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1. Seiter K, Feldman EJ, Sreekantaiah C, Pozzuoli M, Weisberger J, Liu D, Papageorgio C, Weiss M, Kancherla R, Ahmed T: Secondary acute myelogenous leukemia and myelodysplasia without abnormalities of chromosome 11q23 following treatment of acute leukemia with topoisomerase II-based chemotherapy. Leukemia; 2001 Jun;15(6):963-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute myelogenous leukemia and myelodysplasia without abnormalities of chromosome 11q23 following treatment of acute leukemia with topoisomerase II-based chemotherapy.
  • Therapy-related MDS and AML are complications of intensive chemotherapy regimens.
  • Traditionally, patients exposed to topoisomerase II inhibitors are reported to develop secondary AML with abnormalities of chromosome 11q23.
  • We evaluated the long-term hematologic toxicity of topoisomerase II-intensive high-dose mitoxantrone-based chemotherapy in 163 newly diagnosed acute leukemia patients treated over an 8 year period.
  • Nine (5.5%) patients developed new cytogenetic abnormalities.
  • Four patients developed MDS with progression to AML, three patients developed new abnormalities at the time of relapse, and three patients (including one of the former patients) had changes that were not associated with hematologic disease.
  • The abnormalities most frequently involved chromosomes 7q, 20q, 1q, and 13q.
  • 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


2. Saito M, Mori A, Irie T, Tanaka M, Morioka M: [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer]. Rinsho Ketsueki; 2009 Mar;50(3):192-6
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  • [Title] [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer].
  • Among cases of therapy-related acute myeloid leukemia (t-AML) due to DNA topoisomerase II inhibitors, 11q23 abnormality is often detected.
  • The usefulness of paclitaxel as a key drug in chemotherapy for breast cancer has been demonstrated.
  • Few studies have reported t-AML due to paclitaxel.
  • In this study, we report a patient who developed t-AML with 11q23 abnormality and bone marrow metastasis after breast cancer treatment with paclitaxel.
  • Bone marrow aspiration suggested AML (M4) with (11;19)(q23;p13) chromosome abnormalities.
  • This patient had not received any other anticancer drugs.
  • Based on the clinical course, t-AML may have developed after paclitaxel therapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Bone Marrow Neoplasms / secondary. Breast Neoplasms / pathology. Chromosome Aberrations / drug effects. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / etiology. Neoplasms, Second Primary. Paclitaxel / adverse effects


3. Giusiano S, Formisano-Tréziny C, Benziane A, Maroc N, Picard C, Hermitte F, Taranger-Charpin C, Gabert J: Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis. Int J Lab Hematol; 2010 Aug 1;32(4):398-409
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  • [Title] Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis.
  • Three major types of rearrangements are involved in acute myeloid leukemias (AML): t(8;21)(q22;q22), inv(16)(p13q22), and 11q23/MLL abnormalities.
  • Their precise identification becomes essential for diagnosis, prognosis, and therapeutic choices.
  • In this study, we propose a biochip-based assay integrated in a global strategy for identification of rare FT in AML, after fluorescence in situ hybridization detection, as described by the World Health Organization classification.
  • This AMLFusionChip strategy fits into the concept of personalized medicine for the largest number of patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19930410.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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4. Zwaan CM, Kaspers GJ, Pieters R, Hählen K, Huismans DR, Zimmermann M, Harbott J, Slater RM, Creutzig U, Veerman AJ: Cellular drug resistance in childhood acute myeloid leukemia is related to chromosomal abnormalities. Blood; 2002 Nov 1;100(9):3352-60
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  • [Title] Cellular drug resistance in childhood acute myeloid leukemia is related to chromosomal abnormalities.
  • Specific cytogenetic abnormalities predict prognosis in childhood acute myeloid leukemia (AML).
  • However, it is unknown why they are predictive and whether this is related to drug resistance.
  • We previously reported that Down syndrome (DS) AML was associated with favorable resistance profiles.
  • Here, we successfully analyzed drug resistance and (cyto-) genetic abnormalities of 109 untreated childhood AML samples using the 4-day total cell-kill methyl-thiazolyl tetrazolium (MTT) assay.
  • Patients were classified according to the genetic abnormalities in the leukemic cells: t(8;21), inv(16), t(15;17), t(9;11), other 11q23 translocations, abnormalities of chromosome 5/7, trisomy 8 alone, normal karyotype, single random, and multiple (defined as 2 or more) abnormalities.
  • The DS AML samples were excluded from the subgroup analysis.
  • Samples with chromosome 5/7 abnormalities were median 3.9-fold (P =.01) more resistant to cytarabine than other AML samples.
  • The t(9;11) samples were more sensitive to cytarabine (median 2.9-fold, P =.002), etoposide (13.1-fold, P =.001), the anthracyclines (2.9- to 8.0-fold, P <.01), and 2-chlorodeoxyadenosine (10.0-fold, P =.002) than other AML samples.
  • Overall, we found no differences in drug resistance in samples taken at diagnosis between patients remaining in continuous complete remission (CCR) versus the refractory/relapsed patients.
  • We conclude that some, but not all, cytogenetic subgroups in childhood AML display specific drug-resistance profiles.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chromosome Aberrations. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Inversion. Chromosomes, Human / ultrastructure. Cladribine / pharmacology. Cytarabine / pharmacology. Drug Resistance, Multiple / genetics. Etoposide / pharmacology. Female. Humans. Infant. Male. Neoplastic Stem Cells / drug effects. Recurrence. Remission Induction. Tetrazolium Salts. Thiazoles. Translocation, Genetic. Trisomy

