[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 414
1. Grundler R, Miething C, Thiede C, Peschel C, Duyster J: FLT3-ITD and tyrosine kinase domain mutants induce 2 distinct phenotypes in a murine bone marrow transplantation model. Blood; 2005 Jun 15;105(12):4792-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Activating mutations of the Fms-like tyrosine kinase 3 (FLT3) receptor are the most common genetic alteration in acute myeloid leukemia (AML).
  • Recently, point mutations within the activation loop of FLT3 have also been described in childhood acute lymphoblastic leukemia (ALL).
  • The lymphoid manifestation and longer latency of FLT3-TKD compared with FLT3-ITD mutants together with the lack of influence of FLT3-TKD mutations on the clinical outcome of patients with AML suggest differences in cell signaling between FLT3-TKD mutants and FLT3-ITDs.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Tyrosine Kinases / chemistry. Proto-Oncogene Proteins / chemistry. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / chemistry. Receptor Protein-Tyrosine Kinases / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15718420.001).
  • [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 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Milk Proteins; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


2. Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C: Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Dec;171(2):122-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
  • The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.
  • We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics
  • [MeSH-minor] Child. Humans. Male. Molecular Sequence Data

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17116492.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB040537/ AB040538
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Number-of-references] 12
  •  go-up   go-down


3. Hollink IH, van den Heuvel-Eibrink MM, Zimmermann M, Balgobind BV, Arentsen-Peters ST, Alders M, Willasch A, Kaspers GJ, Trka J, Baruchel A, de Graaf SS, Creutzig U, Pieters R, Reinhardt D, Zwaan CM: Clinical relevance of Wilms tumor 1 gene mutations in childhood acute myeloid leukemia. Blood; 2009 Jun 4;113(23):5951-60
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical relevance of Wilms tumor 1 gene mutations in childhood acute myeloid leukemia.
  • Wilms tumor 1 (WT1) mutations have recently been identified in approximately 10% of adult acute myeloid leukemia (AML) with normal cytogenetics (CN-AML) and are associated with poor outcome.
  • Using array-based comparative genome hybridization in pediatric CN-AML samples, we detected a WT1 deletion in one sample.
  • This prompted us to further investigate the role of WT1 aberrations in childhood AML.
  • Mutations were found in 35 of 298 (12%) diagnostic pediatric AML samples.
  • WT1 mutations clustered significantly in the CN-AML subgroup (22%; P < .001) and were associated with FLT3/ITD (43 vs 17%; P < .001).
  • WT1 mutations occur at a significant rate in childhood AML and are a novel independent poor prognostic marker.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. WT1 Proteins / metabolism
  • [MeSH-minor] Base Sequence. Child. Child, Preschool. Female. Humans. Male. Multivariate Analysis. Mutation / genetics. Prognosis. Recurrence. Survival Rate


Advertisement
4. Poppe B, Yigit N, De Moerloose B, De Paepe A, Benoit Y, Speleman F: HOXA gene cluster rearrangement in a t(7;9)(p15;q34) in a child with MDS. Cancer Genet Cytogenet; 2005 Oct 1;162(1):82-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HOXA gene cluster rearrangement in a t(7;9)(p15;q34) in a child with MDS.
  • We describe the molecular characterization of a t(7;9)(p15;q34) found in a 15-month-old female patient, diagnosed with refractory anemia with excess blasts in transformation (RAEBt), in progression to acute myeloid leukemia (AML) M7.
  • Our findings suggest a causal role for HOXA genes in childhood myelodysplasia and warrant investigation of this locus in a larger series of patients.

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16157206.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  •  go-up   go-down


5. Barnard DR, Alonzo TA, Gerbing RB, Lange B, Woods WG, Children's Oncology Group: Comparison of childhood myelodysplastic syndrome, AML FAB M6 or M7, CCG 2891: report from the Children's Oncology Group. Pediatr Blood Cancer; 2007 Jul;49(1):17-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of childhood myelodysplastic syndrome, AML FAB M6 or M7, CCG 2891: report from the Children's Oncology Group.
  • BACKGROUND: Myelodysplastic syndromes (MDS), acute erythroleukemia (FAB M6), and acute megakaryocytic leukemia (FAB M7) have overlapping features.
  • PROCEDURE: Children without Down syndrome or acute promyelocytic leukemia who were newly diagnosed with primary myelodysplastic syndrome or acute myeloid leukemia (AML) M6 or M7 were compared to children with de novo AML M0-M5.
  • RESULTS: The presentation and outcomes of the 132 children diagnosed with MDS (60 children), AML FAB M6 (19 children), or AML FAB M7 (53 children) were similar.
  • Children with AML FAB M7 were diagnosed at a significantly younger age (P = 0.001).
  • All three groups had significantly inferior overall survival (OS) (P < 0.001) and event free survival (P < 0.001) compared with the 748 children diagnosed with AML FAB M0-M5 when assessed from entry on study.
  • However, when assessed from successful completion of induction therapy, the 5-year OS (P = 0.090)(49.1 vs. 56.9%) and disease-free survival (DFS) (P = 0.113)(38.0 vs. 46.3%) therapy were not significantly different from other children with AML.
  • CONCLUSIONS: Childhood AML FAB M6 and AML M7 resemble MDS in presentation, poor induction success rates, and outcomes.
  • [MeSH-major] Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Prognosis. Remission Induction. Survival Rate. Treatment Outcome


6. Choi HW, Shin MG, Sawyer JR, Cho D, Kee SJ, Baek HJ, Kook H, Kim HJ, Shin JH, Suh SP, Hwang TJ, Ryang DW: Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22). Cancer Genet Cytogenet; 2006 Jun;167(2):172-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22).
  • We report on a case of pediatric acute myelocytic leukemia showing 47,XX,+10,t(16;21)(p11;q22) that resulted in an unusual TLS/FUS-ERG chimeric transcript.
  • The leukemic cells showed erythrophagocytosis, positive reactions for myeloperoxidase and Sudan black B stains, and negative reactions for periodic acid-Schiff and alpha-naphtyl butyrate esterase stains as well as expression of myeloid antigens.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Bone Marrow Cells / cytology. Child, Preschool. Chromosomes, Human, Pair 10. Female. Humans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Trisomy

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16737920.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
  •  go-up   go-down


7. Bellezza I, Tucci A, Minelli A: 2-Chloroadenosine and human prostate cancer cells. Anticancer Agents Med Chem; 2008 Oct;8(7):783-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cladribine, i.e.2-deoxy-Chloroadenosine is currently in use as chemotherapeutic agent in chronic lymphoid malignancies and pediatric acute myelogenous leukemia whereas the structurally related counterpart, 2-Chloroadenosine, has been less studied.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18855579.001).
  • [ISSN] 1871-5206
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-23; 0 / Receptor, PAR-1; 146-77-0 / 2-Chloroadenosine
  • [Number-of-references] 137
  •  go-up   go-down


8. Eden T: Aetiology of childhood leukaemia. Cancer Treat Rev; 2010 Jun;36(4):286-97
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aetiology of childhood leukaemia.
  • The acute leukaemias account for about 30% of all malignancy seen in childhood across the Western world.
  • From twin studies and the use of neonatal blood spots it has been possible to back track the first initiating genetic events within critical haemopoietic cells to foetal development in utero for most precursor B cell ALL and some cases of AML.
  • For some leukaemias (e.g. infant MLL positive ALL) the first event appears adequate to create a malignant clone but for the majority of ALL and AML further 'genetic' changes are required, probably postnatal.
  • Many environmental factors have been proposed as causative for leukaemia but only ionising irradiation and certain chemicals, e.g. benzene and cytotoxics (alkylators and topoisomerase II inhibitors) have been confirmed and then principally for acute myeloid leukaemia.
  • It appears increasingly likely that delayed, dysregulated responses to 'common' infectious agents play a major part in the conversion of pre-leukaemic clones into overt precursor B cell ALL, the most common form of childhood leukaemia.
  • High penetrance germ-line mutations are involved in only about 5% of childhood leukaemias (more in AML than ALL).
  • There is no single cause for childhood leukaemia and for most individuals a combination of factors appears to be necessary; all involving gene-environment interactions.
  • [MeSH-major] Leukemia / etiology
  • [MeSH-minor] Alcohol Drinking / adverse effects. Background Radiation / adverse effects. Child. Electromagnetic Fields. Folic Acid / metabolism. Genetic Predisposition to Disease. Humans. Incidence. Seasons. Smoking / adverse effects

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FOLIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010. Published by Elsevier Ltd.
  • (PMID = 20223594.001).
  • [ISSN] 1532-1967
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid
  • [Number-of-references] 141
  •  go-up   go-down


