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1. Büchner T, Berdel WE, Schoch C, Haferlach T, Serve HL, Kienast J, Schnittger S, Kern W, Tchinda J, Reichle A, Lengfelder E, Staib P, Ludwig WD, Aul C, Eimermacher H, Balleisen L, Sauerland MC, Heinecke A, Wörmann B, Hiddemann W: Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia. J Clin Oncol; 2006 Jun 1;24(16):2480-9
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  • [Title] Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia.
  • PURPOSE: Intensification by high-dose cytarabine in postremission or induction therapy and prolonged maintenance are established strategies to improve the outcome in patients with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: A total of 1,770 patients (age 16 to 85 years) with de novo or secondary AML or high-risk myelodysplastic syndrome (MDS) were randomly assigned upfront for induction therapy containing one course with standard dose and one course with high-dose cytarabine, or two courses with high-dose cytarabine, and in the same step received postremission prolonged maintenance or busulfan/cyclophosphamide chemotherapy with autologous stem-cell transplantation.
  • There was no significant difference in any prognostic subgroup according to secondary AML/MDS, cytogenetics, WBC, lactate dehydrogenase, and early blast clearance.
  • CONCLUSION: The regimen of one course with standard-dose cytarabine and one course with high-dose cytarabine for induction, and prolonged maintenance for postremission chemotherapy in patients with AML is not improved by additional escalation in cytotoxic treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Drug Administration Schedule. Female. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Mitoxantrone / administration & dosage. Multivariate Analysis. Prognosis. Prospective Studies. Remission Induction. Risk Factors. Transplantation, Autologous. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2006 Dec 1;24(34):5471-2; author reply 5472-3 [17135654.001]
  • [ErratumIn] J Clin Oncol. 2011 Jul 1;29(19):2739
  • (PMID = 16735702.001).
  • [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; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 1.1.1.27 / L-Lactate Dehydrogenase
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2. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • Moreover, the serial application of high resolution genomic array analysis at different disease stages allowed the description of cryptic abnormalities and the demonstration of their enrichment in the AML phase.
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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3. Szotkowski T, Rohon P, Zapletalova L, Sicova K, Hubacek J, Indrak K: Secondary acute myeloid leukemia - a single center experience. Neoplasma; 2010;57(2):170-8
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  • [Title] Secondary acute myeloid leukemia - a single center experience.
  • Secondary acute myeloid leukemia (sAML) may arise from the previous clonal disorder of hematopoiesis, usually from myelodysplastic syndrome (MDS) or from chronic myeloproliferative neoplasia (cMPN) or after exposure to a leukemogenic agent (previous chemotherapy or radiotherapy, some immunosuppressive drugs or environmental leukemogenic agents).
  • Secondary origin of AML is associated with unfavorable prognosis and it is not considered to be conventionally curable (with the exception of secondary acute promyelocytic leukemia).
  • Over that period of time, a total 574 patients with AML were diagnosed.
  • Of those, 430 patients were diagnosed as having primary AML; in 86 patients, sAML transformed from myelodysplastic syndrome and 58 patients were followed or treated for various malignancies or were treated with potentially leukemogenic agents because of non-malignant disorders.
  • Patients with secondary AML are older and less commonly treated with curative intention than those with primary AML.
  • With the exception of secondary acute promyelocytic leukemia, the prognosis of which does not differ from very good prognosis of the primary forms, secondary AML is not considered a conventionally curable disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Neoplasm Recurrence, Local / etiology. Neoplasms, Second Primary / etiology


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4. Kröger N, Shimoni A, Zabelina T, Schieder H, Panse J, Ayuk F, Wolschke C, Renges H, Dahlke J, Atanackovic D, Nagler A, Zander A: Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS). Bone Marrow Transplant; 2006 Feb;37(4):339-44
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  • [Title] Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS).
  • We investigated a dose-reduced conditioning regimen consisting of treosulfan and fludarabine followed by allogeneic stem cell transplantation (SCT) in 26 patients with secondary AML or MDS.
  • Acute graft-versus-host disease (GvHD) grade II-IV was seen in 23% and severe grade III GvHD in 12% of the patients.
  • No patients experienced grade IV acute GvHD.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Disease-Free Survival. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. HLA Antigens / analysis. Humans. Male. Middle Aged. Prospective Studies. Recurrence. Siblings. Survival Rate. Transplantation, Homologous. Treatment Outcome


5. Roche-Lestienne C, Deluche L, Corm S, Tigaud I, Joha S, Philippe N, Geffroy S, Laï JL, Nicolini FE, Preudhomme C, Fi-LMC group: RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood; 2008 Apr 1;111(7):3735-41
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  • [Title] RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.
  • Acquired molecular abnormalities (mutations or chromosomal translocations) of the RUNX1 transcription factor gene are frequent in acute myeloblastic leukemias (AMLs) and in therapy-related myelodysplastic syndromes, but rarely in acute lymphoblastic leukemias (ALLs) and chronic myelogenous leukemias (CMLs).
  • Among 18 BCR-ABL+ leukemias presenting acquired trisomy of chromosome 21, we report a high frequency (33%) of recurrent point mutations (4 in myeloid blast crisis [BC] CML and one in chronic phase CML) within the DNA-binding region of RUNX1.
  • In addition, we also report a high frequency of cryptic chromosomal RUNX1 translocation to a novel recently described gene partner, PRDM16 on chromosome 1p36, for 3 (21.4%) of 14 investigated patients: 2 myeloid BC CMLs and, for the first time, 1 therapy-related BCR-ABL+ ALL.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / genetics. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Transcription Factors / genetics. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Benzamides. Chromosomes, Human. Chronic Disease. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / mortality. Phenotype. Point Mutation. Retrospective Studies. Survival Rate. Translocation, Genetic / drug effects. Translocation, Genetic / genetics

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  • (PMID = 18202228.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / PRDM16 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RUNX1 protein, human; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [General-notes] NLM/ Investigator list not found.
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6. Kovitz C, Kantarjian H, Garcia-Manero G, Abruzzo LV, Cortes J: Myelodysplastic syndromes and acute leukemia developing after imatinib mesylate therapy for chronic myeloid leukemia. Blood; 2006 Oct 15;108(8):2811-3
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  • [Title] Myelodysplastic syndromes and acute leukemia developing after imatinib mesylate therapy for chronic myeloid leukemia.
  • During therapy with imatinib, some patients with chronic myeloid leukemia (CML) develop chromosomal abnormalities in Philadelphia chromosome (Ph)-negative cells.
  • Although some reports have suggested that the abnormalities might be associated with secondary myelodysplastic syndrome (MDS), the diagnosis has not always been established using standard criteria.
  • One of them developed acute myelogenous leukemia (AML) and the other 2 developed high-risk MDS that rapidly transformed to AML.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / etiology. Piperazines / adverse effects. Pyrimidines / adverse effects
  • [MeSH-minor] Benzamides. Chromosome Aberrations. Female. Humans. Imatinib Mesylate. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Male. Middle Aged. Risk Factors


7. Han JY, Theil KS: The Philadelphia chromosome as a secondary abnormality in inv(3)(q21q26) acute myeloid leukemia at diagnosis: confirmation of p190 BCR-ABL mRNA by real-time quantitative polymerase chain reaction. Cancer Genet Cytogenet; 2006 Feb;165(1):70-4
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  • [Title] The Philadelphia chromosome as a secondary abnormality in inv(3)(q21q26) acute myeloid leukemia at diagnosis: confirmation of p190 BCR-ABL mRNA by real-time quantitative polymerase chain reaction.
  • The Philadelphia chromosome (Ph) as a secondary cytogenetic abnormality is a rare event.
  • It is observed mostly as an additional, late-appearing cytogenetic change during the evolution of acute leukemia and its presentation as a secondary change at the onset of disease is much rarer.
  • We describe here a patient with acute myelogenous leukemia (AML) who had Ph as a secondary chromosome abnormality at diagnosis.
  • To our knowledge, the minor BCR-ABL fusion gene involving a secondary Ph superimposed on inv(3) and monosomy 7 has not been reported in AML at diagnosis.
  • Along with the identification of more cases, it will be possible to understand the exact role of this secondary Ph in a multistep leukemogenesis.
  • [MeSH-major] Chromosome Aberrations. Chromosome Inversion. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Leukemia, Myeloid / genetics. Philadelphia Chromosome. RNA, Messenger / genetics
  • [MeSH-minor] Acute Disease. Aged. Bone Marrow Cells / pathology. Chromosome Mapping. Humans. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 16490599.001).
  • [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 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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8. Szotkowski T, Muzik J, Voglova J, Koza V, Maaloufova J, Kozak T, Jarosova M, Michalova K, Zak P, Steinerova K, Vydra J, Lanska M, Katrincsakova B, Sicova K, Pavlik T, Dusek L, Indrak K: Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic. Neoplasma; 2010;57(6):578-89
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  • [Title] Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic.
  • Acute myeloid leukemia (AML) is a severe condition with a high mortality.
  • The study represents a detailed analysis of the role of these factors and treatment outcomes based on a long-term follow-up of patients treated in 5 hematology intensive care centers in the Czech Republic.The studied group comprised 1,188 patients with de novo AML and 328 patients with secondary AML.
  • Curatively treated patients achieved fewer complete remissions and relapsed more often than those with de novo AML.
  • Patients with secondary AML had lower rates of allogeneic transplantation as part of consolidation therapy and a significantly shorter median overall survival.
  • However, the treatment outcome of de novo AML patients is not satisfactory, the only exception being those with acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality


9. Chau M, Christensen JL, Ajami AM, Capizzi RL: Amonafide, a topoisomerase II inhibitor, is unaffected by P-glycoprotein-mediated efflux. Leuk Res; 2008 Mar;32(3):465-73
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  • Over-expression of P-glycoprotein (Pgp+) has been related to resistance to classical Topo II inhibitors used in the treatment of AML and is common in patients with poor-prognosis, such as those with secondary AML (sAML).
  • Since clinical trials with amonafide, a unique ATP-independent Topo II inhibitor, in combination with cytarabine, have shown significant efficacy for remission induction in patients with sAML, we compared the cytotoxic effect of amonafide (amonafide l-malate, Xanafide) to the classical Topo II inhibitors (daunorubicin, doxorubicin, idarubicin, etoposide, and mitoxantrone) in K562 leukemia cells and in the MDR subline, K562/DOX.
  • Pgp expression was found to be approximately 6.5-fold greater in K562/DOX and causes the rapid efflux of these drugs from the leukemia cell.
  • A similar result was also observed in murine P388 and P388/ADR leukemia cells.
  • These observations suggest that amonafide is a promising therapeutic candidate directed toward bypassing this common mechanism of drug resistance encountered in the treatment of patients with AML, and possibly in other resistant hematological malignancies as well.

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  • (PMID = 17826829.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Imides; 0 / Isoquinolines; 0 / Naphthalimides; 0 / P-Glycoprotein; 0 / Topoisomerase II Inhibitors; 1Q8D39N37L / amonafide
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10. Takahashi W, Arai Y, Tadokoro J, Takeuchi K, Yamagata T, Mitani K: [Disappearance of a Philadelphia chromosome-positive clone and appearance of a -negative clone following treatment with imatinib mesylate in acute myelomonocytic leukemia]. Rinsho Ketsueki; 2006 Feb;47(2):111-4
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  • [Title] [Disappearance of a Philadelphia chromosome-positive clone and appearance of a -negative clone following treatment with imatinib mesylate in acute myelomonocytic leukemia].
  • A 63-year-old female was diagnosed as having Philadelphia chromosome-positive acute myelomonocytic leukemia in June 2002.
  • The transient suppression of the Philadelphia chromosome-positive clone may have brought about amplification of the Philadelphia chromosome-negative cells after the secondary imatinib treatment.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative. Leukemia, Myelomonocytic, Acute / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 16529013.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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11. Raaijmakers MH, Mukherjee S, Guo S, Zhang S, Kobayashi T, Schoonmaker JA, Ebert BL, Al-Shahrour F, Hasserjian RP, Scadden EO, Aung Z, Matza M, Merkenschlager M, Lin C, Rommens JM, Scadden DT: Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia. Nature; 2010 Apr 08;464(7290):852-7
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  • [Title] Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia.
  • Myelodysplasia resulted and acute myelogenous leukaemia emerged that had acquired several genetic abnormalities while having intact Dicer1.
  • Furthermore, primary stromal dysfunction can result in secondary neoplastic disease, supporting the concept of niche-induced oncogenesis.
  • [MeSH-major] Bone and Bones / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology. Stem Cells / pathology
  • [MeSH-minor] Animals. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Female. Gene Deletion. Hematopoiesis / genetics. Male. Mesoderm / cytology. Mice. Osteoblasts / metabolism. Osteoblasts / pathology. Phenotype. Proteins / genetics. Proteins / metabolism. Ribonuclease III / deficiency. Ribonuclease III / genetics. Ribonuclease III / metabolism. Sarcoma, Myeloid / genetics. Sarcoma, Myeloid / metabolism. Sarcoma, Myeloid / pathology. Stem Cell Niche / metabolism. Stem Cell Niche / pathology. Stromal Cells / metabolism. Stromal Cells / pathology


