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1. da Costa Moraes CA, Trompieri NM, Cavalcante Felix FH: Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital. J Pediatr Hematol Oncol; 2008 May;30(5):387-90
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  • [Title] Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital.
  • Acute promyelocytic leukemia (APL) is an uncommon form of pediatric acute nonlymphocytic leukemia.
  • The introduction of all-transretinoic acid (ATRA) or tretinoin, a biologic response modifier, in its therapy was followed by dramatic improvement in its outcome.
  • The clinical charts were searched for data regarding clinical presentation, diagnosis, initial response with induction therapy, toxicity of ATRA, and antracyclic drug (daunorubicin).
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Brazil. Female. Hospitals, Pediatric. Humans. Male. Retrospective Studies

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  • (PMID = 18458575.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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2. Fan Y, Schreiber EM, Giorgianni A, Yalowich JC, Day BW: Myeloperoxidase-catalyzed metabolism of etoposide to its quinone and glutathione adduct forms in HL60 cells. Chem Res Toxicol; 2006 Jul;19(7):937-43
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  • Etoposide is a widely used antineoplastic agent that has provided great success in the treatment of childhood leukemias and other malignancies.
  • Unfortunately, its use is associated with the increased risk of development of secondary acute myelogenous leukemias involving translocations at the MLL gene in chromosome band 11q23.
  • Previous studies showed that the phenoxyl radical of etoposide can be generated by myeloperoxidase (MPO), an enzyme prevalent in myeloid progenitor cells that can derive myelogenous leukemias.
  • We hypothesized that etoposide ortho-quinone could therefore form in myeloid progenitor cells and might be a contributor to the development of treatment-related secondary leukemias.
  • MPO-expressing human myeloid leukemia HL60 cells were treated with etoposide for 0.5 h in the presence and absence of the cosubstrate of MPO, hydrogen peroxide.

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  • [ErratumIn] Chem Res Toxicol. 2007 Jul;20(7):1067
  • (PMID = 16841962.001).
  • [ISSN] 0893-228X
  • [Journal-full-title] Chemical research in toxicology
  • [ISO-abbreviation] Chem. Res. Toxicol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090787
  • [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 / Benzoquinones; 0 / DNA Adducts; 3T006GV98U / benzoquinone; 6PLQ3CP4P3 / Etoposide; EC 1.11.1.7 / Peroxidase; GAN16C9B8O / Glutathione
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3. Dłuzniewska A, Balwierz W, Balcerska A, Chybicka A, Dobaczewski G, Kowalczyk J, Krenke K, Lewandowska D, Malinowska I, Matysiak M, Mikołajczyk M, Niedźwiedzki M, Rokicka-Milewska R, Sońta-Jakimczyk D, Stefaniak J, Styczyński J, Tomaszewska R, Wachowiak J, Wysocki M: [Efficacy of idarubicin in the treatment of childhood acute non-lymphoblastic leukemia: report of Polish Pediatric Leukemia/Lymphoma Study Group]. Przegl Lek; 2003;60 Suppl 5:17-21
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  • [Title] [Efficacy of idarubicin in the treatment of childhood acute non-lymphoblastic leukemia: report of Polish Pediatric Leukemia/Lymphoma Study Group].
  • Results of treatment of childhood ANLL remained unsatisfactory for a long time, and introduction of a new drug seemed justified as the EFS achieved in this disease between 1993-97 was 42%.
  • Between 1998 and 2001, 137 children with ANLL were referred to nine participating centers of PPLLSG.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Idarubicin / therapeutic use. Leukemia, Myeloid, Acute / drug therapy