9. Hawkins LM, Jayanthan AA, Narendran A: Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity. Pediatr Res; 2005 Mar;57(3):430-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity.
  • As more and more effective targeted therapeutics have been developed to treat adults with cancer, it is of critical importance to devise appropriate in vitro experimental models to study their use in pediatric patients.
  • Acute lymphoblastic leukemia (ALL) with Bcr-Abl translocation is one of the most difficult to treat and deadly diseases in children.
  • Recently, the geldanamycin family of antibiotics has been found to induce apoptosis in many malignant cells, including adult CML and AML.
  • Pediatric ALL cell lines with varying Bcr-Abl status and imatinib mesylate sensitivity were generated and their growth inhibition by 17-AAG was studied in vitro.
  • We describe an experimental approach to investigate the complex interaction between Bcr-Abl status, imatinib mesylate sensitivity, and 17-AAG in pediatric ALL.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Genes, abl. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Rifabutin / analogs & derivatives
  • [MeSH-minor] Adult. Apoptosis / drug effects. Benzamides. Benzoquinones. Cell Line, Tumor. Cell Survival / drug effects. Child. Drug Therapy, Combination. Humans. Imatinib Mesylate. Lactams, Macrocyclic. Protein Kinase Inhibitors / metabolism. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use


10. Zwaan CM, den Boer ML, Kazemier KM, Hählen K, Loonen AH, Reinhardt D, Creutzig U, Kaspers GJ, Pieters R: Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia? Blood; 2006 Jun 15;107(12):4975-6; author reply 4976-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia?
  • [MeSH-major] Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Adult. Age Factors. Antibodies, Monoclonal / chemistry. Child. Child, Preschool. Cyclosporine / pharmacology. Female. Flow Cytometry. Humans. Male. Randomized Controlled Trials as Topic. Remission Induction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • (PMID = 16754781.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / P-Glycoprotein; 83HN0GTJ6D / Cyclosporine
  •  go-up   go-down


11. Anagnostopoulos C, Jadwat Y, Wood NH, Meyerov R, Lemmer J, Bouckaert M, Feller L: A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo. SADJ; 2007 Oct;62(9):390, 392-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo.
  • Acute myeloid leukaemia (AML), characterized by proliferation of immature neoplastic myeloid cells, is uncommon in childhood.
  • We present a case of an 8-year-old girl with AML-M4Eo who had an extramedullary leukaemic tumour in the oral cavity.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / pathology. Mouth Neoplasms / pathology
  • [MeSH-minor] Bone Marrow Neoplasms / pathology. Child. Diagnosis, Differential. Eosinophilia / pathology. Fatal Outcome. Female. Humans. Immunophenotyping / methods. Sepsis / drug therapy

  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18260548.001).
  • [ISSN] 1029-4864
  • [Journal-full-title] SADJ : journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging
  • [ISO-abbreviation] SADJ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] South Africa
  •  go-up   go-down


12. Spanaki A, Perdikogianni C, Linardakis E, Kalmanti M: Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia. Leuk Res; 2007 May;31(5):639-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia.
  • The purpose of this study was to investigate PRAME expression levels in children with acute leukemia with real-time PCR analysis.
  • Seventeen children with newly diagnosed or relapsed acute leukemia (11 ALL, 4 AML, 1 acute myeloblastic leukemia secondary to MDS, 1 ALL at relapse) and a control group of seven children were studied.
  • Overexpression of PRAME was found in 52.9% (3 AML, 6 ALL) of the patients studied.
  • The above findings indicate that PRAME expression in acute leukemia does not seem to be of prognostic significance, whereas it might represent a candidate marker for the monitoring of minimal residual disease.
  • [MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Leukemia, Myeloid / genetics. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Humans. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16860864.001).
  • [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 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
  •  go-up   go-down


13. Shimada A, Taki T, Tabuchi K, Tawa A, Horibe K, Tsuchida M, Hanada R, Tsukimoto I, Hayashi Y: KIT mutations, and not FLT3 internal tandem duplication, are strongly associated with a poor prognosis in pediatric acute myeloid leukemia with t(8;21): a study of the Japanese Childhood AML Cooperative Study Group. Blood; 2006 Mar 1;107(5):1806-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] KIT mutations, and not FLT3 internal tandem duplication, are strongly associated with a poor prognosis in pediatric acute myeloid leukemia with t(8;21): a study of the Japanese Childhood AML Cooperative Study Group.
  • Patients with t(8;21) acute myeloid leukemia (AML) are considered to have a good prognosis; however, approximately 50% of them relapse.
  • The genetic alterations associated with a poor outcome in t(8;21) AML remain unknown.
  • Recently, aberrations of receptor tyrosine kinases (RTKs) were frequently found in patients with AML.
  • However, the prevalence and prognostic impact of RTK aberrations in pediatric t(8;21) AML remains undetermined.
  • Here, we found the kinase domain mutations of the KIT gene in 8 (17.4%) of 46 patients with t(8;21) AML among newly diagnosed pediatric patients with AML treated on the AML99 protocol in Japan.
  • These results suggested that KIT mutations are strongly associated with a poor prognosis in pediatric t(8;21) AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Child. DNA Mutational Analysis / methods. Disease-Free Survival. Female. Humans. Infant. Male. Prevalence. Prognosis


14. Sung L, Gamis A, Alonzo TA, Buxton A, Britton K, Deswarte-Wallace J, Woods WG: Infections and association with different intensity of chemotherapy in children with acute myeloid leukemia. Cancer; 2009 Mar 1;115(5):1100-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infections and association with different intensity of chemotherapy in children with acute myeloid leukemia.
  • BACKGROUND: The objectives were to compare infections during different intensities of therapy in children with acute myeloid leukemia (AML).
  • METHODS: Subjects were children enrolled in Children's Cancer Group 2891 with AML.
  • This information sheds insight into the mechanisms behind susceptibility and outcome of infections in pediatric AML.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 American Cancer Society.
  • [Cites] J Clin Oncol. 2000 May;18(9):1845-55 [10784625.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] Clin Infect Dis. 2002 Jan 1;34(1):7-14 [11731939.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Nov;24(8):627-35 [12439034.001]
  • [Cites] Leukemia. 2004 Jan;18(1):72-7 [14586478.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4384-93 [15514380.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):1179-87 [9508206.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):436-44 [10460604.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Ann Intern Med. 2005 Jun 21;142(12 Pt 1):979-95 [15968013.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5207-15 [17114653.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3532-9 [17660380.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [ErratumIn] Cancer. 2009 Jun 15;115(12):2807
  • (PMID = 19156894.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-08; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA095861; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-06; United States / NCI NIH HHS / CA / CA095861-06; None / None / / U10 CA098543-06
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS107661; NLM/ PMC2677372
  •  go-up   go-down


15. Creutzig U, Büchner T, Sauerland MC, Zimmermann M, Reinhardt D, Döhner H, Schlenk RF: Significance of age in acute myeloid leukemia patients younger than 30 years: a common analysis of the pediatric trials AML-BFM 93/98 and the adult trials AMLCG 92/99 and AMLSG HD93/98A. Cancer; 2008 Feb 1;112(3):562-71
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of age in acute myeloid leukemia patients younger than 30 years: a common analysis of the pediatric trials AML-BFM 93/98 and the adult trials AMLCG 92/99 and AMLSG HD93/98A.
  • BACKGROUND: Data on the impact of age in acute myeloid leukemia (AML) patients <30 years treated in pediatric and adult trials are scarce.
  • METHODS: In all, 891 patients <18 years were treated in the pediatric trials AML-BFM 93/98 and 290 adolescents and young adults (>16 to <30 years) in the AMLCG 92/99 and AMLSG HD93/98A trials.
  • When comparing the same age groups, outcome was similar between the trial groups, which differed from reports concerning acute lymphoblastic leukemia.
  • However, the prognosis decreased after childhood independent of other risk factors.
  • [MeSH-major] Aging / physiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / physiopathology
  • [MeSH-minor] Adolescent. Adult. Blast Crisis / pathology. Bone Marrow / pathology. Child. Child, Preschool. Clinical Trials as Topic. Cytarabine / administration & dosage. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Infant. Infant, Newborn. Male. Prognosis. Risk Factors. Survival Analysis. Treatment Outcome


16. Freycon F, Trombert-Paviot B, Casagranda L, Bertrand Y, Plantaz D, Marec-Bérard P: Trends in treatment-related deaths (TRDs) in childhood cancer and leukemia over time: a follow-up of patients included in the childhood cancer registry of the Rhône-Alpes region in France (ARCERRA). Pediatr Blood Cancer; 2008 Jun;50(6):1213-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trends in treatment-related deaths (TRDs) in childhood cancer and leukemia over time: a follow-up of patients included in the childhood cancer registry of the Rhône-Alpes region in France (ARCERRA).
  • BACKGROUND: We assessed the number and causes of treatment-related deaths (TRDs) in childhood cancer over time and correlated them with adherence to therapeutic guidelines.
  • PROCEDURE: We compared two cohorts of children of the Childhood Cancer Registry of the Rhône-Alpes Region: Cohort I (1987-1992, 909 patients) and Cohort II (1996-1999, 648 patients).
  • No difference was observed in treatment- and transplantation-related deaths in patients with acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but OS was better in patients with AML (P = 0.02).
  • CONCLUSION: Although mortality declined, improved adherence to therapeutic guidelines and more restricted indications of allograft are needed to preclude further treatment- and transplantation-related deaths, particularly among those with leukemia.
  • [MeSH-minor] Central Nervous System Neoplasms / mortality. Central Nervous System Neoplasms / therapy. Child. Cohort Studies. Female. France / epidemiology. Guideline Adherence. Hematopoietic Stem Cell Transplantation / mortality. Humans. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Practice Guidelines as Topic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Registries