12. Tavil B, Cetin M, Tuncer M: CD34/CD117 positivity in assessment of prognosis in children with myelodysplastic syndrome. Leuk Res; 2006 Feb;30(2):222-4
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  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal stem cell disorders that are characterized by morphology identifying dysplastic changes in one or more cell lineages, peripheral blood cytopenias and a propensity to evolve into secondary acute myeloid leukemia (AML).
  • CD34 is commonly expressed in all types of childhood leukemias, whereas CD117 is a reliable and specific marker to detect leukemia cells committed to myeloid lineage.
  • Co-expression of CD34/CD117 may strongly suggest the diagnosis of AML (Rytting ME.
  • May; Uçkan D, Hiçsönmez G, Yetgin S, Gürgey A, Cetin M, Karaağaoğlu E, et al. CD34/CD117 co-expression in childhood acute leukemia.
  • Leukemia Res 2000;24:201-6.).
  • We describe the case of a 22 month-old-girl with MDS and Down syndrome who was presented with severe anemia and thrombocytosis at diagnosis, transformed into AML-M7.
  • As the disease progressed, CD34/117 co-existence was increased and MDS transformed into AML.
  • [MeSH-minor] Bone Marrow Examination. Female. Humans. Infant. Leukemia, Myeloid, Acute / etiology. Prognosis


13. McGee SM, Thompson CA, Granberg CF, Hutcheson JC, Vandersteen DR, Reinberg Y, Wolpert JJ: Acute renal infarction due to fungal vascular invasion in disseminated candidiasis. Urology; 2009 Mar;73(3):535-7
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  • [Title] Acute renal infarction due to fungal vascular invasion in disseminated candidiasis.
  • Although renal involvement can be a sequela of disseminated candidiasis, acute renal infarction secondary to Candida invading the renal vasculature has not previously been reported.
  • Our patient, who was being treated for acute myelogenous leukemia, developed complete obstruction of the right renal vessels during the course of 36 hours as documented by serial renal ultrasound scans with Doppler investigation of the vasculature.
  • Histopathologic examination of the nephrectomy specimen revealed complete infarction of the kidney secondary to Candida spp. infiltrating the parenchyma and occluding the hilar vessels.
  • [MeSH-minor] Acute Disease. Child. Female. Humans

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  • (PMID = 18799205.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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14. Creutzig U, Diekamp S, Zimmermann M, Reinhardt D: Longitudinal evaluation of early and late anthracycline cardiotoxicity in children with AML. Pediatr Blood Cancer; 2007 Jun 15;48(7):651-62
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  • [Title] Longitudinal evaluation of early and late anthracycline cardiotoxicity in children with AML.
  • BACKGROUND: Anthracyclines are effective antineoplastic drugs in acute myelogenous leukemia (AML).
  • PROCEDURE: To evaluate anthracycline-associated cardiomyopathy in pediatric AML-patients, the incidence of early and late (>1 year after intensive AML chemotherapy) clinical and subclinical cardiotoxicity was analyzed out of a total of 1,207 patients <18 years treated between 1993 and 2003 in trials AML-BFM93/98: 1,010 protocol patients with de novo AML, 121 with Down syndrome (DS)-AML, and 76 with secondary AML.
  • RESULTS: Thirty-eight patients (4.3%), including 3 DS-AML and 1 secondary AML, suffered from early cardiomyopathy.
  • After 5 years, four patients showed temporarily or persistently a reduced shortening fraction, which led to death in one DS-AML patient.
  • Late clinical cardiomyopathy mainly affected patients with a second anthracycline therapy (secondary malignancy) and those with early cardiotoxicity.
  • CONCLUSION: In spite of a highly intensive and effective treatment, the frequency of anthracycline-associated cardiomyopathy was low in the AML-BFM studies.
  • [MeSH-major] Anthracyclines / adverse effects. Heart / drug effects. Heart Diseases / chemically induced. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug-Related Side Effects and Adverse Reactions. Echocardiography / methods. Female. Follow-Up Studies. Humans. Infant. Longitudinal Studies. Male. Pilot Projects. Risk Factors. Survivors. Time. Treatment Outcome

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2007 Jun 15;48(7):649-50 [17318875.001]
  • (PMID = 17183582.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines
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15. Giles F, Rizzieri D, Karp J, Vey N, Ravandi F, Faderl S, Khan KD, Verhoef G, Wijermans P, Advani A, Roboz G, Kantarjian H, Bilgrami SF, Ferrant A, Daenen SM, Karsten V, Cahill A, Albitar M, Mufti G, O'Brien S: Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia. J Clin Oncol; 2007 Jan 1;25(1):25-31
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  • [Title] Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia.
  • A multicenter phase II study of cloretazine was conducted in patients 60 years of age or older with previously untreated acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS).
  • Patients were stratified by age, performance score, cytogenetic risk category, type of AML, and comorbidity.
  • Response rates in 44 de novo AML patients, 45 secondary AML patients, and 15 high-risk MDS patients were 50%, 11%, and 40%, respectively.
  • CONCLUSION: Cloretazine has significant activity and modest extramedullary toxicity in elderly patients with AML or high-risk MDS.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Hydrazines / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Sulfonamides / therapeutic use


16. Récher C, Beyne-Rauzy O, Demur C, Chicanne G, Dos Santos C, Mas VM, Benzaquen D, Laurent G, Huguet F, Payrastre B: Antileukemic activity of rapamycin in acute myeloid leukemia. Blood; 2005 Mar 15;105(6):2527-34
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  • [Title] Antileukemic activity of rapamycin in acute myeloid leukemia.
  • In this study, we show that mTOR inhibition by rapamycin strongly inhibits the growth of the most immature acute myeloid leukemia (AML) cell lines through blockade in G0/G1 phase of the cell cycle.
  • Accordingly, 2 downstream effectors of mTOR, 4E-BP1 and p70S6K, are phosphorylated in a rapamycin-sensitive manner in a series of 23 AML cases.
  • Interestingly, the mTOR inhibitor markedly impairs the clonogenic properties of fresh AML cells while sparing normal hematopoietic progenitors.
  • Moreover, rapamycin induces significant clinical responses in 4 of 9 patients with either refractory/relapsed de novo AML or secondary AML.
  • Overall, our data strongly suggest that mTOR is aberrantly regulated in most AML cells and that rapamycin and analogs, by targeting the clonogenic compartment of the leukemic clone, may be used as new compounds in AML therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. G0 Phase / drug effects. G1 Phase / drug effects. Leukemia, Myeloid, Acute / metabolism. Protein Kinases / metabolism. Sirolimus / pharmacology


17. Correll PH, Paulson RF, Wei X: Molecular regulation of receptor tyrosine kinases in hematopoietic malignancies. Gene; 2006 Jun 7;374:26-38
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  • Most notably, mutations and chromosomal translocations affecting regulation of tyrosine kinase activity in the Kit receptor, the Flt3 receptor, and the PDGFbeta/FGF1 receptors have been demonstrated in mast cell leukemia, acute myeloid leukemia (AML), and chronic myelogenous leukemias (CML), respectively.
  • In addition, critical but non-overlapping roles for the Ron and Kit receptor tyrosine kinases in the progression of animal models of erythroleukemia have been demonstrated [Persons, D., Paulson, R., Loyd, M., Herley, M., Bodner, S., Bernstein, A., Correll, P. and Ney, P., 1999.
  • The various classes of RTKs implicated in the progression of leukemia have been recently reviewed [Reilly, J., 2003.
  • [MeSH-major] Leukemia / pathology. Leukemia, Experimental / pathology. Receptor Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Binding Sites. Dimerization. Humans. Models, Molecular. Mutation. Phosphorylation. Protein Binding. Protein Conformation. Protein Structure, Secondary. Protein Structure, Tertiary. Translocation, Genetic. Tyrosine / chemistry

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  • (PMID = 16524673.001).
  • [ISSN] 0378-1119
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 42HK56048U / Tyrosine; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 117
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18. Boehm A, Sperr WR, Leitner G, Worel N, Oehler L, Jaeger E, Mitterbauer M, Haas OA, Valent P, Kalhs P, Rabitsch W: Comorbidity predicts survival in myelodysplastic syndromes or secondary acute myeloid leukaemia after allogeneic stem cell transplantation. Eur J Clin Invest; 2008 Dec;38(12):945-52
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  • [Title] Comorbidity predicts survival in myelodysplastic syndromes or secondary acute myeloid leukaemia after allogeneic stem cell transplantation.
  • PATIENTS AND METHODS: We examined the overall survival (OS) and underlying risk factors in 45 adult patients with MDS (n = 38), chronic myelomonocytic leukaemia (n = 1), or secondary acute myeloid leukaemia (AML) arising from MDS (n = 6), who underwent allogeneic SCT at our Institution.
  • CONCLUSIONS: Based on these data and similar published data we recommend selecting patients with MDS or secondary AML for SCT according to the presence of comorbidities.
  • [MeSH-major] Disease-Free Survival. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myelomonocytic, Chronic / mortality. Neoplasms, Second Primary / mortality


19. Devany M, Kappes F, Chen KM, Markovitz DM, Matsuo H: Solution NMR structure of the N-terminal domain of the human DEK protein. Protein Sci; 2008 Feb;17(2):205-15
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  • The human DEK protein has a long-standing association with carcinogenesis since the DEK gene was originally identified in the t(6:9) chromosomal translocation in a subtype of patients with acute myelogenous leukemia (AML).
  • [MeSH-major] Chromosomal Proteins, Non-Histone / chemistry. Oncogene Proteins / chemistry
  • [MeSH-minor] Amino Acid Motifs. Amino Acid Sequence. DNA / metabolism. DNA-Binding Proteins / chemistry. DNA-Binding Proteins / metabolism. Humans. Molecular Sequence Data. Nuclear Magnetic Resonance, Biomolecular. Protein Conformation. Protein Folding. Protein Structure, Secondary. Protein Structure, Tertiary

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  • (PMID = 18227428.001).
  • [ISSN] 0961-8368
  • [Journal-full-title] Protein science : a publication of the Protein Society
  • [ISO-abbreviation] Protein Sci.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2JX3
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Dek protein, human; 0 / Oncogene Proteins; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2222715
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20. Schmid C, Schleuning M, Hentrich M, Markl GE, Gerbitz A, Tischer J, Ledderose G, Oruzio D, Hiddemann W, Kolb HJ: High antileukemic efficacy of an intermediate intensity conditioning regimen for allogeneic stem cell transplantation in patients with high-risk acute myeloid leukemia in first complete remission. Bone Marrow Transplant; 2008 Apr;41(8):721-7
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  • [Title] High antileukemic efficacy of an intermediate intensity conditioning regimen for allogeneic stem cell transplantation in patients with high-risk acute myeloid leukemia in first complete remission.
  • The goal of this analysis was to define the role of the moderate-intensity fludarabin Ara-C amsacrin (FLAMSA)-reduced intensity conditioning (RIC) regimen for patients with high-risk AML undergoing allogeneic SCT (alloSCT) in first CR1.
  • High-risk was defined by (1) AML secondary to MDS or radio/chemotherapy, (2) unfavorable cytogenetics or (3) delayed response to induction chemotherapy.
  • A total of 23 of 44 AML patients referred to the University of Munich for alloSCT in CR1 between 1999 and 2006 fulfilled these criteria and received FLAMSA chemotherapy, followed by RIC (4 Gy TBI/cyclophosphamide/ATG) for alloSCT.
  • Four-year overall and leukemia-free survival was 72.7% (median follow-up among survivors: 35 months).
  • The results of this high-risk cohort were compared to the outcome of 21 consecutive standard-risk patients <55 years, who had received standard, myeloablative sibling SCT in CR1 AML within the same center and time period.
  • In conclusion, the FLAMSA-RIC regimen produces long-term remission in a high proportion of patients with high-risk AML transplanted in CR1.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods


21. Ferrara F, D'Arco AM, De Simone M, Mele G, Califano C, Pocali B, Danise P, Palmieri S: Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia. Haematologica; 2005 Jun;90(6):776-84
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  • [Title] Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: A phase II study was conducted to investigate the effects of a therapeutic program based on the combination of fludarabine and cytarabine (ARA-C) administered as a sequential continuous infusion in untreated elderly patients with acute myeloid leukemia (AML).
  • DESIGN AND METHODS: Sixty-three patients with non-M3 AML, median age 69 years (range 61-81), were accrued.
  • Twenty-four patients (38%) had AML secondary to myelodysplastic syndrome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Vidarabine / analogs & derivatives