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  • (PMID = 12384437.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; 47M74X9YT5 / Cladribine; 6PLQ3CP4P3 / Etoposide
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5. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
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  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • The various aberrations observed were t(8;21)(q22;q22) (5.2%); t(15;17) (q22;q11-21) (9%); t(9;22)(q34;q11)(1.7%); t(14;17)(q32;q11.2)(0.5%); inv(16)(p13;q22)(1.7%); 11q23 rearrangements (4%); monosomy 7 (2.2%) and 22 (1.1%); deletion of 9q (q22q34) (5.1%), 5q (q13q33) (0.5%) and 13q (q13q31) (0.5%); common trisomies like +8 (5.6%), +16 (1.7%), +22 (1.1%), +21 (0.5%), +13 (0.5%), +11 (0.5%), +3 (0.5%); hyperdiploidy (3.4%); hypodiploidy (1.1%); complex karyotype (4%); and other structural abnormalities (4.5%).
  • Apart from these, three novel chromosomal abnormalities viz. t(8;18), t(7;14), t(13;15) were observed in the current study population.
  • CONCLUSION: This study confirms that the incidence of chromosomal abnormalities varies considerably.
  • Similarly, the frequency of other recurrent FAB associated abnormalities viz.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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6. Zwaan CM, Meshinchi S, Radich JP, Veerman AJ, Huismans DR, Munske L, Podleschny M, Hählen K, Pieters R, Zimmermann M, Reinhardt D, Harbott J, Creutzig U, Kaspers GJ, Griesinger F: FLT3 internal tandem duplication in 234 children with acute myeloid leukemia: prognostic significance and relation to cellular drug resistance. Blood; 2003 Oct 1;102(7):2387-94
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  • [Title] FLT3 internal tandem duplication in 234 children with acute myeloid leukemia: prognostic significance and relation to cellular drug resistance.
  • FLT3 internal tandem duplications (FLT3/ITDs) are reported in acute myeloid leukemia (AML) and predict poor clinical outcome.
  • We found FLT3/ITDs in 11.5% of 234 children with de novo AML.
  • FLT3/ITD-positive patients were significantly older and had higher percentages of normal cytogenetic findings or French-American-British (FAB) classification M1/M2 and lower percentages of 11q23 abnormalities or FAB M5.
  • Patients with high ratios (higher than the median) between mutant and wild-type FLT3 had significantly worse 2-year EFS rates than FLT3/ITD-negative patients (pEFS 20% vs 61%; P =.037), whereas patients with ratios lower than the median did not (pEFS 44% vs 61%; P =.26).
  • Using an MTT (methyl-thiazol-tetrazolium)-based assay, we studied cellular drug resistance on 15 FLT3/ITD-positive and 125 FLT3/ITD-negative AML samples, but we found no differences in cellular drug resistance that could explain the poor outcomes in FLT3/ITD-positive patients.
  • We conclude that FLT3/ITD is less common in pediatric than in adult AML.
  • However, poor outcomes in FLT3/ITD-positive patients could not be attributed to increased in vitro cellular drug resistance.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Antibiotics, Antineoplastic / therapeutic use. Child. Child, Preschool. Daunorubicin / therapeutic use. Female. Humans. Idarubicin / therapeutic use. Infant. Infant, Newborn. Male. Prognosis. Risk Factors. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3