  • Genetic Alliance. consumer health - Childhood Cancer.
  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18300318.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


17. Hattori H, Matsuzaki A, Suminoe A, Koga Y, Tashiro K, Hara T: Identification of novel genes with prognostic value in childhood leukemia using cDNA microarray and quantitative RT-PCR. Pediatr Hematol Oncol; 2006 Mar;23(2):115-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of novel genes with prognostic value in childhood leukemia using cDNA microarray and quantitative RT-PCR.
  • The aim of this study was to identify genes distinctively expressed or suppressed in childhood leukemia with different prognoses, using cDNA microarray and quantitative reverse transcription-polymerase chain reaction (RT-PCR).
  • The expression levels of the selected genes by cDNA microarray were quantified in primary leukemic blasts from 44 patients (acute lymphoblastic leukemia, 28; acute myelogenous leukemia (AML), 13; transient myeloproliferative disorder, 3).
  • The expression levels of CDKN2C, CRADD, and IGFBP-2 genes were significantly associated with the event-free survival of the patients in AML.
  • The present results suggest that a combination of cDNA microarray and quantitative RT-PCR may be useful to identify novel genes with prognostic value in childhood AML.
  • [MeSH-major] Genes, Neoplasm. Leukemia / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adolescent. CRADD Signaling Adaptor Protein. Caspase 2. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p18 / genetics. Cysteine Endopeptidases / genetics. Female. Gene Expression Profiling. Humans. Infant. Infant, Newborn. Insulin-Like Growth Factor Binding Protein 2 / genetics. Male. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Prognosis. Protein-Serine-Threonine Kinases / genetics. Receptor-Interacting Protein Serine-Threonine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / genetics

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16651240.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CDKN2C protein, human; 0 / CRADD Signaling Adaptor Protein; 0 / CRADD protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p18; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Neoplasm Proteins; 0 / Tumor Necrosis Factor Receptor-Associated Peptides and Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / RIPK1 protein, human; EC 2.7.11.1 / Receptor-Interacting Protein Serine-Threonine Kinases; EC 3.4.22.- / CASP2 protein, human; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Cysteine Endopeptidases
  •  go-up   go-down


18. Heng JL, Chen YC, Quah TC, Liu TC, Yeoh AE: Dedicated cytogenetics factor is critical for improving karyotyping results for childhood leukaemias - experience in the National University Hospital, Singapore 1989-2006. Ann Acad Med Singapore; 2010 Feb;39(2):102-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dedicated cytogenetics factor is critical for improving karyotyping results for childhood leukaemias - experience in the National University Hospital, Singapore 1989-2006.
  • INTRODUCTION: Childhood leukaemia accounts for more than 40% of new childhood cancer cases.
  • Unfortunately, karyotyping of childhood leukaemia is difficult, laborious and often unsuccessful.
  • Among them, 369 newly diagnosed and relapsed childhood acute leukaemia cases [281 acute lymphoblastic leukaemia (ALL) and 88 acute myeloid leukaemia (AML)] have been diagnosed at NUH.
  • For AML, the success rate also was significantly improved (P = 0.04) from 85% (34/40) to 95.8% (46/48).
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosome Aberrations. Humans. Infant. Infant, Newborn. Karyotyping / methods. Laboratories. Singapore. Universities

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20237730.001).
  • [ISSN] 0304-4602
  • [Journal-full-title] Annals of the Academy of Medicine, Singapore
  • [ISO-abbreviation] Ann. Acad. Med. Singap.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
  •  go-up   go-down


19. Marques-Salles Tde J, Mkrtchyan H, Leite EP, Soares-Ventura EM, Muniz MT, Silva EF, Liehr T, Silva ML, Santos N: Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with acute megakaryoblastic leukemia and neurofibromatosis. Cancer Genet Cytogenet; 2010 Jul 15;200(2):167-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with acute megakaryoblastic leukemia and neurofibromatosis.
  • Acute myeloid leukemia in childhood is a heterogeneous group of diseases, and different epidemiologic factors are involved in the etiopathogenesis.
  • Genetic syndromes are one of the predisposing factors of acute myeloid leukemia (AML), including Down syndrome, Bloom syndrome, and neurofibromatosis.
  • Acute megakaryoblastic leukemia (AMKL) is the main subtype in Down syndrome infants, and acquired chromosomal anomalies are closely related to the physiopathology of the illness.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Megakaryoblastic, Acute / genetics. Neurofibromatoses / genetics
  • [MeSH-minor] Female. Genes, p53. Histone-Lysine N-Methyltransferase. Humans. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics

  • Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.
  • Genetic Alliance. consumer health - Neurofibromatosis.
  • MedlinePlus Health Information. consumer health - Neurofibromatosis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20620601.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


20. Oliansky DM, Rizzo JD, Aplan PD, Arceci RJ, Leone L, Ravindranath Y, Sanders JE, Smith FO 3rd, Wilmot F, McCarthy PL Jr, Hahn T: The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myeloid leukemia in children: an evidence-based review. Biol Blood Marrow Transplant; 2007 Jan;13(1):1-25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myeloid leukemia in children: an evidence-based review.
  • Clinical research examining the role of hematopoietic stem cell transplantation (SCT) in the therapy of acute myeloid leukemia (AML) in children is presented and critically evaluated in this systematic evidence-based review.
  • Treatment recommendations based on the evidence are presented in the table entitled "Summary of Treatment Recommendations Made by the Expert Panel for Pediatric Acute Myeloid Leukemia" and were reached unanimously by a panel of experts in AML.
  • The identified priority areas of needed future research in pediatric AML include: What is the role of risk group stratification, including the role of cytogenetics, in selection of patients for allogeneic SCT, especially those in first CR?
  • and What is the role of biologically targeted agents (ie, tyrosine kinase inhibitors, farnesyl transferase inhibitors, Flt-3 inhibitors, etc) in the treatment of AML, including induction, consolidation, conditioning regimens, and after SCT?
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Transplantation. Child. Child, Preschool. Evidence-Based Medicine. Humans. Remission Induction / methods. Transplantation Conditioning / methods. Transplantation, Autologous. Transplantation, Homologous

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17222748.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 69
  •  go-up   go-down


21. Fronkova E, Madzo J, Zuna J, Reznickova L, Muzikova K, Hrusak O, Stary J, Trka J: TEL/AML 1 real-time quantitative reverse transcriptase PCR can complement minimal residual disease assessment in childhood ALL. Leukemia; 2005 Jul;19(7):1296-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TEL/AML 1 real-time quantitative reverse transcriptase PCR can complement minimal residual disease assessment in childhood ALL.
  • [MeSH-major] Neoplasm, Residual / diagnosis. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Child. Core Binding Factor Alpha 2 Subunit. Humans. Immunoglobulins / genetics. Prospective Studies. Receptors, Antigen, T-Cell / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15858617.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Immunoglobulins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


22. Blair CK, Roesler M, Xie Y, Gamis AS, Olshan AF, Heerema NA, Robison LL, Ross JA, Children's Oncology Group (COG): Vitamin supplement use among children with Down's syndrome and risk of leukaemia: a Children's Oncology Group (COG) study. Paediatr Perinat Epidemiol; 2008 May;22(3):288-95
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because children with DS have a 50-fold increased risk of developing acute leukaemia during the first 5 years of life, we explored the relation between child vitamin and herbal supplement use and the risk of leukaemia in a case-control study.
  • During the period 1997-2002, we enrolled 158 children with DS aged 0-18 years that were diagnosed with acute lymphoblastic leukaemia (ALL) (n = 97) or acute myeloid leukaemia (AML) (n = 61) at participating Children's Oncology Group institutions.
  • Data were collected via telephone interviews with mothers of the index child regarding use of multivitamins, zinc, vitamin C, iron and herbal supplements, including age at first use, frequency and duration.
  • Among controls, 57% reported regular multivitamin use (>/=3 times/week for >/=3 months) compared with 48% of ALL cases and 61% of AML cases.
  • We found no evidence of an association between children's regular multivitamin use and ALL or AML (adjusted odds ratios [OR] = 0.94 [95% CI 0.52, 1.70] and 1.90 [0.73, 4.91] respectively).
  • There was a suggestion of an increased risk for AML associated with regular multivitamin use during the first year of life or for an extended duration (ORs = 2.38 [0.94, 5.76] and 2.59 [1.02, 6.59] respectively).
  • Future research should include larger sample sizes as well as a full assessment of diet including vitamin supplementation to adequately examine the relation between nutritional status and childhood leukaemia.