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  • (PMID = 15951290.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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22. Rizzieri DA, O'Brien JA, Broadwater G, Decastro CM, Dev P, Diehl L, Beaven A, Lagoo A, Gockerman JP, Chao NJ, Moore JO: Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia. Cancer; 2009 Jul 1;115(13):2922-9
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  • [Title] Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia.
  • BACKGROUND: Response and survival in 96 patients with secondary acute myeloid leukemia (sAML) who received aggressive induction chemotherapy was reviewed.
  • Patients with AML after previous chemotherapy or radiation therapy had a higher morphologic remission rate compared with those arising from myelodysplastic syndrome or myeloproliferative disease (82% vs 62%; P = .027).
  • In this population of patients who received aggressive chemotherapy, Charlson comorbidity index or a higher number of factors recognized as high risk in leukemia patients did not affect the chance of OS, DFS, and EFS, although having more recognized leukemia risk factors was related to a lower chance of surviving 1 year.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / drug therapy

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  • (PMID = 19452542.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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23. Fianchi L, Pagano L, Leoni F, Storti S, Voso MT, Valentini CG, Rutella S, Scardocci A, Caira M, Gianfaldoni G, Leone G: Gemtuzumab ozogamicin, cytosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia. Ann Oncol; 2008 Jan;19(1):128-34
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  • [Title] Gemtuzumab ozogamicin, cytosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia.
  • BACKGROUND: Gemtuzumab ozogamicin (GO) is effective as single agent in the treatment of acute myeloid leukemia (AML).
  • We evaluated efficacy and safety of a chemotherapy including growth factors, cytarabine, and GO (G-AraMy) in the treatment of poor-prognosis AML in elderly patients.
  • PATIENTS AND METHODS: In three Italian hematology departments from September 2003 to September 2006, 53 elderly patients [median age 69 years (range 65-77)] with untreated or primary refractory/relapsed AML were enrolled on the combination G-AraMy administered according to two consecutive schedules (G-AraMy1 and G-AraMy2), with intensified consolidation in the second.
  • Twenty-three of 53 patients had a secondary acute myeloid leukemia (sAML).
  • No differences for response rate and toxicity profile were observed between untreated and primary resistant/relapsed patients, de novo AML and sAML, and in the two treatment trials.
  • CONCLUSIONS: G-AraMy therapy may be considered an useful treatment approach for poor-risk elderly AML patients, with a complete remission rate comparable to literature data with reduced side-effects, also in a poor-prognosis population.

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  • (PMID = 17906298.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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24. Varet B, Ifrah N: [Criteria for suspecting a myelodysplastic syndrome]. Rev Prat; 2010 Dec 20;60(10):1404-7
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  • The myelodysplastic syndromes are a group of heterogeneous acquired and clonal disorders that are characterized by the intramedullar, abnormal death of myeloid progenitors leading to peripheral variable cytopenias.
  • It is predictive for the risk of transformation in secondary acute myeloid leukemia.

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  • (PMID = 21425539.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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25. Cole M, Strair R: Acute myelogenous leukemia and myelodysplasia secondary to breast cancer treatment: case studies and literature review. Am J Med Sci; 2010 Jan;339(1):36-40
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  • [Title] Acute myelogenous leukemia and myelodysplasia secondary to breast cancer treatment: case studies and literature review.
  • BACKGROUND AND PURPOSE: Chemotherapy and radiation therapy for breast cancer are known to increase the risk of developing a myelodysplastic syndrome (MDS) and/or acute myelogenous leukemia (AML).
  • Radiation therapy adds to the risk, and there is speculation that granulocyte colony-stimulating factor (G-CSF) may also predispose to leukemia.
  • The purpose of this systemic review is to bring to the attention of family physicians the unintended consequence of leukemia secondary to aggressively treated breast cancer.
  • METHODS: The medical records of several patients from Robert Wood Johnson University Hospital, with previously treated breast cancer admitted for therapy for AML or myelodysplasia, were reviewed.
  • RESULTS: Cases of patients whose AML was likely secondary to their treatment for breast cancer were used to illustrate the role of chemotherapy, radiation therapy, and perhaps G-CSF in the development of leukemia.
  • CONCLUSIONS: Chemotherapy and radiation therapy administered for breast cancer predispose patients to the development of MDS or AML.
  • We hypothesize that the breast cancer (BRCA) gene mutations might add to the risk and that primary care physicians must be aware of the long-term risks of cytotoxic therapy, including the development of MDS or AML.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / etiology


26. Anwar Iqbal M, Al-Omar HM, Owaidah T, Al-Humaidan H, Bhuiyan ZA, Sahovic E: del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality. Eur J Haematol; 2006 Sep;77(3):245-50
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  • [Title] del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.
  • OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary acute myeloid leukemia (AML) as part of complex karyotypes.
  • In this report, we present two young adult patients with de novo AML-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.
  • RESULTS: A diagnosis of AML-M2 was confirmed in both patients by morphological and immunophenotyping studies.
  • The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo AML with deletion 6p23.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Chromosomal Proteins, Non-Histone / genetics. Cytogenetics. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Oncogene Proteins / genetics. Oncogenes. Recurrence

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  • (PMID = 16856925.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins
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27. Kornblau SM, Minden MD, Rosen DB, Putta S, Cohen A, Covey T, Spellmeyer DC, Fantl WJ, Gayko U, Cesano A: Dynamic single-cell network profiles in acute myelogenous leukemia are associated with patient response to standard induction therapy. Clin Cancer Res; 2010 Jul 15;16(14):3721-33
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  • [Title] Dynamic single-cell network profiles in acute myelogenous leukemia are associated with patient response to standard induction therapy.
  • PURPOSE: Complete response to induction chemotherapy is observed in approximately 60% of patients with newly diagnosed non-M3 acute myelogenous leukemia (AML).
  • However, no methods exist to predict with high accuracy at the individual patient level the response to standard AML induction therapy.
  • EXPERIMENTAL DESIGN: We applied single-cell network profiling (SCNP) using flow cytometry, a tool that allows a comprehensive functional assessment of intracellular signaling pathways in heterogeneous tissues, to two training cohorts of AML samples (n = 34 and 88) to predict the likelihood of response to induction chemotherapy.
  • Results were independent of cytogenetics, FLT3 mutational status, and diagnosis of secondary AML.
  • SCNP provides information distinct from other known prognostic factors such as age, secondary AML, cytogenetics, and molecular alterations and is potentially combinable with the latter to improve clinical decision making.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism


28. Tam CS, Seymour JF, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Westerman D: Treatment-related myelodysplasia following fludarabine combination chemotherapy. Haematologica; 2006 Nov;91(11):1546-50
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  • Although myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML) are rare following fludarabine monotherapy, the risk of these diseases may potentially be increased when fludarabine is combined with cyclophosphamide or mitoxantrone due to synergistic effects on the inhibition of DNA repair.


29. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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  • [Title] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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30. Schwarz J, Pytlík R, Doubek M, Brychtová Y, Dulícek P, Campr V, Kren L, Penka M: Analysis of risk factors: the rationale of the guidelines of the Czech Hematological Society for diagnosis and treatment of chronic myeloproliferative disorders with thrombocythemia. Semin Thromb Hemost; 2006 Apr;32(3):231-45
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  • The histopathology-based nosological distinction provided by these classifications yields valuable information on prognosis (including the risks of transition into secondary acute myeloid leukemia and myelofibrosis).

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  • (PMID = 16673277.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Wadhwa PD, Fu P, Koc ON, Cooper BW, Fox RM, Creger RJ, Bajor DL, Bedi T, Laughlin MJ, Payne J, Gerson SL, Lazarus HM: High-dose carmustine, etoposide, and cisplatin for autologous stem cell transplantation with or without involved-field radiation for relapsed/refractory lymphoma: an effective regimen with low morbidity and mortality. Biol Blood Marrow Transplant; 2005 Jan;11(1):13-22
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  • Over a 10-year period (January 1993 to October 2002), 101 relapsed or refractory non-Hodgkin lymphoma patients were treated at our center with high-dose chemotherapy and autologous transplantation.
  • Thirty-two patients had indolent (low-grade), 42 had aggressive (intermediate-grade), and 27 had very aggressive (high-grade) non-Hodgkin lymphoma.
  • Two patients (2%) developed interstitial pneumonitis most likely secondary to high-dose BCNU.
  • Three cases (3%) of secondary acute myelogenous leukemia occurred.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Non-Hodgkin / therapy. Peripheral Blood Stem Cell Transplantation / methods

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  • (PMID = 15625540.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine
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32. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
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  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


33. Yin CC, Cortes J, Barkoh B, Hayes K, Kantarjian H, Jones D: t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy. Cancer; 2006 Apr 15;106(8):1730-8
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  • [Title] t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy.
  • BACKGROUND: The t(3;21)(q26;q22) translocation is associated with myeloid leukemias and results in a chimeric oncoprotein containing AML1/RUNX1 variably fused to EAP, MDS1, and/or EVI1.
  • RESULTS: In all 16 patients with chronic myeloproliferative disorders, including 14 with chronic myelogenous leukemia (CML), the occurrence of t(3;21) heralded myeloid blast transformation.
  • Among 10 cases of t(3;21)-associated acute myeloid leukemia, 8 were secondary tumors after chemotherapy for other neoplasms that had been treated with regimens including fludarabine and 5-fluorouracil in 3 patients each and etoposide in 2 patients.
  • The immunophenotype of the blasts in all 22 tested cases was similar, with uniform expression of myeloid markers and CD34 and variable expression of CD7 and CD9, but minimal morphological myeloid maturation.
  • Among patients with acute myeloid leukemia/myelodysplastic syndrome, 7 died of disease (at a median of 2 mos) and 2 had persistent leukemia with short follow-up.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 21 / drug effects. Chromosomes, Human, Pair 3 / drug effects. Hydroxyurea / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Lymphocyte Activation / drug effects. Myeloproliferative Disorders / drug therapy. Oncogene Proteins, Fusion / analysis. Translocation, Genetic / drug effects

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532439.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; X6Q56QN5QC / Hydroxyurea
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34. Ayash LJ, Ratanatharathorn V, Braun T, Silver SM, Reynolds CM, Uberti JP: Unrelated donor bone marrow transplantation using a chemotherapy-only preparative regimen for adults with high-risk acute myelogenous leukemia. Am J Hematol; 2007 Jan;82(1):6-14
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  • [Title] Unrelated donor bone marrow transplantation using a chemotherapy-only preparative regimen for adults with high-risk acute myelogenous leukemia.
  • Limited data are available for adults undergoing unrelated donor (URD) BMT for AML using chemotherapy-only preparative regimens.
  • Previous studies incorporated irradiation, included adults and children, and excluded secondary leukemia.
  • Herein we report long-term outcomes for adults with poor-prognostic AML receiving a novel regimen of busulfan (16 mg/kg), cytarabine (8,000 mg/m(2)), and cyclophosphamide (120 mg/kg) (BAC), followed by URD BMT.
  • Adverse features included unfavorable cytogenetics (49%), secondary AML (47%), leukemia at transplant (42%), and extramedullary disease (16%).
  • At time of BMT, 23 were in remission (12 CR1) while 22 had leukemia.
  • Acute and chronic GVHD rates were 44 and 67%, respectively.
  • Seventeen (38%) were disease-free 52 months post-BMT; 13 were leukemia-free (eight CR1) at transplant.
  • Secondary leukemia, cytogenetics, cell dose, and GVHD did not influence outcome.
  • In poor-risk AML, BAC provided cytoreduction comparable to reported TBI-containing regimens, when administered for URD BMT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy. Tissue Donors. Transplantation Conditioning
  • [MeSH-minor] Acute Disease. Adult. Chronic Disease. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Factor XIII / administration & dosage. Factor XIII / adverse effects. Female. Fibrinogen / administration & dosage. Fibrinogen / adverse effects. Follow-Up Studies. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Humans. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Thrombin / administration & dosage. Thrombin / adverse effects. Transplantation, Homologous


35. Gondek LP, Tiu R, O'Keefe CL, Sekeres MA, Theil KS, Maciejewski JP: Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML. Blood; 2008 Feb 1;111(3):1534-42
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  • [Title] Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML.
  • We have applied 250K single nucleotide polymorphisms (SNP) arrays (SNP-A) to study chromosomal lesions in samples from 174 patients (94 MDS, 33 secondary acute myeloid leukemia [sAML], and 47 myelodysplastic/myeloproliferative disease [MDS/MPD]) and 76 controls.