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  • (PMID = 12816873.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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7. Sait SN, Claydon MA, Conroy JM, Nowak NJ, Barcos M, Baer MR: Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):143-6
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  • [Title] Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia.
  • Reciprocal chromosomal translocations involving the MLL gene at chromosome region 11q23 are recurring cytogenetic abnormalities in both de novo and therapy-related acute myeloid leukemia (AML) and in acute lymphoblastic leukemia.
  • We report a t(4;11)(p12;q23) with rearrangement of MLL and FRYL (also known as AF4p12), a human homolog to the furry gene of Drosophila, in an adult patient with therapy-related AML after fludarabine and rituximab therapy for small lymphocytic lymphoma and radiation therapy for breast carcinoma.
  • Thus, t(4;11)(p12;q23) with MLL and FRYL involvement represents a new recurring 11q23 translocation, to date seen only in therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Middle Aged. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17854671.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; 4F4X42SYQ6 / Rituximab; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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8. Linassier C, Barin C, Calais G, Letortorec S, Brémond JL, Delain M, Petit A, Georget MT, Cartron G, Raban N, Benboubker L, Leloup R, Binet C, Lamagnère JP, Colombat P: Early secondary acute myelogenous leukemia in breast cancer patients after treatment with mitoxantrone, cyclophosphamide, fluorouracil and radiation therapy. Ann Oncol; 2000 Oct;11(10):1289-94
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  • [Title] Early secondary acute myelogenous leukemia in breast cancer patients after treatment with mitoxantrone, cyclophosphamide, fluorouracil and radiation therapy.
  • BACKGROUND: The topoisomerase II-targeted drugs, epipodophyllotoxins and anthracyclines, have been shown to induce therapy-related AML (t-AML) characterized by a short latency period after chemotherapy, the absence of prior myelodysplastic syndrome and stereotyped chromosome aberrations.
  • We observed 10 cases of such t-AML over a 7-year-period in breast cancer patients treated with mitoxantrone combined with fluorouracil, cyclophosphamide and regional radiotherapy, and in three cases with vindesine.
  • PATIENTS AND METHODS: We retrospectively analyzed patients referred to our hospital for AML with a past history of polychemotherapy for breast cancer, including mitoxantrone, either as adjuvant (8 patients)/neoadjuvant (1 patient) therapy or for metastatic disease (1 patient).
  • We studied the probability of developing t-AML in a prospective series of 350 patients treated with an adjuvant FNC regimen (mitoxantrone, fluorouracil, cyclophosphamide) and radiation therapy.
  • t-AML developed 13-36 months (median 16) after beginning chemotherapy for breast cancer, and 4-28 months (median 10.5) after ending treatment.
  • As described in t-AML following treatment with epipodophyllotoxins or anthracyclines, we found a majority of FAB M4, M5 and M3 phenotypes (7 of 10), and characteristic karyotype abnormalities that also can be found in de novo AML: breakpoint on chromosome 11q23 (3 patients), inv(16)(p13q22) (2 patients), t(15;17)(q22;q11) (1 patient), t(8;21)(q22;q22) (1 patient) and del(20q)(q11) (1 patient).
  • All patients died of AML shortly after diagnosis.
  • Since two patients had been enrolled in a prospective trial for the treatment of breast cancer which included 350 patients, the probability of developing t-AML was calculated to be 0.7% from 25-40 months, using the Kaplan-Meier method (95%, confidence interval (95% CI): 0.1-4.5).
  • CONCLUSIONS: The combination of mitoxantrone with cyclophosphamide, fluorouracil, and radiation therapy can induce t-AML, as with other topoisomerase II-targeted drugs.