  • MedlinePlus Health Information. consumer health - Dietary Supplements.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pediatrics. 1997 Nov;100(5):E4 [9346998.001]
  • [Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1866-72 [15520821.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):40-4 [15390312.001]
  • [Cites] Adv Data. 2004 Nov 9;(349):1-7 [15586828.001]
  • [Cites] J Am Diet Assoc. 2005 May;105(5):763-72; quiz 773-4 [15883554.001]
  • [Cites] Cancer. 2005 Jul 15;104(2):405-10 [15952191.001]
  • [Cites] Proc Nutr Soc. 2005 Nov;64(4):543-53 [16313697.001]
  • [Cites] J Am Diet Assoc. 2006 Jan;106(1 Suppl 1):S52-65 [16376630.001]
  • [Cites] J Pediatr Health Care. 2006 Jan-Feb;20(1):47-54 [16399479.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Mutat Res. 2001 Apr 18;475(1-2):7-20 [11295149.001]
  • [Cites] Ann N Y Acad Sci. 1999;889:87-106 [10668486.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • [Cites] J Am Diet Assoc. 2000 Mar;100(3):371-5 [10719417.001]
  • [Cites] Arch Fam Med. 2000 Mar;9(3):258-62 [10728113.001]
  • [Cites] Dev Med Child Neurol. 2000 Mar;42(3):207-13 [10755461.001]
  • [Cites] Lancet. 2001 Dec 8;358(9297):1935-40 [11747917.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1786-94 [12365028.001]
  • [Cites] Br J Nutr. 2002 Nov;88 Suppl 2:S165-77 [12495459.001]
  • [Cites] Cancer. 2003 Mar 1;97(5):1339-45 [12599243.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):930-8 [12648061.001]
  • [Cites] Lancet. 2003 Apr 12;361(9365):1281-9 [12699967.001]
  • [Cites] Blood. 2004 Jan 15;103(2):399-406 [14512321.001]
  • [Cites] Int J Vitam Nutr Res. 1978;48(2):188-216 [151083.001]
  • [Cites] Endocrinologie. 1988 Apr-Jun;26(2):113-7 [2970667.001]
  • [Cites] Clin Immunol Immunopathol. 1991 Feb;58(2):207-16 [1824686.001]
  • [Cites] Int J Neurosci. 1992 Jul-Aug;65(1-4):259-68 [1341688.001]
  • [Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]
  • [Cites] Cancer Causes Control. 1994 Mar;5(2):141-8 [8167261.001]
  • [Cites] Cancer Causes Control. 1994 Mar;5(2):195-202 [8167267.001]
  • [Cites] N Engl J Med. 1996 May 2;334(18):1150-5 [8602180.001]
  • [Cites] Cancer. 1996 Jan 1;77(1):201-7 [8630931.001]
  • [Cites] Cancer Causes Control. 1997 Sep;8(5):786-802 [9328202.001]
  • [Cites] Am J Epidemiol. 2004 Dec 1;160(11):1098-107 [15561989.001]
  • (PMID = 18426524.001).
  • [ISSN] 1365-3016
  • [Journal-full-title] Paediatric and perinatal epidemiology
  • [ISO-abbreviation] Paediatr Perinat Epidemiol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / R01 CA075169; United States / NCI NIH HHS / CA / R01 CA75169; United States / NCI NIH HHS / CA / U10 CA098543; United States / NIEHS NIH HHS / ES / P30ES10126
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Vitamins
  • [Other-IDs] NLM/ NIHMS378452; NLM/ PMC3365502
  •  go-up   go-down


23. Goulden N, Virgo P, Grimwade D: Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now. Br J Haematol; 2006 Aug;134(3):273-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now.
  • The continued improvement in the prognosis of childhood acute myeloid leukaemia (AML) has been paralleled by the use of increasingly intensive therapy.
  • The article illustrates which children may benefit most from MRD analysis in AML and explores practical issues that should be addressed in the design of clinical trials.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Neoplasm, Residual / drug therapy. Patient Selection. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Clinical Trials as Topic. Drug Costs. Humans. Prognosis. Research Design. Risk Assessment. Salvage Therapy. Stem Cell Transplantation

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16848770.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
  •  go-up   go-down


24. Barbaric D, Byth K, Dalla-Pozza L, Byrne JA: Expression of tumor protein D52-like genes in childhood leukemia at diagnosis: clinical and sample considerations. Leuk Res; 2006 Nov;30(11):1355-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of tumor protein D52-like genes in childhood leukemia at diagnosis: clinical and sample considerations.
  • We used RT-PCR to analyse the expression of three D52-like genes in bone marrow at the time of ALL or AML diagnosis in children.
  • Whereas D53 transcripts were undetectable in all samples, D52 and D54 transcripts were frequently detected in ALL and AML, where they were frequently co-expressed.
  • [MeSH-major] Leukemia, Myeloid. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Proteolipids / genetics. Vesicular Transport Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Cell Line, Tumor. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Infant, Newborn. Male. Myelin and Lymphocyte-Associated Proteolipid Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription, Genetic / genetics

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16620967.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MAL2 protein, human; 0 / Myelin and Lymphocyte-Associated Proteolipid Proteins; 0 / Neoplasm Proteins; 0 / Proteolipids; 0 / TPD52 protein, human; 0 / TPD52L1 protein, human; 0 / TPD52L2 protein, human; 0 / Vesicular Transport Proteins
  •  go-up   go-down


25. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


26. Velardi A, Ruggeri L, Mancusi A, Aversa F, Christiansen FT: Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia. Curr Opin Immunol; 2009 Oct;21(5):525-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia.
  • Donor-versus-recipient natural killer (NK) cell alloreactivity has been established as a key therapeutic element in HLA haplotype mismatched hematopoietic transplants in adult AML and pediatric ALL and as a possible beneficial effector in cord blood transplant for AML.
  • At present NK cell allotherapy for leukemia is deployed through stem cell transplantation (and ensuing NK cell reconstitution) across KIR ligand mismatches.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Adult. Child. Humans. Immunotherapy / methods. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19717293.001).
  • [ISSN] 1879-0372
  • [Journal-full-title] Current opinion in immunology
  • [ISO-abbreviation] Curr. Opin. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 PO1 CA100265
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 46
  •  go-up   go-down


27. Armengol G, Canellas A, Alvarez Y, Bastida P, Toledo JS, Pérez-Iribarne Mdel M, Camós M, Tuset E, Estella J, Coll MD, Caballín MR, Knuutila S: Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia. Leuk Lymphoma; 2010 Jan;51(1):114-24
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.
  • We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH).
  • Six genes (AKT1, RUNX1, LTB, SDC1, RUNX1T1, and JAK2) from the imbalanced regions have been reported to be involved in AML, whereas other 30 cancer genes, not previously reported in an AML context, were identified as imbalanced.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. Male. Polymerase Chain Reaction. Prognosis. Translocation, Genetic


28. Chen SH, Yang CP, Hung IJ, Jaing TH, Shih LY, Tsai MH: Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan. Pediatr Blood Cancer; 2010 Dec 15;55(7):1264-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan.
  • BACKGROUND: Infant leukemia is rare and quite distinct from other childhood leukemias.
  • Differentiating between leukemia and transient myeloproliferative disorder (TMD) in phenotypically normal infants is sometimes difficult.
  • The clinical features and molecular analyses for the fusion transcripts of mixed lineage leukemia (MLL) gene rearrangement in infant leukemia have not been well documented in the Chinese population.
  • PROCEDURE: Forty-five consecutive infants diagnosed with leukemia between 1995 and 2007 in a tertiary medical center in Taiwan were studied.
  • Acute lymphoblastic leukemia (ALL) was diagnosed in 23 infants, acute myeloid leukemia (AML) in 21 (including TMD in 4), and juvenile myelomonocytic leukemia (JMML) in 1.
  • RESULTS: The median white count at diagnosis was higher in ALL than in AML (154.4 × 10(9)/l vs. 58.3 × 10(9)/l, P = 0.05).
  • Chromosome 11q23/MLL abnormalities were present in 77% of ALL and 31% of AML.
  • The 5-year event-free survival (EFS) in infant ALL and AML showed no difference (18% vs. 12%, respectively).
  • However, no factor was associated with an adverse outcome for infants with AML.
  • CONCLUSIONS: The molecular assessments and prognostic factors of infant leukemia in Taiwan mirror those in developed Western countries.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Gene Rearrangement. Humans. Infant. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Leukemia, Myelomonocytic, Juvenile / diagnosis. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / therapy. Leukocyte Count. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloproliferative Disorders / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis. Taiwan. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Pediatr Blood Cancer. 2010 Dec 15;55(7):1247-9 [20981686.001]
  • (PMID = 20979094.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  •  go-up   go-down


29. Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH: CEBPalpha mutations in childhood acute myeloid leukemia. Leukemia; 2005 Mar;19(3):410-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CEBPalpha mutations in childhood acute myeloid leukemia.
  • CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.
  • We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product.
  • Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Clone Cells. DNA Mutational Analysis / methods. Gene Frequency. Humans. Infant. Infant, Newborn. Polymerase Chain Reaction / methods


30. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood acute myelogenous leukaemia: association between PRAME, apoptosis- and MDR-related gene expression.
  • 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.
  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