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4. Flotho C, Kratz C, Niemeyer CM: Targeting RAS signaling pathways in juvenile myelomonocytic leukemia. Curr Drug Targets; 2007 Jun;8(6):715-25
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  • [Title] Targeting RAS signaling pathways in juvenile myelomonocytic leukemia.
  • The RAS proteins function as fundamental signaling switches that control normal cell growth and differentiation.
  • Juvenile myelomonocytic leukemia (JMML) is a rapidly fatal myeloproliferative disorder of early childhood for which no effective treatment other than hematopoietic stem cell transplantation is currently available.
  • Here we give an overview of current concepts on the pathogenesis of JMML, present important aspects of cellular RAS biology that can be exploited for pharmacologic manipulation, and discuss mouse models that have greatly advanced our understanding of the role RAS plays in JMML.
  • In addition, we review recent approaches to develop agents that interfere with the RAS network at the level of the granulocyte-macrophage colony-stimulating factor receptor, posttranslational RAS processing (prenylation and endoprotease cleavage), RAF serine/threonine kinase, MEK mitogen-activated protein kinase, and target of rapamycin activity.
  • Preclinical and clinical data of these pharmaceuticals in JMML and other myeloid malignancies is discussed.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Child. Disease Models, Animal. Humans. Mice. ras Proteins / drug effects. ras Proteins / metabolism

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  • (PMID = 17584027.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.6.5.2 / ras Proteins
  • [Number-of-references] 97
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5. Cohen RJ, Curtis RE, Inskip PD, Fraumeni JF Jr: The risk of developing second cancers among survivors of childhood soft tissue sarcoma. Cancer; 2005 Jun 1;103(11):2391-6
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  • [Title] The risk of developing second cancers among survivors of childhood soft tissue sarcoma.
  • RESULTS: Twenty-seven children developed 28 subsequent primary malignancies, compared with 4.5 expected malignancies based on general population rates (observed-to-expected [O/E] ratio = 6.3 (95% confidence interval [95% CI], 4.2-9.1).
  • The risk of developing a subsequent malignancy was increased among children with rhabdomyosarcoma (observed = 11 malignancies; O/E ratio = 7.7), fibromatous neoplasms (observed = 9 malignancies; O/E ratio = 5.8), and other specified STS (observed = 7 malignancies; O/E ratio = 6.5).
  • Initial therapy with radiation and chemotherapeutic agents was associated with a significantly higher risk of second malignancies compared with surgery alone (O/E ratio = 15.2 vs. 1.4; P < 0.0001).
  • Elevated risks were observed for acute myeloid leukemia, cutaneous melanoma, female breast cancer, and sarcomas of the bone and soft tissue, with generally higher risks among patients who initially received combined modality therapy.
  • For several children, the pattern of multiple malignancies was consistent with a genetic syndrome, particularly neurofibromatosis type 1 and Li-Fraumeni syndrome.
  • CONCLUSIONS: The risk of second malignancies was increased for all histologic types of childhood STS and was particularly high among patients who received combined modality therapy.

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  • (PMID = 15852362.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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6. van Casteren NJ, van der Linden GH, Hakvoort-Cammel FG, Hählen K, Dohle GR, van den Heuvel-Eibrink MM: Effect of childhood cancer treatment on fertility markers in adult male long-term survivors. Pediatr Blood Cancer; 2009 Jan;52(1):108-12
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  • [Title] Effect of childhood cancer treatment on fertility markers in adult male long-term survivors.
  • BACKGROUND: Although it is accepted that pediatric cancer treatment harbors a risk of gonadal damage, large cohort studies using up-to-date fertility markers are lacking.
  • PROCEDURE: The aim of our study was to evaluate the gonadal toxicity of childhood cancer treatment using fertility markers.
  • We included 248 adult male long-term survivors of childhood cancer.
  • Significantly decreased Inhibin B levels and increased FSH levels were found in men treated for Hodgkin and non-Hodgkin lymphoma, acute-myeloid leukemia, neuroblastoma, and sarcoma as compared to other malignancies.
  • CONCLUSIONS: Severe gonadal impairment is a risk in a considerable subgroup of childhood cancer survivors based on current fertility markers like Inhibin B.
  • [MeSH-major] Fertility / drug effects. Infertility / diagnosis. Neoplasms / complications. Survivors
  • [MeSH-minor] Biomarkers / analysis. Child, Preschool. Cyclophosphamide / adverse effects. Female. Follicle Stimulating Hormone / analysis. Follow-Up Studies. Gonads / drug effects. Gonads / physiopathology. Humans. Inhibins / analysis. Leukemia, Myeloid, Acute / complications. Lymphoma / complications. Male. Neuroblastoma / complications. Procarbazine / adverse effects. Sarcoma / complications

