoma; 2010 Nov;51(11):2120-5
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia following fludarabine therapy for non-Hodgkin lymphoma and chronic lymphocytic leukemia in Thai patients.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Lymphoma, Non-Hodgkin / drug therapy. Myelodysplastic Syndromes / chemically induced. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Female. Humans. Male. Middle Aged. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / epidemiology. Prognosis. Retrospective Studies. Thailand / epidemiology. Young Adult


49. Asou N, Iwanaga E, Nanri T, Mitsuya H: Successful treatment with low-dose imatinib mesylate of therapy-related myeloid neoplasm harboring TEL-PDGFRB in a patient with acute promyelocytic leukemia. Haematologica; 2010 Sep;95(9):e1
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with low-dose imatinib mesylate of therapy-related myeloid neoplasm harboring TEL-PDGFRB in a patient with acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / drug therapy. Oncogene Proteins, Fusion / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
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  • (PMID = 20807977.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / TEL-PDGFRbeta fusion protein, human; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC2930974
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50. Andersen MK, Pedersen-Bjergaard J: Therapy-related MDS and AML in acute promyelocytic leukemia. Blood; 2002 Sep 1;100(5):1928-9; author reply 1929
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related MDS and AML in acute promyelocytic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Humans. Tretinoin / adverse effects. Tretinoin / therapeutic use






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