31. Franklin JL, Seibel NL, Krailo M, Fu C, Adamson PC, Reaman G, Children's Oncology Group: Phase 2 study of docetaxel in the treatment of childhood refractory acute leukemias: a Children's Oncology Group report. Pediatr Blood Cancer; 2008 Mar;50(3):533-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase 2 study of docetaxel in the treatment of childhood refractory acute leukemias: a Children's Oncology Group report.
  • BACKGROUND: To determine the response rate and toxicity of docetaxel when administered as a 60 mg/m(2) dose by 1 hr intravenous (IV) infusion weekly x 3 weeks in children with relapsed acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML).
  • PROCEDURE: Patients who were under the age of 22-year-old at the time of the original ALL or AML diagnosis and in a second relapse were accrued from August 2002 to May 2005 for this Children's Oncology Group (COG) phase 2 study (ADVL0023).
  • Ten patients with ALL and two patients with AML were enrolled.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Leukemia / drug therapy. Salvage Therapy. Taxoids / therapeutic use
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Bone Marrow Diseases / chemically induced. Child. Child, Preschool. Drug Administration Schedule. Female. Fever / etiology. Humans. Infant. Infusions, Intravenous. Leukemia, Myeloid / drug therapy. Male. Neutropenia / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Failure

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17668867.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  •  go-up   go-down


32. Lehrnbecher T, Bernig T, Hanisch M, Koehl U, Behl M, Reinhardt D, Creutzig U, Klingebiel T, Chanock SJ, Schwabe D: Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia. Leukemia; 2005 Oct;19(10):1745-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia.
  • Infectious complications represent a substantial cause of morbidity and mortality in children undergoing therapy for acute myeloid leukemia (AML).
  • Since it has been shown that alterations in innate immune pathways contribute to the risk for serious infections, we analyzed well-characterized variants in innate immune genes (TNF, IL6, IL8, MPO, CHIT, FCGR2A, TLR2, and TLR4) to determine their possible contribution to infectious complications during therapy for pediatric AML.
  • The study population consisted of 168 North European Caucasian children enrolled on the clinical trial AML-BFM 93.
  • Our data suggest that variant alleles of both IL6 and CHIT could influence susceptibility to infection with Gram-negative bacteria in children undergoing therapy for AML.
  • [MeSH-major] Gram-Negative Bacterial Infections / etiology. Hexosaminidases / genetics. Interleukin-6 / genetics. Leukemia, Myeloid / genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Alleles. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Female. Genetic Variation. Genotype. Gram-Negative Bacteria / isolation & purification. Humans. Infant. Infant, Newborn. Male

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107886.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; EC 3.2.1.- / Hexosaminidases; EC 3.2.1.- / chitotriosidase
  •  go-up   go-down


33. Savaşan S, Buck S, Ozdemir O, Hamre M, Asselin B, Pullen J, Ravindranath Y: Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2005 Jun;46(6):833-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia.
  • Risk-based treatment strategies have improved outcome in childhood B-precursor acute lymphoblastic leukemia, and in vitro drug sensitivity assessment using methyl-thiazol-tetrazolium (MTT) assay has been shown to be an independent prognostic marker.
  • To date, such strategies in childhood T-cell acute lymphoblastic leukemia (T-ALL) have proved elusive, and in vitro drug sensitivity testing has had limited success in T-ALL due to poor T-cell lymphoblast survival in vitro.
  • We studied 68 cases of childhood T-ALL for cytarabine (Ara-C) and daunorubicin sensitivity by FCDSA and compared the results with those obtained by MTT assay.
  • Comparison of T-ALL sensitivity with acute myeloid leukemia (AML) cases revealed a unique pattern difference.
  • Median cytotoxicity (expressed in arbitrary units) for Ara-C was 8 (0-47) and 27 (0-81), and daunorubicine cytotoxicity for T-ALL and AML samples was 79 (5-100) and 34 (0-98), respectively.
  • [MeSH-major] Drug Screening Assays, Antitumor. Flow Cytometry / methods. Medical Oncology / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Apoptosis. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Child. Daunorubicin / pharmacology. Humans. Immunophenotyping / methods. Inhibitory Concentration 50. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / drug therapy. Reproducibility of Results. Sensitivity and Specificity. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology


34. Gra OA, Glotov AS, Kozhekbaeva Zhm, Makarova OV, Nasedkina TV: [Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia]. Mol Biol (Mosk); 2008 Mar-Apr;42(2):214-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia].
  • In the present work the frequencies of xenobiotic-metabolizing gene polymorphisms in 332 children with the diagnosis acute lymphoblastic leukemia (ALL), 71 children with the diagnosis acute myeloblastic leukemia (AML) and 490 healthy donors have been determined using allele-specific hybridization on the biochip.
  • Statistically significant increase in the frequency of GSTT1 "null" genotype (OR = 1.9, p = 4.7E-5) and GSTT1/GSTM1 double "null" genotype (OR = 3.1, p = 2.5E-8) in children with acute leukemia relative to healthy donors group has been revealed.
  • Also 1.8-fold increase in the frequency of NAT2 genotype 341T/T, 481C/C, 590G/G in children with acute leukemia relative to healthy donors group (p = 0.026) has been recognized.
  • Analysis of gene-gene interactions has showed that in patients with acute leukemia genotype NAT2 341T/T, 481C/C, 590G/G in combination with GSTT1 "null" and/or GSTM1 "null" genotype is significantly more frequent than in population control.
  • Besides the reduction of MTRR genotype 66G/G frequency in girls with acute leukemia relative to female healthy donors has been found (OR = 0.50, p = 0.0015).
  • Analysis of gene-gene interactions has shown that the presence of GSTT1 "null" and/or GSTM1 "null" genotype in combination with MTRR genotype 66A/- may consider as risk factor of acute leukemia in girls.
  • Thus, the studied polymorphic variants of genes GSTT1, GSTM1, NAT2 and MTRR can modulate the risk of childhood acute leukemia, residents of European part of Russia.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Ferredoxin-NADP Reductase / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Alleles. Child. Child, Preschool. Female. Gene Frequency / genetics. Humans. Infant. Male. Risk Factors. Russia. Sex Factors

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18610829.001).
  • [ISSN] 0026-8984
  • [Journal-full-title] Molekuliarnaia biologiia
  • [ISO-abbreviation] Mol. Biol. (Mosk.)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
  •  go-up   go-down


35. Bachas C, Schuurhuis GJ, Hollink IH, Kwidama ZJ, Goemans BF, Zwaan CM, van den Heuvel-Eibrink MM, de Bont ES, Reinhardt D, Creutzig U, de Haas V, Assaraf YG, Kaspers GJ, Cloos J: High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine. Blood; 2010 Oct 14;116(15):2752-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine.
  • Although virtually all pediatric patients with acute myeloid leukemia (AML) achieve a complete remission after initial induction therapy, 30%-40% of patients will encounter a relapse and have a dismal prognosis.
  • To determine relevance of established AML type I/II mutations that may serve as therapeutic targets, we assessed frequencies of these mutations and their persistence during disease progression in a large group (n = 69) of paired diagnosis and relapse pediatric AML specimens.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precision Medicine
  • [MeSH-minor] Adolescent. Base Sequence. Biomarkers, Tumor / genetics. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Genes, Wilms Tumor. Genes, ras. Humans. Infant. Male. Prognosis. Recurrence. Time Factors. Treatment Outcome. fms-Like Tyrosine Kinase 3 / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2010 Oct 14;116(15):2622-3 [20947687.001]
  • (PMID = 20592250.001).
  • [ISSN] 1528-0020
  • [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 / Biomarkers, Tumor; 0 / DNA Primers; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


36. Ehlers S, Herbst C, Zimmermann M, Scharn N, Germeshausen M, von Neuhoff N, Zwaan CM, Reinhardt K, Hollink IH, Klusmann JH, Lehrnbecher T, Roettgers S, Stary J, Dworzak M, Welte K, Creutzig U, Reinhardt D: Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse. J Clin Oncol; 2010 May 20;28(15):2591-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse.
  • PURPOSE: This prospective, multicenter Acute Myeloid Leukemia Berlin-Frankfurt-Muenster (AML-BFM) 98 study randomly tested the ability of granulocyte colony-stimulating factor (G-CSF) to reduce infectious complications and to improve outcomes in children and adolescents with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: Of 154 SR patients in the AML-BFM 98 cohort, 50 patients were tested for G-CSF receptor (G-CSFR) RNA isoform I and IV expression, G-CSFR cell surface expression, and acquired mutations in the G-CSFR gene.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Receptors, Granulocyte Colony-Stimulating Factor / biosynthesis
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Flow Cytometry. Humans. Incidence. Male. Prospective Studies. Protein Isoforms. Recurrence. Treatment Outcome