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  • (PMID = 18819129.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / inhibin B; 35S93Y190K / Procarbazine; 57285-09-3 / Inhibins; 8N3DW7272P / Cyclophosphamide; 9002-68-0 / Follicle Stimulating Hormone
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7. Zhang JB, Sun Y, Dong J, Liu LX, Ning F: [Expression of lung resistance protein and multidrug resistance-associated protein in naive childhood acute leukemia and their clinical significance]. Ai Zheng; 2005 Aug;24(8):1015-7
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  • [Title] [Expression of lung resistance protein and multidrug resistance-associated protein in naive childhood acute leukemia and their clinical significance].
  • BACKGROUND & OBJECTIVE: Previous studies revealed that lung resistance protein (LRP) and multidrug resistance-associated protein (MRP) relate to drug resistance of childhood leukemia, which is not caused by only one mechanism.
  • This study was to evaluate the expression of LRP and MRP genes in childhood leukemia and their correlation.
  • METHODS: The expression of LRP and MRP in 38 children with acute leukemia and 6 healthy children were measured with reverse transcription-polymerase chain reaction (RT-PCR); their clinical significance was analyzed according to complete remission (CR) rate of the patients after chemotherapy.
  • The positive rate of LRP was significantly lower in acute lymphoblastic leukemia (ALL) than in acute nonlymphocytic leukemia (ANLL) [18.5% (5/27) vs. 45.5% (6/11), P < 0.05]; however, the positive rate of MRP was 59.3% (16/27) in ALL, and 45.5% (5/11) in ANLL (P > 0.05).
  • CONCLUSION: Childhood acute leukemia patients with overexpression of LRP and MRP suffer severe disease and achieve low remission rateû lower remission rate of childhood ANLL patients may relate to LRP expression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Multidrug Resistance-Associated Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vault Ribonucleoprotein Particles / metabolism

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  • (PMID = 16086885.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
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8. Brassesco MS, Montaldi AP, Gras DE, Camparoto ML, Martinez-Rossi NM, Scrideli CA, Tone LG, Sakamoto-Hojo ET: Cytogenetic and molecular analysis of MLL rearrangements in acute lymphoblastic leukaemia survivors. Mutagenesis; 2009 Mar;24(2):153-60
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  • [Title] Cytogenetic and molecular analysis of MLL rearrangements in acute lymphoblastic leukaemia survivors.
  • The successful treatment of paediatric malignancies by multimodal therapy has improved outcomes for children with cancer, especially those with acute lymphoblastic leukaemia (ALL).
  • Depending on dosage, 2-12% of patients treated with topoisomerase II inhibitors and/or alkylating agents develop treatment-related acute myeloid leukaemia characterized by translocations at 11q23.
  • Our goal was to study MLL rearrangements in peripheral lymphocytes using cytogenetic and molecular methods in order to evaluate the late effects of cancer therapy in patients previously treated for childhood ALL.
  • Chromosomal rearrangements at 11q23 were analysed in cytogenetic preparations from 49 long-term ALL survivors and 49 control individuals.
  • Thirty-five patients (81%) presented putative translocations; among those, 91% corresponded with t(4;11) (q21;q23), while the other 9% corresponded with t(11;X), t(8;11)(q23;q23) and t(11;16).
  • Our results indicate an increase in MLL aberrations in childhood ALL survivors years after completion of therapy.
  • The higher frequency in this cohort might be associated with therapy using anti-tumoural drugs, independent of the inclusion of topoisomerase II inhibitors.
  • Even though the biological significance of these rearrangements needs further investigation, they demonstrate a degree of genome instability, indicating the relevance of cytogenetic and molecular studies during the follow-up of patients in complete clinical remission.
  • [MeSH-major] Cytogenetic Analysis. Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Survivors