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  • (PMID = 17954704.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2214746
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36. Junghanss C, Waak M, Knopp A, Kleine HD, Kundt G, Leithäuser M, Hilgendorf I, Wolff D, Casper J, Freund M: Multivariate analyses of prognostic factors in acute myeloid leukemia: relevance of cytogenetic abnormalities and CD34 expression. Neoplasma; 2005;52(5):402-10
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  • [Title] Multivariate analyses of prognostic factors in acute myeloid leukemia: relevance of cytogenetic abnormalities and CD34 expression.
  • Identification of additional prognostic factors besides karyotype is important for the improvement of the risk adapted treatment strategies in acute myeloid leukemia (AML).
  • The aim of this study was to investigate whether other factors besides karyotype could be used as a prognostic tool in newly diagnosed AML.
  • Biological and disease related established and potential prognostic factors were retrospectively analysed in 124 consecutive AML patients treated between 1993 and 2002 at the University hospital Rostock (Germany).
  • In patients that received potential curative therapies LDH >or=2000 U/l, WBC >50 GPT/l, CD34 surface expression on the AML blasts, secondary AML, unfavorable karyotype and no allogeneic HSCT at some point of treatment course were associated with unfavorable prognosis.
  • However, in the multivariate risk factor analyses only unfavorable karyotype (p=0.012), CD34 positivity of AML blasts (p=0.046), no allogeneic HSCT (p=0.008) and first diagnosis after 1997 (p=0.025) were independent unfavourable prognostic factors.
  • In conclusion, karyotype and CD34 expression are independent prognostic markers in newly diagnosed AML.
  • Furthermore, receiving an allogeneic HSCT at some point of the treatment course seems to be of benefit for AML patients.
  • [MeSH-major] Antigens, CD34 / metabolism. Biomarkers, Tumor / analysis. Chromosome Aberrations. Leukemia, Myeloid / genetics. Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease / therapy. Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Flow Cytometry. Hematopoietic Stem Cell Transplantation. Humans. Karyotyping. Middle Aged. Multivariate Analysis. Palliative Care. Prognosis. Remission Induction. Retrospective Studies. Risk Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 16151585.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor
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37. Patel JK, Perez OA, Viera MH, Halem M, Berman B: Ecthyma gangrenosum caused by Escherichia coli bacteremia: a case report and review of the literature. Cutis; 2009 Nov;84(5):261-7
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  • We describe a 50-year-old man previously diagnosed with acute myelogenous leukemia (AML) who developed an E coli-colonized EG lesion secondary to E coli bacteremia.
  • This case represents the seventh of its kind in the literature and the first case in a patient with AML.
  • [MeSH-major] Bacteremia / complications. Bacteremia / microbiology. Ecthyma / microbiology. Escherichia coli. Escherichia coli Infections / complications. Gangrene / microbiology. Leukemia, Myeloid, Acute / complications


38. Dale DC: Advances in the treatment of neutropenia. Curr Opin Support Palliat Care; 2009 Sep;3(3):207-12
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  • Current guidelines recommend the prophylactic use of the myeloid growth factors for the first cycle of chemotherapy for patients with more than a 20% risk of febrile neutropenia.
  • Meta analysis from randomized trials shows that granulocyte colony-stimulating factor prophylaxis is associated with patients receiving more intensive chemotherapy, having better survival, but also having a higher risk of secondary acute myeloid leukemia.
  • SUMMARY: The myeloid growth factor granulocyte colony-stimulating factor has radically changed our approach to the prevention of febrile neutropenia.

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  • [Cites] Value Health. 2008 Mar-Apr;11(2):172-9 [18380630.001]
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  • (PMID = 19550332.001).
  • [ISSN] 1751-4266
  • [Journal-full-title] Current opinion in supportive and palliative care
  • [ISO-abbreviation] Curr Opin Support Palliat Care
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R24 AI049393; United States / NIAID NIH HHS / AI / R24 AI049393-09
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Number-of-references] 48
  • [Other-IDs] NLM/ NIHMS202938; NLM/ PMC3390973
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39. Willems L, Suarez F, Messas E, Baubion N, Decaudin D, Fourquet A, Ghez D, Delarue R, Hermine O, Buzyn A, Varet B, Rubio MT: [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer]. Bull Cancer; 2010 Feb;97(2):245-54
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  • [Title] [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer].
  • Secondary acute myeloid leukaemia (AML) occurring after breast cancer is a rare long-term complication of the chemo- and/or radiation therapy required to treat breast cancer.
  • The usually recognized curative option of these secondary AML includes courses of anthracycline-based chemotherapy followed by haematopoietic stem cell transplantation (HSCT).
  • Cardiac dysfunction during AML treatment of these patients previously treated with anthracyclines for breast cancer has not been reported to date.
  • We evaluated the evolution of cardiac function in seven patients treated with anthracyclines and/or autologous or allogeneic bone marrow transplantation for secondary AML occurring after breast cancer.
  • All of the patients who received a cumulative anthracycline dose above the cardiac toxicity threshold developed cardiac symptoms during AML chemotherapy courses.
  • Thus, the risk of severe cardiac dysfunction after treatment of secondary AML following breast cancer must be taken in account as part of the therapeutic strategy of those patients.
  • As discussed here, an accurate evaluation of risk factors, the use of sensitive detection tests and of cardioprotective drugs as well as that of non-cardiotoxic chemotherapy might decrease the occurrence and severity of this life-threatening complication.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Acute Disease. Adult. Chemotherapy, Adjuvant / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Heart Diseases / chemically induced. Heart Diseases / drug therapy. Heart Diseases / physiopathology. Humans. Middle Aged. Remission Induction. Stroke Volume / drug effects. Stroke Volume / physiology

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  • (PMID = 19819776.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; ZS7284E0ZP / Daunorubicin; FEC protocol
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40. Tangen JM, Fløisand Y, Foss-Abrahamsen J, Haukås E, Naess IA, Skjelbakken T: [Survival in adults with acute myelogenous leukemia]. Tidsskr Nor Laegeforen; 2008 May 15;128(10):1164-7
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  • [Title] [Survival in adults with acute myelogenous leukemia].
  • BACKGROUND: Acute myelogenous leukemia is the most common type of acute leukemia in adults.
  • MATERIAL AND METHODS: Survival data were retrieved from the Norwegian Registry for Acute Leukemias and Lymphoblastic Lymphomas for patients with acute myelogenous leukemia (aged from 16 to 60 years) who were registered in the period 1.1.2000-31.12.2005.
  • Patients with secondary acute myelogenous leukemia were classified as high-risk.
  • RESULTS AND INTERPRETATION: 4-year survival was 94.5% in acute promyelocytic leukemia, 77.7% in other low-risk acute myelogenous leukemia, 39.0% in standard risk patients and 29.1% in high-risk patients.
  • The increase is most probably due to an intensification of chemotherapy after remission and to the implementation of all-trans-retinoic acid in the treatment of promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Female. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / mortality. Male. Middle Aged. Neoplasm Recurrence, Local / mortality. Norway / epidemiology. Risk Factors. Survival Rate

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  • [CommentIn] Tidsskr Nor Laegeforen. 2008 Aug 14;128(15):1681-2; author reply 1682 [18704137.001]
  • (PMID = 18480864.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Norway
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41. Snyder DS, Stein AS, O'Donnell MR, Gaal K, Slovak ML, Forman SJ: Philadelphia chromosome-positive acute lymphoblastic leukemia secondary to chemoradiotherapy for Ewing sarcoma. Report of two cases and concise review of the literature. Am J Hematol; 2005 Jan;78(1):74-8
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  • [Title] Philadelphia chromosome-positive acute lymphoblastic leukemia secondary to chemoradiotherapy for Ewing sarcoma. Report of two cases and concise review of the literature.
  • Survivors of childhood solid tumors including Ewing sarcoma (ES) have an increased risk of secondary malignant neoplasms (SMNs) as a consequence of exposure to chemotherapy and/or radiation (see: Bhatia S, Sklar C.
  • The most common hematologic SMNs are myelodysplasia (MDS) and acute myelogenous leukemia (AML).
  • Acute lymphoblastic leukemia (ALL) is uncommon in this patient population, and Philadelphia chromosome positive (Ph+) ALL in particular, is rare.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Bone Neoplasms / drug therapy. Bone Neoplasms / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Radiation Injuries / complications. Sarcoma, Ewing / drug therapy. Sarcoma, Ewing / radiotherapy


42. Ferrara F, Mele G, Palmieri S, Pedata M, Copia C, Riccardi C, Izzo T, Criscuolo C, Musto P: Continuous infusion idarubicin and intravenous busulphan as conditioning regimen to autologous stem cell transplantation for patients with acute myeloid leukaemia. Hematol Oncol; 2009 Dec;27(4):198-202
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  • [Title] Continuous infusion idarubicin and intravenous busulphan as conditioning regimen to autologous stem cell transplantation for patients with acute myeloid leukaemia.
  • The current study aimed to evaluate the efficacy and toxicity of a combination of intravenous (iv) busulfan (Bu) and continuous infusion Idarubicin (IDA) as a conditioning regimen to autologous haematopoietic stem cell transplantation (ASCT) in patients with acute myeloid leukaemia (AML).
  • In order to perform a comparison in terms of haematological and non haematological toxicity, a group of 30 patients, who were previously autografted after conditioning with IDA and oral Bu was considered.
  • Selection of factors for a matched pair analysis included median age, percentage of subjects aged over 60 years, median CD34+ cell received, cytogenetic and molecular findings and per cent of secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods. Transplantation Conditioning / methods

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19475701.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] G1LN9045DK / Busulfan; ZRP63D75JW / Idarubicin
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43. Lozzi GP, Massone C, Citarella L, Kerl H, Cerroni L: Rimming of adipocytes by neoplastic lymphocytes: a histopathologic feature not restricted to subcutaneous T-cell lymphoma. Am J Dermatopathol; 2006 Feb;28(1):9-12
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  • In this study we reviewed a series of 45 biopsy specimens of primary and secondary cutaneous B- and T-cell lymphomas and one of myeloid leukemia involving the subcutaneous tissues and showing rimming of adipocytes (subcutaneous panniculitis-like T-cell lymphoma: n = 16; mycosis fungoides, tumor stage: n = 3; aggressive epidermotropic CD8(+) T-cell lymphoma: n = 2; cutaneous gamma/delta T-cell lymphoma: n = 4; extranodal NK/T-cell lymphoma, nasal type: n = 4; cutaneous medium-large pleomorphic T-cell lymphoma, NOS: n = 5; CD4(+)/CD56(+) hematodermic neoplasm (blastic NK-cell lymphoma): n = 7; secondary cutaneous large B-cell lymphoma: n = 3; secondary cutaneous lymphoplasmacytic lymphoma: n = 1; specific cutaneous manifestations of acute myelogenous leukemia: n = 1).

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  • (PMID = 16456318.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell, gamma-delta
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44. Bastianutto C, Mian A, Symes J, Mocanu J, Alajez N, Sleep G, Shi W, Keating A, Crump M, Gospodarowicz M, Medin J, Minden M, Liu FF: Local radiotherapy induces homing of hematopoietic stem cells to the irradiated bone marrow. Cancer Res; 2007 Nov 1;67(21):10112-6
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  • Local breast radiation therapy (RT) is associated with a 3-fold increased risk of secondary acute myeloid leukemia.
  • Our data also suggest some opportunities for leukemia prevention in breast cancer patients undergoing RT.
  • [MeSH-major] Bone Marrow Cells / radiation effects. Hematopoietic Stem Cells / radiation effects. Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Radiotherapy / adverse effects

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  • (PMID = 17974951.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Cxcl12 protein, mouse; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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45. Sakai R, Fujimaki K, Yamazaki E, Sakamoto H, Kanamori H, Miura I, Ishigatsubo Y: Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22). Int J Hematol; 2006 Dec;84(5):417-20
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  • [Title] Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22).
  • inv(16)(p13q22) is associated with de novo acute myelomonocytic leukemia with dysplastic bone marrow eosinophils (AMML Eo), which has a relatively favorable clinical course with a longer remission duration and better survival prospects.
  • On the other hand, t(5; 17)(q13;q11), although relatively rare, has been reported to be a component of complex chromosomal abnormalities in myelodysplastic syndromes and secondary acute myeloid leukemia (AML).
  • In general, certain secondary chromosomal abnormalities are associated with the phenotype of the disease, which retains its essential biologic characteristics established by the primary abnormality.
  • Accordingly, the primary nature of the leukemic cells in this case differs from the findings for core-binding factor AML with inv(16)(p13q22).
  • We believe this report is the first of de novo AMML Eo with t(5; 17)(q13;q11) showing as a secondary chromosomal aberration with inv(16)(p13q22).
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosome Inversion. Chromosomes, Human / genetics. Eosinophils / pathology. Leukemia, Myelomonocytic, Acute. Translocation, Genetic

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  • (PMID = 17189222.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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46. Ling X, Konopleva M, Zeng Z, Ruvolo V, Stephens LC, Schober W, McQueen T, Dietrich M, Madden TL, Andreeff M: The novel triterpenoid C-28 methyl ester of 2-cyano-3, 12-dioxoolen-1, 9-dien-28-oic acid inhibits metastatic murine breast tumor growth through inactivation of STAT3 signaling. Cancer Res; 2007 May 1;67(9):4210-8
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  • Our previous studies indicated that prolonged CDDO-Me treatment inactivated extracellular signal-regulated kinase signaling in acute myelogenous leukemia cells.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Growth Processes / drug effects. Dendritic Cells / drug effects. Dendritic Cells / immunology. Female. Genetic Vectors / genetics. Lentivirus / genetics. Luciferases, Renilla. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Signal Transduction / drug effects. Spleen / cytology. Spleen / drug effects. Spleen / immunology