37. Roberson JR, Onciu M, Pounds S, Rubnitz JE, Pui CH, Razzouk BI: Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 Mar;50(3):542-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia.
  • BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia (AML), but this association is unsubstantiated in pediatric AML.
  • PROCEDURE: We retrospectively compared cytochemical MPO results with outcome in 154 patients younger than 21 years treated on three consecutive institutional protocols for newly diagnosed AML (1987-2001).
  • Patients with FAB M0 and M7 AML (no MPO expression) or M3 AML (100% MPO expression) and Down's syndrome were excluded.
  • CONCLUSIONS: The percentage of MPO-positive blast cells is related to FAB subtype in pediatric AML but has limited prognostic relevance.
  • [MeSH-major] Leukemia, Myeloid / blood. Myeloid Cells / enzymology. Neoplastic Stem Cells / enzymology. Peroxidase / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Prognosis. Retrospective Studies. Risk. Survival Analysis

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763467.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [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 / Biomarkers; EC 1.11.1.7 / Peroxidase
  •  go-up   go-down


38. Robazzi TC, Barreto JH, Silva LR, Santiago MB, Mendonça N: Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil. J Pediatr Hematol Oncol; 2007 Sep;29(9):622-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil.
  • OBJECTIVE: This study was to determine the prevalence and characteristics of the osteoarticular manifestations on initial clinical presentation of acute leukemias (ALs) on childhood in the state of Bahia, Brazil.
  • RESULTS: Acute lymphocytic leukemia (ALL) was diagnosed in 313 (77.1%) patients and acute myeloid leukemia (AML), in 93 (22.9%) patients, including 241 males (59.4%) and 165 females (40.6%).
  • Prior referral to our center, the most frequent initial diagnosis was anemia (15.8%), leukemia (15.0%), amygdalitis (3.7%), and rheumatic fever (2.7%).
  • The presence of joint tenderness (16.2% in ALLx5.4% in AML), arthritis (26.6% in ALLx9.7 in AML), bone tenderness (26.1% in ALLx16.1% in AML), limb tenderness (49.5% in ALLx25.8% in AML), and antalgic gait (32.8% in ALLx9.7% in AML) had higher prevalence on ALL.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Osteoarthritis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Brazil. Child. Child, Preschool. Female. Humans. Infant. Male

  • MedlinePlus Health Information. consumer health - Osteoarthritis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17805037.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


39. Shimada A, Taki T, Kubota C, Itou T, Tawa A, Horibe K, Tsuchida M, Hanada R, Tsukimoto I, Hayashi Y, Japanese childhood AML cooperative study group: N822 mutation of KIT gene was frequent in pediatric acute myeloid leukemia patients with t(8;21) in Japan: a study of the Japanese childhood AML cooperative study group. Leukemia; 2007 Oct;21(10):2218-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] N822 mutation of KIT gene was frequent in pediatric acute myeloid leukemia patients with t(8;21) in Japan: a study of the Japanese childhood AML cooperative study group.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Mutation. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / physiology. Translocation, Genetic
  • [MeSH-minor] Bone Marrow Cells / metabolism. Child. Exons. Humans. Japan. Oncogenes. Protein Structure, Tertiary. Remission Induction


40. Flotho C, Paulun A, Batz C, Niemeyer CM: AKAP12, a gene with tumour suppressor properties, is a target of promoter DNA methylation in childhood myeloid malignancies. Br J Haematol; 2007 Sep;138(5):644-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AKAP12, a gene with tumour suppressor properties, is a target of promoter DNA methylation in childhood myeloid malignancies.
  • We hypothesized that epigenetic repression of the AKAP12 gene might occur in malignant myeloid disorders.
  • AKAP12 hypermethylation was found in one case of refractory anaemia with excess blasts (RAEB) and two cases of acute myeloid leukaemia (AML) in a panel of 21 blood or bone marrow samples from children with malignant myeloid disorders including refractory cytopenia, RAEB, juvenile myelomonocytic leukaemia and AML.
  • While AKAP12 function has not been previously linked to leukaemogenesis, our results raise the possibility that epigenetic silencing of AKAP12 is involved in myeloid malignancies.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA Methylation. DNA, Neoplasm / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] A Kinase Anchor Proteins. Adolescent. Anemia, Refractory, with Excess of Blasts / genetics. Anemia, Refractory, with Excess of Blasts / metabolism. Child. Child, Preschool. Epigenesis, Genetic. Female. Gene Silencing. Humans. Infant. Infant, Newborn. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Male. Neoplasm Proteins / metabolism. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17686059.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / A Kinase Anchor Proteins; 0 / AKAP12 protein, human; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  •  go-up   go-down


41. Slats AM, Egeler RM, van der Does-van den Berg A, Korbijn C, Hählen K, Kamps WA, Veerman AJ, Zwaan CM: Causes of death--other than progressive leukemia--in childhood acute lymphoblastic (ALL) and myeloid leukemia (AML): the Dutch Childhood Oncology Group experience. Leukemia; 2005 Apr;19(4):537-44
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Causes of death--other than progressive leukemia--in childhood acute lymphoblastic (ALL) and myeloid leukemia (AML): the Dutch Childhood Oncology Group experience.
  • We analyzed causes of death, other than resistant disease or relapse, in 875 children with acute lymphoblastic leukemia (ALL) and 229 with acute myeloid leukemia (AML), treated on three different Dutch Childhood Oncology Group (DCOG) ALL and three AML protocols.
  • Overall, 23 (2.6%) ALL and 44 (19.2%) AML patients died.
  • Early death (ED, before remission was reached) occurred in nine ALL (1%) and thirty AML (13.1%) patients, including three and ten deaths before treatment was initiated.
  • Chemotherapy-related mortality in remission (CRM) occurred in nine ALL (1.1%) and eight AML (4.4%) patients.
  • For AML a decrease in ED was observed (from 26% to approximately 10%), but counter-balanced by an increase in CRM (from 3 to 8%), maybe related to the scheduling of intensification blocks in AML-92/94.
  • Including transplant-related mortality, death in CR rates in AML increased from 3 to 15% in the last study.
  • We conclude that mortality dropped favorably in ALL, but not in AML.
  • Especially for AML, effective but less toxic therapy and better supportive care guidelines need to be developed.
  • [MeSH-major] Leukemia, Myeloid / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Agents / adverse effects. Cause of Death. Child. Child, Preschool. Female. Humans. Infant. Male. Netherlands / epidemiology. Remission Induction


42. Jurek AM, Maldonado G, Spector LG, Ross JA: Periconceptional maternal vitamin supplementation and childhood leukaemia: an uncertainty analysis. J Epidemiol Community Health; 2009 Feb;63(2):168-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Periconceptional maternal vitamin supplementation and childhood leukaemia: an uncertainty analysis.
  • BACKGROUND: Recent studies in childhood cancer suggest that maternal vitamin supplementation may reduce the risk of leukaemia, neuroblastoma and certain types of childhood brain tumours.
  • For example, a previous study found a significantly reduced risk of acute lymphoblastic leukaemia (ALL) but not acute myeloid leukaemia (AML) in children with Down syndrome whose mothers reported any vitamin supplement use prior to knowledge of pregnancy (ALL OR adjusted for confounders 0.51, 95% confidence limits (CL): 0.30, 0.89; AML OR adjusted for confounders 0.92, 95% CL 0.48, 1.76).

  • MedlinePlus Health Information. consumer health - Dietary Supplements.
  • MedlinePlus Health Information. consumer health - Preconception Care.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Epidemiol Community Health. 2009 Feb;63(2):91 [19141660.001]
  • (PMID = 18977808.001).
  • [ISSN] 1470-2738
  • [Journal-full-title] Journal of epidemiology and community health
  • [ISO-abbreviation] J Epidemiol Community Health
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075169; United States / NCI NIH HHS / CA / R01 CA75169
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Vitamins
  •  go-up   go-down


43. Taub JW, Ge Y: Down syndrome, drug metabolism and chromosome 21. Pediatr Blood Cancer; 2005 Jan;44(1):33-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been recognized that chromosomal abnormalities in childhood leukemia, are linked to both leukemogenesis and segregate patients into prognostic treatment groups.
  • This is best exemplified in cases of children with Down syndrome (DS), who have significantly higher risks of developing leukemia compared to non-DS children and distinctive treatment outcomes, particularly in cases of acute myeloid leukemia (AML).
  • The high event-free survival (EFS) rates of DS AML patients and in particular, patients with megakaryocytic leukemia (AMkL), at least in part reflects an increased sensitivity to cytosine arabinoside (ara-C) secondary to increased expression of the chromosome 21-localized gene, cystathionine-beta-synthase, and potentially global mechanisms which increase the susceptibility of cells to undergo apoptosis.
  • Hyperdiploid acute lymphoblastic leukemia (ALL) cells with extra copies of chromosome 21, generate higher levels of the active methotrexate (MTX) metabolite, MTX polyglutamates.
  • Microarray technology should lead to the identification of additional gene targets linked to the treatment response of specific cytogenetic leukemia subgroups.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 21. Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / metabolism. Antineoplastic Agents, Alkylating / therapeutic use. Child. Disease-Free Survival. Humans. Methotrexate / adverse effects. Methotrexate / metabolism. Methotrexate / therapeutic use. Prognosis

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15390307.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 45
  •  go-up   go-down