9. Ishizawa S, Slovak ML, Popplewell L, Bedell V, Wrede JE, Carter NH, Snyder DS, Arber DA: High frequency of pro-B acute lymphoblastic leukemia in adults with secondary leukemia with 11q23 abnormalities. Leukemia; 2003 Jun;17(6):1091-5
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  • [Title] High frequency of pro-B acute lymphoblastic leukemia in adults with secondary leukemia with 11q23 abnormalities.
  • To evaluate the frequency and cytogenetic and immunophenotypic features of therapy-related, precursor B-cell acute lymphoblastic leukemia (ALL), 152 cases of immature B-cell ALL were reviewed.
  • These were compared to the frequency of therapy-related acute myeloid leukemia (t-AML) during the same time period.
  • Eight ALL cases with a prior diagnosis of malignancy were identified, including six (4.0%) with prior therapy considered to be therapy-related ALL (t-ALL).
  • All t-ALL cases had a pro-B (CD10-negative) immunophenotype with significantly higher expression of CD15 and CD65, compared to the de novo CD10-positive ALL cases.
  • All six t-ALL cases had MLL abnormalities by fluorescence in situ hybridization, and four showed t(4;11)(q21;q23).
  • These represented half of all 11q23-positive adult ALL cases.
  • During the same time period, 4.9% of all AML cases were considered t-AML.
  • There was a 16.7% frequency of 11q23 abnormalities in the t-AML group.
  • Despite the similar frequency in therapy-related disease among ALL and AML cases, there were differences in the frequency of the diseases and t-ALL represented 12% of all therapy-related leukemias.
  • However, t-ALL represented 46% of all 11q23-positive therapy-related leukemias.
  • The immunogenetic features of t-ALL appear distinct and may aid in identifying more cases of this disease type in the future.
  • [MeSH-major] Burkitt Lymphoma / etiology. Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid / etiology. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / immunology. Antineoplastic Agents / therapeutic use. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Neoplasms / drug therapy. Neoplasms / radiotherapy. Translocation, Genetic

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  • (PMID = 12764373.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30206; United States / NCI NIH HHS / CA / CA 33572
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents
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10. de Jesus Marques-Salles T, Liehr T, Mkrtchyan H, Raimondi SC, Tavares de Souza M, de Figueiredo AF, Rouxinol S, Jordy Macedo FC, Abdelhay E, Santos N, Macedo Silva ML: A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):59-62
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  • [Title] A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia.
  • Infants diagnosed with acute myelogenous leukemia (AML) are likely to have subtypes M4 or M5 characterized by 11q23 abnormalities like a t(9;11)(p22;q23).
  • Detection of all possible types of chromosomal abnormalities, including mixed lineage leukemia (MLL) gene rearrangements at 11q23, is of importance for the identification of biological subgroups, which might differ in drug resistance and/or clinical outcome.
  • Here, we report the clinical, conventional banding and molecular cytogenetics data of a 6-month-old boy with an AML-M5 presenting with a unique cryptic rearrangement involving the MLL gene: a three-way t(9;19;11)(p11.2;p13.1;q23).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 19167614.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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11. Kawakami K, Watanabe Y, Kadowaki S: [Therapy-related acute myelogenous leukemia (AML-M6) with add(11) (q23) and del(20) (q11.2) developing via myelodysplastic syndrome after chemotherapy for malignant lymphoma]. Rinsho Ketsueki; 2003 Mar;44(3):168-73
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  • [Title] [Therapy-related acute myelogenous leukemia (AML-M6) with add(11) (q23) and del(20) (q11.2) developing via myelodysplastic syndrome after chemotherapy for malignant lymphoma].
  • A 62-year-old woman was diagnosed as having malignant lymphoma, diffuse large B-cell type.
  • Four months later, the myelodysplastic syndrome of RA (refractory anemia) with pancytopenia developed and rapidly progressed to acute myelogenous leukemia (AML-M6) in 4 months.
  • Cytogenetic analysis for the bone marrow specimens of both periods of MDS and AML-M6 revealed complex karyotypic abnormalities involving chromosome 5, 7, 11q23 and 20q11.2.
  • The patient was died from progression of leukemia and pneumonia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosome Aberrations. Leukemia, Erythroblastic, Acute / etiology. Leukemia, Erythroblastic, Acute / genetics. Myelodysplastic Syndromes / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 5. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Ifosfamide / administration & dosage. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Middle Aged. Mitoguazone / administration & dosage. Prednisolone / administration & dosage. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives. Vincristine / administration & dosage