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  • [ErratumIn] Cancer Res. 2008 Jun 15;68(12):4958
  • (PMID = 17483332.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 P50 CA100632; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P50 CA116199
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 6SMK8R7TGJ / Oleanolic Acid; CEG1Q6OGU1 / methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate; EC 1.13.12.5 / Luciferases, Renilla
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47. De Vita S, De Matteis S, Laurenti L, Chiusolo P, Reddiconto G, Fiorini A, Leone G, Sica S: Secondary Ph+ acute lymphoblastic leukemia after temozolomide. Ann Hematol; 2005 Oct;84(11):760-2
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  • [Title] Secondary Ph+ acute lymphoblastic leukemia after temozolomide.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / chemically induced

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  • (PMID = 16044311.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 8A1O1M485B / Imatinib Mesylate
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48. Lichtman MA: Is there an entity of chemically induced BCR-ABL-positive chronic myelogenous leukemia? Oncologist; 2008 Jun;13(6):645-54
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  • [Title] Is there an entity of chemically induced BCR-ABL-positive chronic myelogenous leukemia?
  • Advances in the therapy of malignancy have been accompanied by an increased frequency of cases of secondary acute myelogenous leukemia and related clonal cytopenias and oligoblastic (subacute) myelogenous leukemia (myelodysplastic syndromes).
  • The acute myelogenous leukemia incidence can be increased by high-dose acute ionizing radiation exposure, alkylating agents, topoisomerase II inhibitors, possibly other DNA-damaging therapeutic agents, heavy, prolonged cigarette smoking, and high dose-time exposure to benzene, the latter less frequently seen in industrialized countries with worksite regulations.
  • Acute myelogenous leukemia and myelodysplastic syndromes may result from innumerable primary types of chromosome damage.
  • In the case of chronic myelogenous leukemia, a specific break in chromosome bands 9q34 and 22q11 must occur to result in the causal fusion oncogene (BCR-ABL).
  • A review of 11 studies of the chromosomal abnormalities found in presumptive cases of cytotoxic therapy-induced leukemia and of 40 studies of the subtypes of leukemia that occur following cytotoxic therapy for other cancers has not provided evidence of an increased risk for chemically induced BCR-ABL-positive chronic myelogenous leukemia.
  • Studies of the effects of alkylating agents, topoisomerase inhibitors, and benzene on chromosomes of hematopoietic cells in vitro, coupled with the aforementioned epidemiological studies of secondary leukemia after cytotoxic therapy or of persons exposed to high dose-time concentrations of benzene in the workplace, do not indicate a relationship among chemical exposure, injury to chromosome bands 9q34 and 22q11, and an increased risk for BCR-ABL-positive chronic myelogenous leukemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / chemically induced

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  • (PMID = 18586919.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 113
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49. Sovinz P, Urban C, Hausegger K: Life-threatening hemangiomatosis of the liver in an infant: multimodal therapy including cyclophosphamide and secondary acute myeloid leukemia. Pediatr Blood Cancer; 2006 Dec;47(7):972-3
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  • [Title] Life-threatening hemangiomatosis of the liver in an infant: multimodal therapy including cyclophosphamide and secondary acute myeloid leukemia.
  • [MeSH-major] Cyclophosphamide / adverse effects. Hemangioma / therapy. Leukemia, Myeloid, Acute / etiology. Liver Neoplasms / therapy. Neoplasms, Second Primary / etiology


50. Ersvaer E, Kittang AO, Hampson P, Sand K, Gjertsen BT, Lord JM, Bruserud O: The protein kinase C agonist PEP005 (ingenol 3-angelate) in the treatment of human cancer: a balance between efficacy and toxicity. Toxins (Basel); 2010 01;2(1):174-94
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  • Direct pro-apoptotic effects of this drug have been demonstrated in several malignant cells, including melanoma cell lines and primary human acute myelogenous leukemia cells.
  • At micromolar concentrations required to kill melanoma cells this agent causes PKC-independent secondary necrosis.

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  • (PMID = 22069553.001).
  • [ISSN] 2072-6651
  • [Journal-full-title] Toxins
  • [ISO-abbreviation] Toxins (Basel)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.7.11.13 / Protein Kinase C-delta
  • [Other-IDs] NLM/ PMC3206618
  • [Keywords] NOTNLM ; cancer-protein kinase C-PEP005 (major topic)
  • [General-notes] NLM/ Original DateCompleted: 20111110
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51. Harousseau JL, Martinelli G, Jedrzejczak WW, Brandwein JM, Bordessoule D, Masszi T, Ossenkoppele GJ, Alexeeva JA, Beutel G, Maertens J, Vidriales MB, Dombret H, Thomas X, Burnett AK, Robak T, Khuageva NK, Golenkov AK, Tothova E, Mollgard L, Park YC, Bessems A, De Porre P, Howes AJ, FIGHT-AML-301 Investigators: A randomized phase 3 study of tipifarnib compared with best supportive care, including hydroxyurea, in the treatment of newly diagnosed acute myeloid leukemia in patients 70 years or older. Blood; 2009 Aug 6;114(6):1166-73
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  • [Title] A randomized phase 3 study of tipifarnib compared with best supportive care, including hydroxyurea, in the treatment of newly diagnosed acute myeloid leukemia in patients 70 years or older.
  • This phase 3, multicenter, open-label study evaluated the efficacy and safety of tipifarnib compared with best supportive care (BSC), including hydroxyurea, as first-line therapy in elderly patients (>or=70 years) with newly diagnosed, de novo, or secondary acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hydroxyurea / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Quinolones / administration & dosage

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  • (PMID = 19470696.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00093990
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib; X6Q56QN5QC / Hydroxyurea
  • [Investigator] Bezares R; Calahonra R; Fernandez I; Bosly J; Bries G; Bron D; Demuynck H; Ferrant A; Maertens J; Noens L; Selleslag D; Zachee P; Del Giglio; Figueiras R; Hungria V; Brandwein J; Kassis J; Sheridan D; Van der Jagt R; Mayer J; Dufva I; Juul Nielsen O; Friis L; Scholer Kristensen J; Bordessoule D; Dombret H; Fenaux P; Harousseau JL; Huguet F; Ifrah N; Pigneaux A; Quesnel B; Randriamalala E; Rossi JF; Thomas X; Vey N; Ganser A; Germing U; Hänel M; Moritz T; Niederwieser; Noppeney R; Borbényi Z; Losonczy H; Masszi T; Radványi G; Udvardy M; Conneally E; O'Dwyer M; Alimena G; Baccarani M; De Fabritiis P; Fanin R; Martinelli G; Kim I; Lee KH; Min YH; Garcés O; Plasencia A; Sobrevilla P; Vela J; Dmoszynska A; Jedrzejczak W; Kloczko J; Kuliczkowski K; Robak T; Skotnicki A; Sulek K; Alexeeva JA; Abdulkadyrov KM; Domnikova N; Dunaev YA; Gaisarova G; Gavrilenko A; Golenkov AK; Khuageva NK; Khlevnaya N; Loginov AB; Patrin VF; Pristupa A; Rossiev VA; Samoilova OS; Shneider TV; Suvorov A; Yablokova VV; Demeckova E; Tothova E; Wild A; Brunet S; Esteve J; Garcia J; Laraña; San Miguel J; Björkholm M; Mollgard L; Tidefelt U; Chou WC; Hsiao LT; Kuo CY; Lin TL; Löwenberg B; Van Marwijk Kooy M; Muus P; Ossenkoppele GJ; Schipperus MR; Schouten HC; Wittebol S; Gülbas Z; Burnett AK; Carr R; El-Agnaf M; Mufti GJ; Rudin C; Kaplan PE; Kryachok IA; Lysa I; Masliak ZV; Pylypenko HV; Stulginskaya MA; Manges RF
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52. Klepin HD, Balducci L: Acute myelogenous leukemia in older adults. Oncologist; 2009 Mar;14(3):222-32
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  • [Title] Acute myelogenous leukemia in older adults.
  • The incidence of acute myelogenous leukemia (AML) increases with age.
  • Older AML patients, generally defined by age > or = 60 years, have worse treatment outcomes than younger patients.
  • Older patients are more likely to present with unfavorable cytogenetic abnormalities, multidrug resistance phenotypes, and secondary AML.
  • Investigations of hypomethylating agents and signal transduction inhibitors hold promise for the treatment of AML patients.
  • [MeSH-major] Geriatrics / methods. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy


53. Sekeres MA, Elson P, Kalaycio ME, Advani AS, Copelan EA, Faderl S, Kantarjian HM, Estey E: Time from diagnosis to treatment initiation predicts survival in younger, but not older, acute myeloid leukemia patients. Blood; 2009 Jan 1;113(1):28-36
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  • [Title] Time from diagnosis to treatment initiation predicts survival in younger, but not older, acute myeloid leukemia patients.
  • Acute myeloid leukemia (AML) is considered an oncologic emergency.
  • We examined the effect of time from AML diagnosis to treatment (TDT) on complete remission (CR) and overall survival (OS), using patient characteristics available at diagnosis.
  • Regression models were applied to older (> or = 60 years) and younger (< 60 years) adults, controlling for age, baseline white blood cell count, secondary AML (sAML), and performance status.
  • AML therapy should be initiated immediately in younger patients.


54. Linsenmeier C, Thoennessen D, Negretti L, Bourquin JP, Streller T, Lütolf UM, Oertel S: Total body irradiation (TBI) in pediatric patients. A single-center experience after 30 years of low-dose rate irradiation. Strahlenther Onkol; 2010 Nov;186(11):614-20
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  • A total of 18 patients suffered from acute lymphoblastic leukemia (ALL), 5 from acute and 2 from chronic myelogenous leukemia, 1 from non-Hodgkin lymphoma, and 2 from anaplastic anemia.
  • The cohort consisted of 15 patients referred after first remission and 13 patients with relapsed leukemia.
  • Eight patients died of recurrent disease, 1 of graft vs. host reaction, 2 of sepsis, and 2 patients died of a secondary malignancy.
  • Overall survival was significantly inferior in patients treated after relapse compared to those treated for newly diagnosed leukemia (24% versus 74%; p=0.004).
  • Late effects (RTOG ≥ 3) were pneumonitis in 1 patient, chronic bronchitis in 1 patient, cardiomyopathy in 2 patients, severe cataractogenesis in 1 patient (48 months after TBI with 10 Gy in a single dose) and secondary malignancies in 2 patients (36 and 190 months after TBI).
  • CONCLUSION: As severe late sequelae after TBI, we observed 2 secondary malignancies in 11 patients who survived in excess of 36 months.
  • [MeSH-major] Anemia, Aplastic / radiotherapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radiotherapy. Leukemia, Myeloid, Acute / radiotherapy. Lymphoma, Non-Hodgkin / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Whole-Body Irradiation

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  • (PMID = 21069270.001).
  • [ISSN] 1439-099X
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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55. Verma D, O'Brien S, Thomas D, Faderl S, Koller C, Pierce S, Kebriaei P, Garcia-Manero G, Cortes J, Kantarjian H, Ravandi F: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens. Cancer; 2009 Jan 1;115(1):101-6
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  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens.
  • BACKGROUND: Secondary malignancies including myeloid neoplasms occur infrequently in acute lymphoblastic leukemia (ALL) and to the authors' knowledge have not been as well documented in adults as in children.
  • RESULTS: Sixteen patients (2.49%) developed secondary acute myelogenous leukemia (AML) (6 patients) or myelodysplastic syndrome (MDS) (10 patients).
  • Karyotype at time of AML/MDS diagnosis was -5, -7 in 9 patients, normal in 1 patient, complex in 1 patient, inv(11) in 1 patient, t(4;11) in 1 patient, del(20) in 1 patient, and unavailable in 2 patients.
  • Secondary AML/MDS developed at a median of 32 months after ALL diagnosis.
  • Cytarabine plus anthracycline-based treatment was given to 12 patients with AML and high-risk MDS.
  • Eight patients (1 with AML and 7 with MDS) underwent allogeneic stem cell transplantation, and all but 2 died at a median of 3 months (range, 0.5-11 months) after transplantation.
  • The median overall survival after a diagnosis of secondary AML and MDS was 9.25 months (range, 1+ to 26+ months).
  • CONCLUSIONS: Secondary AML and MDS occur infrequently in adult patients with de novo ALL treated with the hyper-CVAD regimens, and response to therapy is poor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


56. Rubio S, Martins C, Lacerda JF, Carmo JA, Lourenço F, Lacerda JM: Allogeneic stem cell transplantation in patients with myelodysplastic syndrome: outcome analysis according to the International Prognostic Scoring System. Acta Med Port; 2006 Sep-Oct;19(5):343-7
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  • We determined the outcome of patients with myelodysplastic syndrome (MDS) and secondary acute myeloid leukemia (sAML) after allogeneic stem cell transplantation according to their international prognostic scoring system (IPSS) risk categories at diagnosis.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Leukemia, Myeloid / surgery. Male. Middle Aged. Prognosis. Recurrence. Risk Assessment. Treatment Outcome


57. Tefferi A: Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1. Leukemia; 2010 Jun;24(6):1128-38
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  • Beginning in early 2005, a number of novel mutations involving Janus kinase 2 (JAK2), Myeloproliferative Leukemia Virus (MPL), TET oncogene family member 2 (TET2), Additional Sex Combs-Like 1 (ASXL1), Casitas B-lineage lymphoma proto-oncogene (CBL), Isocitrate dehydrogenase (IDH) and IKAROS family zinc finger 1 (IKZF1) have been described in BCR-ABL1-negative MPNs.
  • The incidence of TET2, ASXL1, CBL, IDH or IKZF1 mutations in these disorders ranges from 0 to 17%; these latter mutations are more common in chronic (TET2, ASXL1, CBL) or juvenile (CBL) myelomonocytic leukemias, mastocytosis (TET2), myelodysplastic syndromes (TET2, ASXL1) and secondary acute myeloid leukemia, including blast-phase MPN (IDH, ASXL1, IKZF1).