44. Whitworth KW, Symanski E, Coker AL: Childhood lymphohematopoietic cancer incidence and hazardous air pollutants in southeast Texas, 1995-2004. Environ Health Perspect; 2008 Nov;116(11):1576-80
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood lymphohematopoietic cancer incidence and hazardous air pollutants in southeast Texas, 1995-2004.
  • There is increasing interest in the role of air pollutants, including benzene and 1,3-butadiene, in the etiology of childhood cancers.
  • OBJECTIVE: Our goal was to assess whether census tracts with the highest benzene or 1,3-butadiene ambient air levels have increased childhood lymphohematopoietic cancer incidence.
  • METHODS: Our ecologic analysis included 977 cases of childhood lymphohematopoietic cancer diagnosed from 1995-2004.
  • RESULTS: Census tracts with the highest benzene levels had elevated rates of all leukemia [rate ratio (RR) = 1.37; 95% confidence interval (CI), 1.05, 1.78].
  • This association was higher for acute myeloid leukemia (AML) (RR = 2.02; 95% CI, 1.03-3.96) than for acute lymphocytic leukemia (ALL) (RR = 1.24; 95% CI, 0.92-1.66).
  • Among census tracts with the highest 1,3-butadiene levels, we observed RRs of 1.40 (95% CI, 1.07-1.81), 1.68 (95% CI, 0.84-3.35), and 1.32 (95% CI, 0.98-1.77) for all leukemia, AML, and ALL, respectively.
  • CONCLUSIONS: Our ecologic analysis suggests an association between childhood leukemia and hazardous air pollution; further research using more sophisticated methodology is warranted.

  • Genetic Alliance. consumer health - Childhood Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Air Waste Manag Assoc. 2000 Feb;50(2):175-80 [10680346.001]
  • [Cites] Occup Environ Med. 1999 Nov;56(11):774-80 [10658564.001]
  • [Cites] J Am Stat Assoc. 1995 Mar;90(429):64-71 [12155398.001]
  • [Cites] Cancer Causes Control. 2002 Sep;13(7):665-73 [12296514.001]
  • [Cites] Environ Health Perspect. 2003 Apr;111(4):663-8 [12676632.001]
  • [Cites] Epidemiology. 2003 Jul;14(4):386-91 [12843760.001]
  • [Cites] Int J Cancer. 2004 Feb 10;108(4):596-9 [14696126.001]
  • [Cites] Environ Health Perspect. 2004 Feb;112(2):257-65 [14754581.001]
  • [Cites] Occup Environ Med. 2004 Sep;61(9):773-8 [15317919.001]
  • [Cites] Environ Health Perspect. 2004 Oct;112(14):1386-92 [15471730.001]
  • [Cites] IARC Monogr Eval Carcinog Risk Chem Hum. 1982 May;29:1-398 [6957379.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum Suppl. 1987;7:1-440 [3482203.001]
  • [Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:105-10 [8549455.001]
  • [Cites] J Epidemiol Community Health. 1995 Dec;49 Suppl 2:S20-7 [8594128.001]
  • [Cites] Milbank Q. 1996;74(2):215-38 [8632735.001]
  • [Cites] Int Arch Occup Environ Health. 1997;70(1):57-60 [9258708.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1999;71 Pt 1:1-315 [10507919.001]
  • [Cites] Science. 2004 Dec 3;306(5702):1774-6 [15576619.001]
  • [Cites] J Epidemiol Community Health. 2005 Feb;59(2):101-5 [15650139.001]
  • [Cites] Cancer Invest. 2005;23(1):60-75 [15779869.001]
  • [Cites] J Epidemiol Community Health. 2005 Sep;59(9):755-60 [16100313.001]
  • [Cites] Mutat Res. 2006 Jan;612(1):14-39 [16027031.001]
  • [Cites] J Epidemiol Community Health. 2006 Feb;60(2):136-41 [16415262.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):2920-9 [16425269.001]
  • [Cites] J Expo Sci Environ Epidemiol. 2006 Nov;16(6):538-43 [16736057.001]
  • [Cites] Environ Health Perspect. 2007 Jan;115(1):138-45 [17366834.001]
  • [Cites] Environ Health Perspect. 2007 Oct;115(10):1388-93 [17938725.001]
  • [Cites] J Expo Sci Environ Epidemiol. 2008 Jan;18(1):45-58 [17878926.001]
  • [Cites] Cancer. 2008 Jan 15;112(2):416-32 [18074355.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:13-8 [8549460.001]
  • [Cites] Am J Epidemiol. 2001 Mar 1;153(5):433-43 [11226975.001]
  • (PMID = 19057714.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA128106; United States / NCI NIH HHS / CA / 1 R03 CA128106-01A1
  • [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 / Air Pollutants
  • [Other-IDs] NLM/ PMC2592281
  • [Keywords] NOTNLM ; 1,3-butadiene / air toxics / benzene / childhood cancer / epidemiology / hazardous air pollution
  •  go-up   go-down


45. Zou Y, Wang H, Chen XJ, Wang SC, Zhang L, Chen YM, Zhu XF: [Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Sep;27(9):621-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia].
  • OBJECTIVE: To analyse the clinical outcome and the prognostic factor of childhood acute myeloid leukemia (AML).
  • METHODS: Disease-free survival (DFS), event-free survival (EFS) and overall survival (OS) rates were estimated by Kaplan-Meier method and prognostic factors were evaluated by Cox regression with SPSS in 141 childhood AML in our hospital from August 1995 to July 2004.
  • The patients were divided into 2 groups: acute promyelocytic leukemia (APL) as group A and AML other than APL as group B.
  • The cumulative 5 year DFS and OS rate for group B patients were (28.4 +/- 9.0)% and (35.5 +/- 6.3)%, the 51 group A patients were (94.3 +/- 4.0)% and (81.4 +/- 5.7)%, and for total 141 AML patients were (56.9 +/- 6.3)% and (53.3 +/- 4.8)% respectively.
  • Multivariate analysis demonstrated that higher bone marrow blast cell percentage at diagnosis, CR after more than one course of chemotherapy and less than six courses of consolidation chemotherapy were risk prognostic factors in childhood AML other than APL (P < 0.05).
  • CONCLUSION: The prognosis of childhood APL is better, while of childhood t(8;21) AML is no better than other FAB subtypes.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Prognosis. Regression Analysis. Retrospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17278430.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


46. Deschler B, Lübbert M: Acute myeloid leukemia: epidemiology and etiology. Cancer; 2006 Nov 1;107(9):2099-107
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • With an incidence of 3.7 per 100,000 persons and an age-dependent mortality of 2.7 to nearly 18 per 100,000 persons, there is a rising awareness in the Western world of AML's special attributes resulting from an ever-aging population.
  • A review of the literature is presented, reflecting highlights of current research with respect to AML etiology.
  • 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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


47. Walter RB, Alonzo TA, Gerbing RB, Ho PA, Smith FO, Raimondi SC, Hirsch BA, Gamis AS, Franklin JL, Hurwitz CA, Loken MR, Meshinchi S: High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group. J Clin Oncol; 2010 Jun 10;28(17):2831-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group.
  • PURPOSE: To evaluate the prognostic significance of the integrin cell adhesion molecule very late antigen-4 (VLA-4) in acute myeloid leukemia (AML).
  • Subgroup analyses indicated that the prognostic role of VLA-4 expression was most prominent in patients with standard-risk AML, in whom low VLA-4 expression was associated with inferior DFS (34% +/- 16% v 69% +/- 14% for high expression; P = .011) and higher RR (61% +/- 16% v 26% +/- 14% for high expression; P = .009).
  • CONCLUSION: High VLA-4 expression is associated with better clinical outcome in pediatric AML and is an independent predictor of relapse that may refine our abilities to stratify patients without identifiable cytogenetic or molecular risk factors.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Apr 1;97(7):2121-9 [11264180.001]
  • [Cites] Cell. 2002 Sep 20;110(6):673-87 [12297042.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):579-89 [12899713.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1158-65 [12897778.001]
  • [Cites] Blood. 1993 Nov 15;82(10):3125-32 [7693037.001]
  • [Cites] Leukemia. 1996 Apr;10(4):682-6 [8618447.001]
  • [Cites] Blood. 2009 Oct 1;114(14):3008-17 [19636064.001]
  • [Cites] Nat Rev Immunol. 2007 Sep;7(9):678-89 [17717539.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):845-6 [18023867.001]
  • [Cites] Blood. 2009 Jan 22;113(4):866-74 [18927435.001]
  • [Cites] Annu Rev Immunol. 2009;27:339-62 [19302044.001]
  • [Cites] Leuk Res. 2009 Jun;33(6):764-8 [19042019.001]
  • [Cites] Genome Biol. 2007;8(5):215 [17543136.001]
  • (PMID = 20421533.001).
  • [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 / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K23 CA137161; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alpha4beta1
  • [Other-IDs] NLM/ PMC2903318
  •  go-up   go-down