12. Ramkumar B, Chadha MK, Barcos M, Sait SN, Heyman MR, Baer MR: Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis. Cancer Genet Cytogenet; 2008 Apr 15;182(2):126-9
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  • [Title] Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis.
  • Mitoxantrone is a DNA-topoisomerase 2 inhibitor used as a single agent for treatment of relapsing-remitting or progressive multiple sclerosis (MS).
  • We present here two patients treated with mitoxantrone for MS who subsequently developed acute promyelocytic leukemia (APL).
  • Topoisomerase 2 inhibitors are associated with therapy-related acute myeloid leukemia (t-AML) with 11q23 abnormalities, but therapy-related APL (t-APL) is less common, and documentation of nine cases of t-APL after mitoxantrone therapy for MS suggests a specific association.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / chemically induced. Mitoxantrone / adverse effects. Multiple Sclerosis / drug therapy

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  • [ErratumIn] Cancer Genet Cytogenet. 2008 Oct 15;186(2):130
  • (PMID = 18406875.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone
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13. Taylor HJ, Gravett P, Plowman PN: Secondary acute myeloblastic leukaemia (AML) (expressing 11q23 mutation) occurring 11 months after chemotherapy/radiotherapy for paediatric non-Hodgkin lymphoma (NHL). Clin Oncol (R Coll Radiol); 2000;12(2):112-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute myeloblastic leukaemia (AML) (expressing 11q23 mutation) occurring 11 months after chemotherapy/radiotherapy for paediatric non-Hodgkin lymphoma (NHL).
  • The occurrence of 11q23 cytogenetic abnormalities in drug-induced acute myeloid leukaemia (AML) is now well recognized.
  • We here describe the case history of a 15-year-old child who presented with Stage III B-cell non-Hodgkin's lymphoma (NHL) and was treated with anthracyclines, alkylating agents and low-dose mediastinal radiotherapy.
  • She developed an 11q23 mutation-related secondary AML at 11 months after therapy (15 months after her first exposure to drugs; 12 months after the first radiotherapy exposure), possibly the earliest yet reported in a paediatric patient.
  • We discuss this newly recognized early form of refractory, secondary AML and its relationship to chemoradiotherapy.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Lymphoma, Large B-Cell, Diffuse / radiotherapy. Mediastinal Neoplasms / radiotherapy


14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • The advice is to treat patients early after diagnosis and preferably before progression as these patients have the highest chance of a favorable outcome.
  • [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


15. Dann EJ, Rowe JM: Biology and therapy of secondary leukaemias. Best Pract Res Clin Haematol; 2001 Mar;14(1):119-37
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  • Secondary leukaemias are common, accounting for more than 40% of all patients with acute myeloid leukaemia (AML) or myelodysplastic syndrome (MDS).
  • The specific cytogenetic abnormalities common to MDS, alkylating-agent-related AML and poor-prognosis AML (3q-, -5, 5q-, -7, 7q-, +8, +9, 11q-, 12p-, -18, -19,20q-, +21, t(1;7), t(2;11)), probably reflect a common pathogenesis distinct from that of other de novo AMLs, although the pathogenetic pathway has yet to be elucidated.
  • Typically, these patients are either elderly or have a history of exposure to alkylating agents or environmental exposure 5-7 years prior to diagnosis.
  • Another distinct entity affects the mixed lineage leukaemia (MLL) gene located on 11q23.
  • Other therapy-related patients with t(8:21), inv16 or t(15;17) translocations should be treated as any other de novo AML with similar cytogenetics.
  • [MeSH-major] Leukemia / chemically induced. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / therapy