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  • (PMID = 20428194.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Thrombopoietin; 0 / Repressor Proteins; 0 / TET2 protein, human; 143641-95-6 / MPL protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Number-of-references] 171
  • [Other-IDs] NLM/ PMC3035972
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58. Shinder R, Oellers P, Esmaeli B, Schiffman JS: Superior ophthalmic vein thrombosis in a patient with chronic myeloid leukemia receiving antifibrinolytic and thrombopoietin receptor agonist therapy. J Ocul Pharmacol Ther; 2010 Jun;26(3):293-6
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  • [Title] Superior ophthalmic vein thrombosis in a patient with chronic myeloid leukemia receiving antifibrinolytic and thrombopoietin receptor agonist therapy.
  • Patients present with acute orbital signs, including proptosis, ophthalmoplegia, globe dystopia, and periorbital edema, and may have diminished vision secondary to optic neuropathy.
  • [MeSH-minor] Aged. Eye / blood supply. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Male


59. Yesilipek MA, Karasu GT, Kupesiz A, Uygun V, Hazar V: Better posttransplant outcome with fludarabine based conditioning in multitransfused fanconi anemia patients who underwent peripheral blood stem cell transplantation. J Pediatr Hematol Oncol; 2009 Jul;31(7):512-5
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  • We lost 3 patients in regimen A group and 1 of them from secondary acute myeloid leukemia.

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  • (PMID = 19564748.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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60. Lehrnbecher T, Zimmermann M, Reinhardt D, Dworzak M, Stary J, Creutzig U: Prophylactic human granulocyte colony-stimulating factor after induction therapy in pediatric acute myeloid leukemia. Blood; 2007 Feb 1;109(3):936-43
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  • [Title] Prophylactic human granulocyte colony-stimulating factor after induction therapy in pediatric acute myeloid leukemia.
  • Children with acute myelogenous leukemia (AML) have a high risk of infectious complications that might be reduced by prophylactic granulocyte colony-stimulating factor (G-CSF).
  • However, G-CSF could induce AML blast proliferation.
  • The prospective randomized trial AML-BFM 98 investigated the impact of G-CSF on hematopoetic recovery and infectious complications (primary endpoints) and on outcome (secondary endpoint) in children (aged 0-18 years) with de novo AML.
  • Between 1998 and 2003, 161 children with AML were randomized to receive G-CSF after inductions 1 and 2, whereas 156 patients were assigned to the control group.
  • Since G-CSF does not influence the risk of infectious complications or outcome in children undergoing therapy for AML, one cannot advocate the routine use of G-CSF in this patient group.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 17008536.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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61. Ko MW, Tamhankar MA, Volpe NJ, Porter D, McGrath C, Galetta SL: Acute promyelocytic leukemic involvement of the optic nerves following mitoxantrone treatment for multiple sclerosis. J Neurol Sci; 2008 Oct 15;273(1-2):144-7
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  • [Title] Acute promyelocytic leukemic involvement of the optic nerves following mitoxantrone treatment for multiple sclerosis.
  • Mitoxantrone, the first immunosuppressant to receive FDA approval for treatment of worsening relapsing-remitting, secondary progressive, and progressive-relapsing multiple sclerosis (MS) is a DNA topoisomerase II inhibitor that has been associated with the development of acute promyelocytic myelogenous leukemia (APML).
  • [MeSH-major] Analgesics / adverse effects. Leukemia, Promyelocytic, Acute / chemically induced. Leukemia, Promyelocytic, Acute / pathology. Mitoxantrone / adverse effects. Optic Nerve / drug effects

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  • (PMID = 18687447.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Analgesics; BZ114NVM5P / Mitoxantrone
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62. Kuptsova-Clarkson N, Ambrosone CB, Weiss J, Baer MR, Sucheston LE, Zirpoli G, Kopecky KJ, Ford L, Blanco J, Wetzler M, Moysich KB: XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia. Int J Mol Epidemiol Genet; 2010;1(4):278-94
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  • [Title] XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia.
  • We evaluated these polymorphisms and XPD haplotypes in adult de novo (n=214) and secondary (n=79) acute myeloid leukemia (AML) patients treated with cytarabine and anthracycline chemotherapy.
  • Differential responses were observed in secondary, but not de novo, AML.
  • Among secondary AML patients, the odds of achieving complete remission (CR) were higher for the XPD 312Asn/Asn (OR= 11.23; 95% CI, 2.23-56.63) and XPD 751Gln/Gln (OR= 7.07; 95% CI, 1.42-35.18) genotypes.
  • If validated, these findings could support stratification of chemotherapy in secondary AML.

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  • (PMID = 21394217.001).
  • [ISSN] 1948-1756
  • [Journal-full-title] International journal of molecular epidemiology and genetics
  • [ISO-abbreviation] Int J Mol Epidemiol Genet
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353; United States / NCI NIH HHS / CA / CA108353-01; United States / NCI NIH HHS / CA / R03 CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353-01
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS247623; NLM/ PMC3049908
  • [Keywords] NOTNLM ; Acute Myeloid Leukemia (AML) / DNA repair gene polymorphisms / pharmacogenetics/pharmacogenomics / secondary AML
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63. Ferrara F, Palmieri S, Izzo T, Criscuolo C, Riccardi C: Continuous sequential infusion of fludarabine and cytarabine for elderly patients with acute myeloid leukaemia secondary to a previously diagnosed myelodysplastic syndrome. Hematol Oncol; 2010 Dec;28(4):202-8
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  • [Title] Continuous sequential infusion of fludarabine and cytarabine for elderly patients with acute myeloid leukaemia secondary to a previously diagnosed myelodysplastic syndrome.
  • Acute myeloid leukaemia (AML) secondary to myelodysplastic syndrome (MDS) is characterized by poor prognosis, namely in older patients.
  • The combination of fludarabine (F) with cytarabine (ARA-C) ± G-CSF was proven as effective in patients with poor risk AML.
  • The efficacy and toxicity of a regimen including F + ARA-C as sequential continuous infusion (CI-FLA) in 64 untreated patients aged >60 years, in which AML arose after a previous MDS, was investigated.
  • CI-FLA is effective in elderly patients with AML secondary to previously diagnosed MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / complications
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Combined Modality Therapy. Cytarabine / administration & dosage. Cytarabine / adverse effects. Diarrhea / chemically induced. Disease-Free Survival. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Remission Induction. Transplantation, Autologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / adverse effects. Vidarabine / analogs & derivatives


64. Cornely OA, Böhme A, Reichert D, Reuter S, Maschmeyer G, Maertens J, Buchheidt D, Paluszewska M, Arenz D, Bethe U, Effelsberg J, Lövenich H, Sieniawski M, Haas A, Einsele H, Eimermacher H, Martino R, Silling G, Hahn M, Wacker S, Ullmann AJ, Karthaus M, Multinational Case Registry of the Infectious Diseases Working Party of the German Society for Hematology and Oncology: Risk factors for breakthrough invasive fungal infection during secondary prophylaxis. J Antimicrob Chemother; 2008 Apr;61(4):939-46
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  • [Title] Risk factors for breakthrough invasive fungal infection during secondary prophylaxis.
  • Secondary prophylaxis of IFI is widely administered, but reliable data on outcome and risk factors for recurrent IFI during subsequent chemotherapy are not available.
  • METHODS: From 25 European cancer centres, 166 consecutive patients with acute myelogenous leukaemia (AML) and a recent history of proven or probable pulmonary IFI were included.
  • Multiple logistic regressions yielded predisposing factors: duration of neutropenia [per additional day; odds ratio (OR) 1.043, confidence interval (CI) 1.008-1.078], high-dose cytarabine (OR 3.920, CI 1.120-12.706), number of antibiotics (per antibiotic; OR 1.504, CI 1.089-2.086), partial response as outcome of prior IFI (OR 4.037, CI 1.301-12.524) and newly diagnosed AML (OR 3.823, CI 0.953-15.340).
  • CONCLUSIONS: Duration of neutropenia, high-dose cytarabine, prior antibiotic therapy and a partial response to the first IFI therapy were risk factors for recurrent IFI and should be considered in AML patients with prior pulmonary IFI undergoing further chemotherapy.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemoprevention. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Logistic Models. Male. Middle Aged. Recurrence. Risk Factors. Treatment Outcome

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  • (PMID = 18272515.001).
  • [ISSN] 1460-2091
  • [Journal-full-title] The Journal of antimicrobial chemotherapy
  • [ISO-abbreviation] J. Antimicrob. Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents
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65. Allen SL, Kolitz JE, Lundberg AS, Bennett JM, Capizzi RL, Budman DR: Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia. Leuk Res; 2010 Apr;34(4):487-91
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  • [Title] Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia.
  • Amonafide-l-malate (amonafide) is a unique DNA intercalator that maintains activity in the presence of MDR mechanisms, a frequent cause of treatment-failure in secondary AML.
  • 43 patients with relapsed/refractory or secondary AML or CML blast crisis were enrolled into two phase I dose-escalation studies investigating amonafide as monotherapy or in combination with cytarabine.
  • Between both trials responses occurred in 9/20 patients with secondary AML.
  • Both trials demonstrated an acceptable safety profile and significant antileukemic activity in patients with poor-risk AML, especially those with secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Naphthalimides / administration & dosage

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748672.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Naphthalimides; 04079A1RDZ / Cytarabine; 1Q8D39N37L / amonafide
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66. Mittal R, Ramaswamy NV, Pandita R, Al Bahar S, Khalifa N, Omar S: Secondary acute myeloid leukemia after successful treatment for osteosarcoma. Indian J Med Paediatr Oncol; 2010 Jan;31(1):33-5
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  • [Title] Secondary acute myeloid leukemia after successful treatment for osteosarcoma.
  • Secondary acute myeloid leukemia (sAML) is a rare complication following chemotherapy for osteogenic sarcoma.
  • Eight months after completion of therapy, while on follow-up, he presented with leukocytosis and thrombocytopenia and confirmed to have AML.

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  • (PMID = 20931020.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2941602
  • [Keywords] NOTNLM ; Acute myeloid leukemia / chemotherapy / osteosarcoma / secondary malignancy
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67. Bhojwani D, Moskowitz N, Raetz EA, Carroll WL: Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia. Paediatr Drugs; 2007;9(3):149-56
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  • [Title] Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is a heterogeneous disease.
  • Identification of patients who are predicted to have an unfavorable outcome may allow for early intervention such as intensification of therapy or avoidance of drugs that are associated with specific secondary effects such as therapy-related acute myelogenous leukemia.
  • [MeSH-major] Gene Expression Profiling. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Child. Diploidy. Drug Resistance, Neoplasm / genetics. Humans. Oligonucleotide Array Sequence Analysis. Oncogene Proteins / genetics. Secondary Prevention


68. Winter SS, Holdsworth MT, Devidas M, Raisch DW, Chauvenet A, Ravindranath Y, Ducore JM, Amylon MD: Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296. Pediatr Blood Cancer; 2006 Feb;46(2):179-86
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  • [Title] Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296.
  • PURPOSE: A previous Pediatric Oncology Group (POG) study showed high incidence of secondary acute myelogenous leukemia (AML) in children treated for T-cell acute lymphoblastic leukemia (T-ALL) or higher-stage lymphoblastic lymphoma.
  • To prevent secondary neoplasms, induce prolonged asparagine depletion, and maintain high event-free survival (EFS) in children with newly diagnosed T-ALL or higher-stage non-Hodgkins lymphoma (NHL), we designed this pilot study to determine feasibility and safety of substituting methotrexate/mercaptopurine for teniposide/cytarabine and PEG-asparaginase for native asparaginase.
  • No patients treated entirely on this study developed secondary neoplasms.
  • One patient taken off study for asparaginase toxicity was treated with multiagent therapy that contained teniposide, and died from secondary myelodysplasia (sMDS)/AML.
  • EFS was not compromised and secondary neoplasms were decreased.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Anthracyclines / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child. Child, Preschool. Disease-Free Survival. Drug Hypersensitivity / etiology. Female. Follow-Up Studies. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / mortality. Male. Pilot Projects. Remission Induction. Sepsis / etiology. Sepsis / mortality