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  • (PMID = 19028982.001).
  • [ISSN] 1464-3804
  • [Journal-full-title] Mutagenesis
  • [ISO-abbreviation] Mutagenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; 957E6438QA / Teniposide
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9. Ansari M, Krajinovic M: Pharmacogenomics in cancer treatment defining genetic bases for inter-individual differences in responses to chemotherapy. Curr Opin Pediatr; 2007 Feb;19(1):15-22
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  • PURPOSE OF REVIEW: Pharmacogenomics is evolving rapidly due to the expansion of genomics and proteomics, the emerging technologies, knowledge of the molecular basis of neoplasms and of drug pathways.
  • This article will give an update on the genetic basis of variable therapeutic responses to anticancer agents in children.
  • RECENT FINDINGS: The majority of recent findings concern the pharmacogenetics of key components of acute lymphoblastic leukemia treatment, 6-mercaptopurine and methotrexate.
  • This is not surprising given that leukemia is the most common cancer affecting children, accounting for 25-35% of childhood malignancies worldwide with acute lymphoblastic leukemia comprising 80% of leukemia cases.
  • In certain patients treatment fails due to drug resistance, rendering acute lymphoblastic leukemia the leading cause of cancer-related death in children.
  • Recent findings relating to other childhood tumors and the potential to optimize treatment of these malignancies are briefly discussed.
  • SUMMARY: Interindividual differences in drug responses are an important cause of resistance to treatment and adverse drug reactions.
  • Pharmacogenetics tends to identify the genetic basis of these suboptimal responses allowing traditional treatment to be complemented by genotype-based drug dose adjustment.
  • [MeSH-major] Genetic Variation. Neoplasms / drug therapy. Neoplasms / genetics
  • [MeSH-minor] Child. Child, Preschool. Drug Resistance, Neoplasm. Genetic Predisposition to Disease. Genotype. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Pharmacogenetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis

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  • (PMID = 17224657.001).
  • [ISSN] 1040-8703
  • [Journal-full-title] Current opinion in pediatrics
  • [ISO-abbreviation] Curr. Opin. Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 53
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10. Goellner S, Steinbach D, Schenk T, Gruhn B, Zintl F, Ramsay E, Saluz HP: Childhood acute myelogenous leukaemia: association between PRAME, apoptosis- and MDR-related gene expression. Eur J Cancer; 2006 Nov;42(16):2807-14
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  • [Title] Childhood acute myelogenous leukaemia: association between PRAME, apoptosis- and MDR-related gene expression.
  • The mRNA level of PRAME is used as a tumour marker due to its overexpression in various malignancies.
  • Furthermore, it is known that the overexpression of genes encoding antiapoptotic proteins leads to the survival of leukaemic cells via exclusion of apoptosis.
  • On the other hand, overexpression of genes encoding ABC transporters may lead to multi drug resistance (MDR).
  • Therefore, we investigated whether there is a relationship between PRAME overexpression and the expression of apoptosis- and MDR-related genes in childhood de novo acute myelogenous leukaemia (AML) patient samples and, furthermore, whether this is a general or an AML-subtype specific event.
  • Microarray analysis and real time quantitative PCR revealed that clinical samples showing PRAME upregulation are associated with a decreasing expression of genes coding for apoptotic proteins and an overexpression of genes encoding ABC transporters.
  • [MeSH-major] Antigens, Neoplasm / genetics. Genes, MDR / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Apoptosis. Child. Child, Preschool. Drug Resistance, Multiple / genetics. Female. Gene Expression. Humans. Infant. Infant, Newborn. Male. Microarray Analysis. Up-Regulation