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  • [Copyright] Copyright 2001 Harcourt Publishers Ltd.
  • (PMID = 11355927.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 102
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16. Olney HJ, Mitelman F, Johansson B, Mrózek K, Berger R, Rowley JD: Unique balanced chromosome abnormalities in treatment-related myelodysplastic syndromes and acute myeloid leukemia: report from an international workshop. Genes Chromosomes Cancer; 2002 Apr;33(4):413-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unique balanced chromosome abnormalities in treatment-related myelodysplastic syndromes and acute myeloid leukemia: report from an international workshop.
  • A total of 123 balanced rearrangements, including 26 occurring as a sole anomaly, not known to be recurrent in myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML) prior to the Workshop, were ascertained retrospectively from 104 patients with treatment-related MDS/AML (t-MDS/t-AML).
  • Among 85 cases with secondary chromosomal abnormalities, -5, -7, del(5q), and del(7q) were observed in 76%, which is significantly higher (P < or = 0.007 for all pairwise comparisons) than the frequencies found in the Workshop subgroups of patients with previously known recurring aberrations.
  • Treatment exposure was significantly different (less topoisomerase II inhibitor exposure, more radiotherapy-only exposure) than for patients with 11q23 (P < 0.001 and P = 0.002, respectively) and 21q22 (P = 0.007 and P = 0.002, respectively) abnormalities.
  • The median time from the first toxic exposure to secondary disease, 59 months, was significantly longer (P < or = 0.016 for all significant pairwise comparisons) than the median latency of all other patients except those in the Rare subgroup, and the median survival time, 7 months, was significantly shorter than for patients in the 21q22, inv(16), and t(15;17) subgroups (P < or = 0.002 for all pairwise comparisons), but similar to patients in the 11q23 and Rare subgroups.
  • In contrast to known recurring abnormalities, significantly more patients (61%, all P < 0.001) presented with t-MDS, with over one-third of these patients progressing to t-AML.
  • Thus, this group of patients appears to be more similar to the typical t-MDS/t-AML patients, with complex karyotypes as well as chromosome 5 and 7 abnormalities, than to those with recurrent balanced rearrangements.
  • [MeSH-major] Chromosome Aberrations / chemically induced. Chromosome Aberrations / statistics & numerical data. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Chromosome Breakage / genetics. Female. Humans. Male. Middle Aged. Survival. Translocation, Genetic / drug effects. Translocation, Genetic / genetics


17. Block AW, Carroll AJ, Hagemeijer A, Michaux L, van Lom K, Olney HJ, Baer MR: Rare recurring balanced chromosome abnormalities in therapy-related myelodysplastic syndromes and acute leukemia: report from an international workshop. Genes Chromosomes Cancer; 2002 Apr;33(4):401-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare recurring balanced chromosome abnormalities in therapy-related myelodysplastic syndromes and acute leukemia: report from an international workshop.
  • Seventy-seven patients were identified with Rare recurring (excluding 11q23, 21q22, inv(16), and t(15;17)) chromosome abnormalities among 511 patients with treatment-related myelodysplastic syndromes and acute leukemia accepted from centers in the United States, Europe, and Japan.
  • Among 54 cases with secondary abnormalities, chromosome 5 and/or 7 abnormalities were observed in 59%.
  • The most frequent primary diseases were breast cancer (24 cases), Hodgkin disease (14 cases), non-Hodgkin lymphoma (10 cases), and de novo ALL (5 cases).
  • Thirty-seven patients received alkylating agents plus topoisomerase II inhibitors with or without radiation therapy.
  • The presenting diagnosis was t-AML in 47 cases, t-MDS in 23 cases (10 progressed to t-AML), and t-ALL in seven cases, five of whom had a t(9;22).
  • The median latency time from initiation of original therapy to therapy-related disease diagnosis was quite long (69 months), and the overall median survival from the date of therapy-related disease diagnosis was very short (7 months).
  • Comparison with previously reported cases showed increased karyotypic complexity and adult presentation of pediatric-associated chromosome abnormalities.
  • [MeSH-major] Chromosome Aberrations / chemically induced. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasm Recurrence, Local / chemically induced
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Translocation, Genetic / drug effects. Translocation, Genetic / genetics


18. Sato Y, Izumi T, Kanamori H, Davis EM, Miura Y, Larson RA, Le Beau MM, Ozawa K, Rowley JD: t(1;3)(p36;p21) is a recurring therapy-related translocation. Genes Chromosomes Cancer; 2002 Jun;34(2):186-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chromosome bands 1p36 and 3p21 are known to be recurring breakpoints in therapy-related (t-) leukemia.
  • We identified a recurring translocation, t(1;3)(p36;p21), in eight patients with various hematologic malignancies: three patients with ALL, one with chronic myelogenous leukemia (CML) in accelerated phase (AP), two with MDS, and two with AML(M3).
  • Five of the eight patients had a history of chemotherapy, including alkylating agents in three, before the translocation was detected.
  • The karyotypes of the patients were complex, including -7 and structural abnormalities of 5q, 6q, 7q, 9p, and 11q23.
  • The results of the present study suggest that t(1;3)(p36;p21) in hematologic diseases is associated with prior exposure to mutagens, including alkylating agents.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 3 / genetics. Translocation, Genetic / drug effects. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Child. Chromosome Breakage / genetics. Chromosome Mapping / methods. Female. Humans. In Situ Hybridization, Fluorescence / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / chemically induced. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Promyelocytic, Acute / chemically induced. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Recurrence

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 11979552.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA42557
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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