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  • (PMID = 16007607.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 U10 CA5312; United States / NCI NIH HHS / CA / CA29139
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; EC 3.5.1.1 / Asparaginase
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69. Alioglu B, Avci Z, Ozcay F, Arda S, Ozbek N: Neutropenic enterocolitis in children with acute leukemia or aplastic anemia. Int J Hematol; 2007 Nov;86(4):364-8
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  • [Title] Neutropenic enterocolitis in children with acute leukemia or aplastic anemia.
  • Neutropenic enterocolitis (NE) and acute appendicitis are life-threatening conditions that develop in children with severe or prolonged neutropenia secondary to acute leukemia and lymphoma.
  • The medical records of 118 patients who were treated for acute lymphoblastic leukemia (69 patients), acute myelogenous leukemia (22 patients), or aplastic anemia (27 patients) between 1997 and 2006 in our hospital pediatric hematology department were examined retrospectively.
  • Conservative treatment was favored for all patients, but 1 patient with acute appendicitis underwent surgery.
  • NE and acute appendicitis should always be considered in the differential diagnosis of abdominal pain.
  • [MeSH-major] Anemia, Aplastic / pathology. Enterocolitis, Neutropenic / complications. Enterocolitis, Neutropenic / pathology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


70. Kuendgen A, Schmid M, Schlenk R, Knipp S, Hildebrandt B, Steidl C, Germing U, Haas R, Dohner H, Gattermann N: The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia. Cancer; 2006 Jan 1;106(1):112-9
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  • [Title] The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia.
  • BACKGROUND: Valproic acid (VPA) inhibits histone deacetylase activity and, synergizing with all-trans retinoic acid (ATRA), achieves differentiation induction of myeloid blast cells in vitro.
  • METHODS: We used VPA in 58 patients with acute myeloid leukemia (AML) who were too old and/or medically unfit to receive intensive chemotherapy (32 AML secondary to myelodysplastic syndrome [MDS], 22 de novo AML, 4 AML secondary to myeloproliferative syndrome).
  • RESULTS: The response rate was only 5% according to International Working Group (IWG) criteria for AML but was 16% when IWG response criteria for MDS were used, which capture hematologic improvement and stabilization of the disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Tretinoin / therapeutic use. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Treatment Outcome


71. Ravoet C, Mineur P, Robin V, Debusscher L, Bosly A, André M, El Housni H, Soree A, Bron D, Martiat P: Farnesyl transferase inhibitor (lonafarnib) in patients with myelodysplastic syndrome or secondary acute myeloid leukaemia: a phase II study. Ann Hematol; 2008 Nov;87(11):881-5
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  • [Title] Farnesyl transferase inhibitor (lonafarnib) in patients with myelodysplastic syndrome or secondary acute myeloid leukaemia: a phase II study.
  • We prospectively studied efficiency and tolerance of lonafarnib, a compound able to inhibit Ras signalling pathway through an inhibition of farnesyl transferase, in patients with MDS or secondary acute myeloid leukaemia (sAML).
  • Sixteen patients were included: FAB/RAEB (n = 10), RAEB-T (n = 2), sAML (n = 2) and chronic myelomonocytic leukaemia (CMML; n = 2); WHO/RAEB-1 (n = 4), RAEB-2 (n = 5), AML (n = 5), CMML (n = 2).
  • Lonafarnib alone, administered following our schedule, has shown limited activity in patients with MDS or secondary AML.
  • [MeSH-major] Farnesyltranstransferase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Piperidines / adverse effects. Pyridines / adverse effects


72. NAKAMURA S, TAKEICHI T, YAMANAKA C, SHICHIJO K, TAKAHASHI K, HIASA Y, MATSUSHITA T, HORIUCHI N, TAMAKI Y, KIMURA S, FUJIMOTO H, MASUDA K, SHINOMIYA S: Multiple hepatocellular carcinomas developed 15 months after commencement of chemotherapy for elderly acute myelogenous leukemia. Rinsho Ketsueki; 2009 Nov;50(11):1616-20
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  • [Title] Multiple hepatocellular carcinomas developed 15 months after commencement of chemotherapy for elderly acute myelogenous leukemia.
  • In May 2006, a 72-year-old man with acute myelogenous leukemia (M4Eo) was admitted to our hospital.
  • He received chemotherapy according to the JALSG GML200 protocol, which led to complete remission; however, in January 2007, his leukemia recurred.
  • He eventually died because of aggressive enlargement of liver tumors during the following month accompanied by the simultaneous recurrence of leukemia and unsuccessful embolization of the hepatic artery.
  • Autopsy specimens showed fibrosis and considerable iron deposition in the liver, suggested secondary hemochromatosis due to transfusion.
  • Secondary hemochromatosis, androgen imbalance, and humoral factors from leukemic cells were believed to be the causes of the rapid onset and development of HCCs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Hepatocellular. Leukemia, Myeloid, Acute / drug therapy. Liver Neoplasms. Neoplasms, Second Primary

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  • (PMID = 20009436.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgen Antagonists; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin; CAG protocol
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73. Figueroa ME, Skrabanek L, Li Y, Jiemjit A, Fandy TE, Paietta E, Fernandez H, Tallman MS, Greally JM, Carraway H, Licht JD, Gore SD, Melnick A: MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation. Blood; 2009 Oct 15;114(16):3448-58
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  • [Title] MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation.
  • Increasing evidence shows aberrant hypermethylation of genes occurring in and potentially contributing to pathogenesis of myeloid malignancies.
  • To determine the extent of promoter hypermethylation in such tumors, we compared the distribution of DNA methylation of 14 000 promoters in MDS and secondary acute myeloid leukemia (AML) patients enrolled in a phase 1 trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34(+) bone marrow cells.
  • The MDS and secondary AML patients displayed more extensive aberrant DNA methylation involving thousands of genes than did the normal CD34(+) bone marrow cells or de novo AML blasts.
  • Aberrant methylation in MDS and secondary AML tended to affect particular chromosomal regions, occurred more frequently in Alu-poor genes, and included prominent involvement of genes involved in the WNT and MAPK signaling pathways.
  • [MeSH-major] Azacitidine / administration & dosage. DNA Methylation / drug effects. DNA, Neoplasm / metabolism. Enzyme Inhibitors / administration & dosage. Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / metabolism

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  • (PMID = 19652201.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00101179
  • [Grant] United States / NCI NIH HHS / CA / R21 CA110507; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / U54 CA143876-01; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / R01 CA125635; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / U54 CA143876; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Wnt Proteins; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2765680
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74. Karp JE, Smith BD, Levis MJ, Gore SD, Greer J, Hattenburg C, Briel J, Jones RJ, Wright JJ, Colevas AD: Sequential flavopiridol, cytosine arabinoside, and mitoxantrone: a phase II trial in adults with poor-risk acute myelogenous leukemia. Clin Cancer Res; 2007 Aug 1;13(15 Pt 1):4467-73
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  • [Title] Sequential flavopiridol, cytosine arabinoside, and mitoxantrone: a phase II trial in adults with poor-risk acute myelogenous leukemia.
  • In a phase I study of flavopiridol followed by 1-beta-d-arabinofuranosylcytosine (ara-C) and mitoxantrone, overall response rate for adults with relapsed and refractory acute myelogenous leukemias (AML) was 31%.
  • We have now completed a phase II study of sequential flavopiridol, ara-C, and mitoxantrone in 62 adults with poor-risk AML.
  • Complete remissions (CR) were achieved in 12 of 15 (75%) newly diagnosed secondary AML, 18 of 24 (75%) first relapse after short CR (median CR, 9 months, including prior allotransplant), and 2 of 13 (15%) primary refractory but 0 of 10 multiply refractory AML.
  • CONCLUSIONS: Flavopiridol has anti-AML activity directly and in combination with ara-C and mitoxantrone.
  • This timed sequential regimen induces durable CRs in a significant proportion of adults with newly diagnosed secondary AML (including complex cytogenetics) and adults with AML in first relapse after short first CR.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 17671131.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01-RR0052; United States / NCI NIH HHS / CA / U01 CA70095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 04079A1RDZ / Cytarabine; 45AD6X575G / alvocidib; BZ114NVM5P / Mitoxantrone
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75. Bai XT, Gu BW, Yin T, Niu C, Xi XD, Zhang J, Chen Z, Chen SJ: Trans-repressive effect of NUP98-PMX1 on PMX1-regulated c-FOS gene through recruitment of histone deacetylase 1 by FG repeats. Cancer Res; 2006 May 1;66(9):4584-90
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  • The formation of fusion genes between NUP98 and members of the HOX family represents a critical factor for the genesis of acute leukemia or acute transformation of chronic myeloid leukemia (CML).
  • To gain insights into the molecular mechanisms underlying the leukemogenesis of NUP98-HOX fusion products, we cloned NUP98-PMX1 from a CML-blast crisis patient with t(1;11) as a secondary chromosomal translocation, and functionally studied the fusion products in detail through various molecular and protein biochemical assays.
  • Accordingly, we have hypothesized that this dual binding activity is shared by most, if not all, NUP98-HOX-involved fusion proteins, enabling these fusion proteins to act as both trans-activators and trans-repressors, and contributing to the genesis of acute leukemia or acute transformation of CML.
  • [MeSH-major] Genes, fos. Histone Deacetylases / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

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  • (PMID = 16651408.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NUP98-PMX1 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
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76. de Witte T, Hagemeijer A, Suciu S, Belhabri A, Delforge M, Kobbe G, Selleslag D, Schouten HC, Ferrant A, Biersack H, Amadori S, Muus P, Jansen JH, Hellström-Lindberg E, Kovacsovics T, Wijermans P, Ossenkoppele G, Gratwohl A, Marie JP, Willemze R: Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial. Haematologica; 2010 Oct;95(10):1754-61
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  • [Title] Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy

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  • (PMID = 20494931.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002926
  • [Grant] United States / NCI NIH HHS / CA / 5U10 CA11488-32; United States / NCI NIH HHS / CA / 5U10 CA11488-27; United States / NCI NIH HHS / CA / 5U10 CA11488-38; United States / NCI NIH HHS / CA / 5U10 CA11488-28; United States / NCI NIH HHS / CA / 5U10 CA11488-35; United States / NCI NIH HHS / CA / 5U10 CA11488-31; United States / NCI NIH HHS / CA / 5U10 CA11488-26; United States / NCI NIH HHS / CA / 5U10 CA11488-37; United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / 5U10 CA11488-29; United States / NCI NIH HHS / CA / 5U10 CA11488-36; United States / NCI NIH HHS / CA / 5U10 CA11488-33; United States / NCI NIH HHS / CA / 5U10 CA11488-34; United States / NCI NIH HHS / CA / 5U10 CA11488-30
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2948102
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77. Gupta V, Chun K, Yi QL, Minden M, Schuh A, Wells R, Brandwein J: Disease biology rather than age is the most important determinant of survival of patients &gt; or = 60 years with acute myeloid leukemia treated with uniform intensive therapy. Cancer; 2005 May 15;103(10):2082-90
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  • [Title] Disease biology rather than age is the most important determinant of survival of patients > or = 60 years with acute myeloid leukemia treated with uniform intensive therapy.
  • BACKGROUND: The objectives of the current study were to evaluate the outcome of patients > or = 60 years with acute myeloid leukemia (AML) treated uniformly with high-dose daunorubicin containing induction and modified high-dose cytosine arabinoside containing postremission therapy, and to identify factors predictive of complete disease remission (CR) and survival.
  • METHODS: Between 1998 and 2002, the authors treated 117 newly diagnosed patients (acute promyelocytic leukemia excluded) with AML > or = 60 years (median, 67 years; range, 60-82 years).
  • A normal karyotype was seen in 41 patients and 40 (34%) had secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Aged, 80 and over. Antibiotics, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Hematologic Diseases / complications. Humans. Karyotyping. L-Lactate Dehydrogenase / analysis. Leukocyte Count. Male. Middle Aged. Myelodysplastic Syndromes / complications. Remission Induction. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 15830348.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 1.1.1.27 / L-Lactate Dehydrogenase; ZS7284E0ZP / Daunorubicin
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78. D'Andrea AD: Targeting DNA repair pathways in AML. Best Pract Res Clin Haematol; 2010 Dec;23(4):469-73
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  • [Title] Targeting DNA repair pathways in AML.
  • DNA repair inhibitors, such as poly-ADP-ribose polymerase (PARP) inhibitors, may be useful in a small subset of acute myeloid leukemia (AML) patients, especially those who have complex karyotypes or those with secondary AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Repair / drug effects. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21130409.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Poly(ADP-ribose) Polymerase Inhibitors; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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79. Roboz GJ, Giles FJ, List AF, Cortes JE, Carlin R, Kowalski M, Bilic S, Masson E, Rosamilia M, Schuster MW, Laurent D, Feldman EJ: Phase 1 study of PTK787/ZK 222584, a small molecule tyrosine kinase receptor inhibitor, for the treatment of acute myeloid leukemia and myelodysplastic syndrome. Leukemia; 2006 Jun;20(6):952-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase 1 study of PTK787/ZK 222584, a small molecule tyrosine kinase receptor inhibitor, for the treatment of acute myeloid leukemia and myelodysplastic syndrome.
  • The objective of this Phase I study was to evaluate the safety, tolerability, biologic activity and pharmacologic profile of PTK/ZK administered orally, twice daily, on a continuous dosing schedule in patients with primary refractory or relapsed acute myeloid leukemia (AML), secondary AML, poor-prognosis de novo AML or advanced myelodysplastic syndrome (MDS).
  • Acute myeloid leukemia patients for whom PTK/ZK monotherapy was ineffective could receive PTK/ZK combined with standard induction chemotherapy.
  • Complete remission was observed in five of 17 AML patients treated with PTK/ZK combined with chemotherapy.
  • The drug is generally well tolerated and can be given in combination with chemotherapy for patients with MDS and AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Phthalazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Proliferation / drug effects. Cohort Studies. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Treatment Outcome. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors


80. Bug G, Ritter M, Wassmann B, Schoch C, Heinzel T, Schwarz K, Romanski A, Kramer OH, Kampfmann M, Hoelzer D, Neubauer A, Ruthardt M, Ottmann OG: Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia. Cancer; 2005 Dec 15;104(12):2717-25
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  • [Title] Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia.
  • BACKGROUND: Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, induced in vitro differentiation of primary acute myeloid leukemia (AML) blasts, an effect enhanced by all-trans retinoic acid (ATRA).
  • Herein, the authors have described results of a clinical trial with VPA plus ATRA in 26 patients with poor-risk AML.
  • No patient achieved complete remission, one with de novo AML had a minor response, and two patients with secondary AML arising from myeloproliferative disorder (MPD) achieved a partial remission and clearance of PB blasts, respectively.
  • The latter responses were accompanied by profound granulocytosis and erythrocytosis in both patients, reminiscent of the response pattern known from ATRA treatment of acute promyelocytic leukemia.
  • CONCLUSIONS: Treatment with VPA/ATRA results in transient disease control in a subset of patients with AML that has evolved from a myeloproliferative disorder but not in patients with a primary or MDS-related AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / administration & dosage. Valproic Acid / administration & dosage


81. Wadehra N, Farag S, Bolwell B, Elder P, Penza S, Kalaycio M, Avalos B, Pohlman B, Marcucci G, Sobecks R, Lin T, Andrèsen S, Copelan E: Long-term outcome of Hodgkin disease patients following high-dose busulfan, etoposide, cyclophosphamide, and autologous stem cell transplantation. Biol Blood Marrow Transplant; 2006 Dec;12(12):1343-9
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  • Five patients died between 5.3 and 9.3 years of late complications, including secondary myelodysplasia or acute myeloid leukemia, secondary solid malignancies, and pulmonary toxicity.

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  • [CommentIn] Biol Blood Marrow Transplant. 2007 Jun;13(6):746-7 [17531785.001]
  • (PMID = 17162217.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan
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82. Suzuki K, Ohishi K, Sekine T, Masuya M, Katayama N: Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone. Int J Hematol; 2007 May;85(4):344-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone.
  • The management of elderly patients with acute myeloid leukemia (AML) and a poor performance status is challenging.
  • An 89-year-old man with AML secondary to myelodysplastic syndrome (MDS) and a poor performance status (4) underwent treatment with methylprednisolone (mPSL) (125 mg/body), which resulted in a remarkable reduction of blast cells in the peripheral blood.
  • On the basis of this experience, we gave the same mPSL dose to other elderly patients with MDS/AML (n=5) or AML-M4 (n=1) who had a poor performance status (3 or higher) and appeared unable to tolerate standard cytotoxic chemotherapies.
  • Selective and significant blast cell reduction was observed in 4 of the 5 patients with MDS/AML, whereas no effects were seen in the AML patient.
  • Although our experience is limited, these findings may provide a clue to understanding the mechanisms regulating the survival of blast cells of MDS/AML and indicate that mPSL may provide a benefit to a subset of these patients.
  • [MeSH-major] Blast Crisis / drug therapy. Blast Crisis / etiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Methylprednisolone / administration & dosage. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy


83. Sergeeva A, Ono Y, Rios R, Molldrem JJ: High titer autoantibodies to GM-CSF in patients with AML, CML and MDS are associated with active disease. Leukemia; 2008 Apr;22(4):783-90
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  • [Title] High titer autoantibodies to GM-CSF in patients with AML, CML and MDS are associated with active disease.
  • Neutralizing anti-GM-CSF IgG has been associated with pulmonary alveolar proteinosis (PAP), and secondary PAP has been linked to myeloid leukemia.
  • We studied 69 patients with acute myeloid leukemia, chronic myeloid leukemia and myelodysplastic syndrome, including 19 patients who received GM-CSF with peptide antigen and incomplete Freund's adjuvant in a vaccine trial for the presence or induction of anti-GM-CSF antibodies.
  • Anti-GM-CSF IgG were present in 36 (52%) patients with myeloid leukemia compared to only 1 of 33 (3%) healthy subjects (P=0.008) and in none of 6 patients with lymphoid leukemia (P=0.0001).
  • These data are first to show that anti-GM-CSF antibodies of multiple isotypes are present in patients with active myeloid leukemia without PAP and may be useful markers of disease activity.


84. Norian JM, Stratton P: Labial fusion: a rare complication of chronic graft-versus-host disease. Obstet Gynecol; 2008 Aug;112(2 Pt 2):437-9
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  • CASE: A 22-year-old woman with a history of Ewing's sarcoma and acute myelogenous leukemia received chemotherapy and total-body irradiation followed by a matched, unrelated donor hematopoetic stem cell transplantation.
  • Labial fusion secondary to chronic GVH disease may be treated successfully with surgery and medical therapy.
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 18669755.001).
  • [ISSN] 0029-7844
  • [Journal-full-title] Obstetrics and gynecology
  • [ISO-abbreviation] Obstet Gynecol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 HD999999
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS82568; NLM/ PMC2617771
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85. Infante-Rivard C, Vermunt JK, Weinberg CR: Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia. Am J Epidemiol; 2007 Jun 1;165(11):1248-54
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  • [Title] Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia.
  • Topoisomerase II is a DNA-processing enzyme, and secondary acute myeloid leukemia has been associated with exposure to drugs that inhibit its action.
  • Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood leukemia.
  • To assess its role in the etiology of childhood acute lymphoblastic leukemia, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000).
  • [MeSH-major] Family Health. Inheritance Patterns. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17332311.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES045005-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; J64922108F / Benzene
  • [Other-IDs] NLM/ NIHMS33454; NLM/ PMC2080583
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86. Gyurkocza B, Storb R, Storer BE, Chauncey TR, Lange T, Shizuru JA, Langston AA, Pulsipher MA, Bredeson CN, Maziarz RT, Bruno B, Petersen FB, Maris MB, Agura E, Yeager A, Bethge W, Sahebi F, Appelbaum FR, Maloney DG, Sandmaier BM: Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia. J Clin Oncol; 2010 Jun 10;28(17):2859-67
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  • [Title] Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia.
  • PURPOSE: Allogeneic hematopoietic cell transplantation (HCT) after high-dose conditioning regimens imposes prohibitively high risks of morbidity and mortality for patients with high-risk acute myeloid leukemia (AML) who are older or have comorbid conditions.
  • PATIENTS AND METHODS: Two hundred seventy-four patients (median age, 60 years) with de novo or secondary AML underwent allogeneic HCT from related (n = 118) or unrelated donors (n = 156) after conditioning with 2 Gy of total-body irradiation (TBI) with or without fludarabine.
  • The cumulative incidences of grades 2, 3, and 4 acute graft-versus-host disease (GVHD) were 38%, 9%, and 5%, respectively.
  • CONCLUSION: Allogeneic HCT from related or unrelated donors after conditioning with low-dose TBI and fludarabine, relying almost exclusively on graft-versus-leukemia effects, can result in long-term remissions in older or medically infirm patients with AML.

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  • (PMID = 20439626.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / R21 CA106177; United States / NCI NIH HHS / CA / CA15704; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / CA106177; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2903320
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87. Coyle TE, Bair AK, Stein C, Vajpayee N, Mehdi S, Wright J: Acute leukemia associated with valproic acid treatment: a novel mechanism for leukemogenesis? Am J Hematol; 2005 Apr;78(4):256-60
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  • [Title] Acute leukemia associated with valproic acid treatment: a novel mechanism for leukemogenesis?
  • We now report three cases of acute leukemia with features of secondary leukemia associated with valproic acid therapy: two cases of acute myelogenous leukemia with multilineage dysplasia, one with trisomy 8 and one with monosomy 7, and one case of secondary acute lymphoblastic leukemia with del (7) (q22q34), del (9) (q21.11q22), del (11) (q12q23).
  • We propose that valproic acid therapy may lead to secondary leukemia by increasing DNA damage through chronic inhibition of histone deacetylase.
  • [MeSH-major] Leukemia / chemically induced. Valproic Acid / adverse effects
  • [MeSH-minor] Acute Disease. Adult. Anticonvulsants / adverse effects. Chromosome Aberrations. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9. DNA Damage. Epilepsy / drug therapy. Female. Gene Deletion. Humans. Male

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  • (PMID = 15795916.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 614OI1Z5WI / Valproic Acid
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88. Rison RA: Ascending sensory motor polyradiculoneuropathy with cranial nerve involvement following administration of intrathecal methotrexate and intravenous cytarabine in a patient with acute myelogenous leukemia: a case report*. Cases J; 2008;1(1):255
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  • [Title] Ascending sensory motor polyradiculoneuropathy with cranial nerve involvement following administration of intrathecal methotrexate and intravenous cytarabine in a patient with acute myelogenous leukemia: a case report*.
  • BACKGROUND: Acute inflammatory polyradiculoneuropathy secondary to chemotherapy for leukemia has been described in the pediatric literature.
  • However, the reports are rare and have been mainly from intrathecal methotrexate in pediatric acute lymphoblastic leukemia patients who developed demyelinating polyradiculoneuropathy.
  • CASE PRESENTATION: A case report is presented of an unfortunate 53 year old Hispanic woman with acute myelogenous leukemia who developed profound weakness with cranial nerve palsies following both intravenous and intrathecal chemotherapy.
  • CONCLUSION: This is an interesting and unusual case of predominantly axonal ascending sensory motor polyradiculoneuropathy with cranial nerve involvement in an adult patient with acute myelogenous leukemia following intravenous Cytosine arabinoside and intrathecal methotrexate.

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  • (PMID = 18937872.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2577643
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89. Larson RA: Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia? Best Pract Res Clin Haematol; 2007 Mar;20(1):29-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia?
  • Secondary leukemia is a poorly defined term that often refers to the development of acute myeloid leukemia (AML) following the history of a previous disease, such as a myelodysplastic syndrome or a chronic myeloproliferative disorder.
  • Secondary leukemia can also be a consequence of treatment with chemotherapy, including alkylating agents and topoisomerase II inhibitors, and/or radiotherapy, or due to exposure to environmental carcinogens.
  • Outcomes for this large and variable group of patients with secondary AML have been poor compared to people who develop AML de novo.
  • The question arises whether a diagnosis of secondary leukemia per se indicates a poor prognosis or whether their bad outcomes result from an association with certain morphologic and biologic characteristics.
  • Morphologic dysplasia in de novo AML is related to unfavorable cytogenetics, but has no independent prognostic relevance under the conditions of intensive chemotherapy.
  • While there is no significant correlation between cytogenetic risk groups and dysplasia, cytogenetic features do have an impact on outcome among both de novo and secondary AML patients.
  • In various subgroups of secondary AML, the spectrum of cytogenetic abnormalities is similar to de novo AML, but the frequency of abnormalities associated with unfavorable and intermediate risk cytogenetics, such as a complex karyotype, trisomy 8, monosomy 7, and others, is higher in secondary AML.
  • The survival of patients with therapy-related myeloid leukemia (t-AML) is generally shorter than for those with de novo AML within the same cytogenetic risk group.
  • Across the population of t-AML, however, survival varies according to cytogenetic risk group, with longer survival in patients with favorable-risk karyotypes.
  • The term secondary AML is too broad and imprecise to be of importance and should not be used.
  • These AML patients should be enrolled on front-line chemotherapy trials and should be stratified by pretreatment disease status and exposure history, if necessary.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Humans. Myelodysplastic Syndromes. Myeloproliferative Disorders. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / genetics. Prognosis. Survival Analysis

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  • (PMID = 17336252.001).
  • [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] 23
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90. Ko M, Huang Y, Jankowska AM, Pape UJ, Tahiliani M, Bandukwala HS, An J, Lamperti ED, Koh KP, Ganetzky R, Liu XS, Aravind L, Agarwal S, Maciejewski JP, Rao A: Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2. Nature; 2010 Dec 9;468(7325):839-43
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  • [Title] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2.
  • The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies.
  • Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
  • We show here that TET2 mutations associated with myeloid malignancies compromise catalytic activity.
  • Our results demonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzymatic activity favours myeloid tumorigenesis.
  • Measurement of 5hmC levels in myeloid malignancies may prove valuable as a diagnostic and prognostic tool, to tailor therapies and assess responses to anticancer drugs.