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  • (PMID = 16978861.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / PRAME protein, human
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11. Peters GJ, van der Wilt CL, van Moorsel CJ, Kroep JR, Bergman AM, Ackland SP: Basis for effective combination cancer chemotherapy with antimetabolites. Pharmacol Ther; 2000 Aug-Sep;87(2-3):227-53
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  • (1) possible metabolic and biological interactions between drugs, (2) scheduling, and (3) different pharmacokinetic profiles.
  • Ideally, the combination of two or more agents should be more effective than each agent separately (synergism), although additive and even antagonistic combinations may result in a higher therapeutic efficacy in the clinic.
  • The median-drug effect analysis method is one of the most widely used methods for in vitro evaluation of combinations.
  • Several examples of classical effective antimetabolite-(anti)metabolite combinations are discussed, such as that of methotrexate with 6-mercaptopurine or leucovorin in (childhood) leukemia and 5-fluorouracil (5FU) with leucovorin in colon cancer.
  • More recent combinations include treatment of acute-myeloid leukemia with fludarabine and arabinosylcytosine.
  • Other combinations, currently frequently used in the treatment of solid malignancies, include an antimetabolite with a DNA-damaging agent, such as gemcitabine with cisplatin and 5FU with the cisplatin analog oxaliplatin.
  • The latter combinations have dramatically changed the treatment of incurable cancers, such as lung and colon cancer, and have demonstrated that rationally designed drug combinations offer new possibilities to treat solid malignancies.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Fluorouracil / pharmacology. Neoplasms / drug therapy
  • [MeSH-minor] Colonic Neoplasms / drug therapy. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Deoxycytidine Kinase / metabolism. Drug Therapy / trends. Humans. Leucovorin / pharmacology. Leukemia / drug therapy. Thymidylate Synthase / metabolism

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  • (PMID = 11008002.001).
  • [ISSN] 0163-7258
  • [Journal-full-title] Pharmacology & therapeutics
  • [ISO-abbreviation] Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.1.1.45 / Thymidylate Synthase; EC 2.7.1.74 / Deoxycytidine Kinase; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
  • [Number-of-references] 229
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12. Deschler B, Lübbert M: Acute myeloid leukemia: epidemiology and etiology. Cancer; 2006 Nov 1;107(9):2099-107
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  • [Title] Acute myeloid leukemia: epidemiology and etiology.
  • Acute myeloid leukemias (AMLs) are infrequent, yet highly malignant neoplasms responsible for a large number of cancer-related deaths.
  • It continuously shows 2 peaks in occurrence in early childhood and later adulthood.
  • To estimate outcome and discuss informed treatment decisions with AML patients of different age groups and different biologic risk categories, it is mandatory to consider that the outcome results reported in clinical trials were until now heavily biased toward younger patients, whereas the overall dismal prognosis documented in population-based studies most likely reflects the exclusion of older patients from aggressive treatment.
  • The etiology for most cases of AML is unclear, but a growing knowledge concerning leukemogenenic agents within chemotherapy regimens for other malignancies is already available.
  • This includes specific associations of the most frequent balanced translocations in AML, including the "good-risk" abnormalities comprised by the core binding factor leukemias (i.e., AML with the translocation (8;21) and inversion of chromosome 16, and acute promyelocytic leukemia with the translocation (15;17)).
  • In contrast to these genetic alterations, epigenetic lesions, e.g., promoter silencing by hypermethylation of the p15/INK4b and other genes, are increasingly recognized as important in the pathogenesis of AML.
  • [MeSH-major] Leukemia, Myeloid / epidemiology. Leukemia, Myeloid / etiology

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17019734.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 89
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13. Zwerdling T, Krailo M, Monteleone P, Byrd R, Sato J, Dunaway R, Seibel N, Chen Z, Strain J, Reaman G, Children's Oncology Group: Phase II investigation of docetaxel in pediatric patients with recurrent solid tumors: a report from the Children's Oncology Group. Cancer; 2006 Apr 15;106(8):1821-8
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  • [Title] Phase II investigation of docetaxel in pediatric patients with recurrent solid tumors: a report from the Children's Oncology Group.
  • BACKGROUND: Docetaxel, which is an antitubulin agent, has demonstrable activity against murine and human tumors.
  • The current study was designed to determine response rates to docetaxel in various strata of recurrent solid tumors of childhood and to assess toxicity in a group of patients who were assigned to receive it.
  • RESULTS: There were no deaths attributable to study drug.
  • One patient each had acute myeloid leukemia, acute lymphoid leukemia, and high-grade glioma reported as secondary malignancies.
  • CONCLUSIONS: Docetaxel demonstrated activity in patients with recurrent Ewing sarcoma but was found to be ineffective for treating the other types of recurrent solid tumors that were studied.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Glioma / drug therapy. Glioma / secondary. Neoplasm Recurrence, Local / drug therapy. Sarcoma / drug therapy. Sarcoma / secondary. Taxoids / therapeutic use

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DOCETAXEL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532433.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
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