48. Rihani R, Bazzeh F, Faqih N, Sultan I: Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry. Cancer; 2010 Sep 15;116(18):4385-94
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry.
  • The main histological subtype of secondary hematological malignancy was acute myeloid leukemia (AML) (49%), which had the shortest median latency time and the worst 5-year survival (18% ± 5.3%; P = .044).
  • The risk of secondary AML steadily increased from 1986 to 2005, whereas SIRs for acute lymphoblastic leukemia did not change over time.
  • CONCLUSIONS: Childhood cancer survivors are at increased risk of developing secondary hematological malignancies, particularly secondary AML.
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Incidence. Infant. Infant, Newborn. Male. SEER Program. Time Factors

  • Genetic Alliance. consumer health - Childhood Cancer.
  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 American Cancer Society.
  • (PMID = 20549819.001).
  • [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
  •  go-up   go-down


49. Linabery AM, Jurek AM, Duval S, Ross JA: The association between atopy and childhood/adolescent leukemia: a meta-analysis. Am J Epidemiol; 2010 Apr 1;171(7):749-64
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The association between atopy and childhood/adolescent leukemia: a meta-analysis.
  • Atopic disease is hypothesized to be protective against several malignancies, including childhood/adolescent leukemia.
  • To summarize the available epidemiologic evidence, the authors performed a meta-analysis of associations between atopy/allergies, asthma, eczema, hay fever, and hives and childhood/adolescent leukemia, acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML).
  • Odds ratios for atopy/allergies were 1.42 (95% confidence interval (CI): 0.60, 3.35) for 3 studies of leukemia overall, 0.69 (95% CI: 0.54, 0.89) for 6 studies of ALL, and 0.87 (95% CI: 0.62, 1.22) for 2 studies of AML, with high levels of heterogeneity detected for leukemia overall and ALL.

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Obstet Gynaecol. 1987 Aug;94(8):721-3 [3311129.001]
  • [Cites] Int J Cancer. 2009 Jun 1;124(11):2658-70 [19173295.001]
  • [Cites] Pediatr Infect Dis J. 1988 May;7(5 Suppl):S10-2 [2840629.001]
  • [Cites] Lancet. 1988 Dec 10;2(8624):1323-7 [2904050.001]
  • [Cites] BMJ. 1989 Nov 18;299(6710):1259-60 [2513902.001]
  • [Cites] J Epidemiol Community Health. 1989 Dec;43(4):352-5 [2614325.001]
  • [Cites] Tumori. 1990 Oct 31;76(5):413-9 [2256184.001]
  • [Cites] J Autoimmun. 1992 Apr;5 Suppl A:363-71 [1503633.001]
  • [Cites] Cancer Causes Control. 1993 Jul;4(4):361-8 [8347786.001]
  • [Cites] Leukemia. 1994 May;8(5):856-64 [8182942.001]
  • [Cites] Cancer Detect Prev. 1994;18(4):241-52 [7982234.001]
  • [Cites] Arch Pediatr Adolesc Med. 1995 May;149(5):553-8 [7735412.001]
  • [Cites] BMJ. 1997 Sep 13;315(7109):629-34 [9310563.001]
  • [Cites] Br J Cancer. 1997;76(9):1241-7 [9365177.001]
  • [Cites] Cancer Causes Control. 1998 May;9(3):285-98 [9684709.001]
  • [Cites] Klin Padiatr. 1998 Jul-Aug;210(4):185-91 [9743951.001]
  • [Cites] BMJ. 1998 Dec 5;317(7172):1562-3 [9836655.001]
  • [Cites] Clin Exp Allergy. 1998 Nov;28 Suppl 5:39-44; discussion 50-1 [9988446.001]
  • [Cites] Curr Probl Dermatol. 1999;28:1-8 [10374044.001]
  • [Cites] Br J Cancer. 1999 May;80(3-4):585-90 [10408870.001]
  • [Cites] Crit Rev Oncog. 1999;10(3):247-60 [10468184.001]
  • [Cites] J Natl Cancer Inst. 1957 Dec;19(6):1087-94 [13502763.001]
  • [Cites] Cancer Causes Control. 2000 Apr;11(4):303-7 [10843442.001]
  • [Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]
  • [Cites] J Paediatr Child Health. 2001 Aug;37(4):397-9 [11532063.001]
  • [Cites] Br J Cancer. 2002 Feb 1;86(3):350-5 [11875698.001]
  • [Cites] Nat Rev Immunol. 2001 Oct;1(1):69-75 [11905816.001]
  • [Cites] Stat Med. 2002 Jun 15;21(11):1539-58 [12111919.001]
  • [Cites] Int J Cancer. 2003 Jun 10;105(2):255-60 [12673688.001]
  • [Cites] Chem Immunol. 2000;78:50-61 [12847718.001]
  • [Cites] J Allergy Clin Immunol. 2003 Aug;112(2):252-62 [12897728.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):139-45 [14710221.001]
  • [Cites] Eur J Cancer. 2004 Mar;40(4):579-84 [14962726.001]
  • [Cites] N Engl J Med. 1972 Jul 20;287(3):107-10 [5032269.001]
  • [Cites] Br Med J. 1973 May 26;2(5864):482-3 [4736507.001]
  • [Cites] J Med. 1973;4(5):276-81 [4520972.001]
  • [Cites] Prev Med. 1974 Mar;3(1):165-70 [4815275.001]
  • [Cites] Prev Med. 1974 Sep;3(3):361-9 [4415641.001]
  • [Cites] J Natl Cancer Inst. 1976 May;56(5):891-8 [994201.001]
  • [Cites] Control Clin Trials. 1986 Sep;7(3):177-88 [3802833.001]
  • [Cites] Br Med J. 1958 Jun 28;1(5086):1495-508 [13546604.001]
  • [Cites] J Chronic Dis. 1965 Feb;18:113-32 [14258467.001]
  • [Cites] JAMA. 1964 May 4;188:459 [14125221.001]
  • [Cites] J Am Acad Dermatol. 2004 Nov;51(5 Suppl):S151-5 [15577757.001]
  • [Cites] Paediatr Perinat Epidemiol. 2005 Mar;19(2):152-64 [15787890.001]
  • [Cites] Immunol Allergy Clin North Am. 2005 Nov;25(4):621-39 [16257629.001]
  • [Cites] J Investig Allergol Clin Immunol. 2005;15(3):161-6 [16261950.001]
  • [Cites] Haematologica. 2006 Feb;91(2):240-3 [16461310.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):3124-32 [16395696.001]
  • [Cites] Lancet. 2006 Aug 26;368(9537):733-43 [16935684.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(17):3028-33 [16945522.001]
  • [Cites] Int J Cancer. 2007 Aug 15;121(4):819-24 [17390373.001]
  • [Cites] Cancer. 2008 Jan 15;112(2):416-32 [18074355.001]
  • [Cites] Eur J Pediatr. 2008 Jun;167(6):697-8 [17619899.001]
  • [Cites] Br J Cancer. 2008 Nov 18;99(10):1668-72 [19002185.001]
  • [Cites] Blood Cells Mol Dis. 2009 Mar-Apr;42(2):99-104 [19049852.001]
  • [Cites] Vital Health Stat 10. 2009 Jan;(239):1-80 [19326838.001]
  • [Cites] Leukemia. 1988 Feb;2(2):120-5 [3278171.001]
  • (PMID = 20228139.001).
  • [ISSN] 1476-6256
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA099936; United States / NCI NIH HHS / CA / T32CA099936
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 67
  • [Other-IDs] NLM/ PMC2877483
  •  go-up   go-down


50. Styczynski J, Wysocki M, Dluzniewska A, Juraszewska E, Balwierz W, Czyzewski K, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M, Kowalczyk J, Stefaniak J, Badowska W, Sonta-Jakimczyk D, Szczepanski T, Matysiak M, Stanczak E, Malinowska I, Wachowiak J, Konatkowska B, Gil L, Balcerska A, Kapuscinska L, Szczepanek J, Kolodziej B, Rafinska B, Kubicka M: Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in childhood acute myeloid leukemia. Anticancer Res; 2008 May-Jun;28(3B):1927-31
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in childhood acute myeloid leukemia.
  • BACKGROUND: The role of cellular drug resistance in childhood acute myeloid leukemia (AML) has not yet been established.
  • The aim of the study was the analysis of the clinical value of ex vivo drug resistance in pediatric AML.
  • PATIENTS AND METHODS: A cohort of 90 children with de novo AML were assayed for drug resistance profile by the 3-4,5-dimethylthiazol-2-yl-2,5-difenyl tetrazolium bromide (MTT) assay and prognostic model of in vitro drug sensitivity was analyzed.
  • A combined in vitro drug resistance profile to fludarabine, treosulfan and mitoxantrone (FTM score) was defined and it had an independent prognostic significance for disease free survival in pediatric AML.
  • CONCLUSION: The combined fludarabine, treosulfan and mitoxantrone resistance profile to possibly may be used for better stratification of children with AML or indicate the necessity for additional therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Busulfan / administration & dosage. Busulfan / analogs & derivatives. Child. Child, Preschool. Cohort Studies. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Female. Humans. Infant. Male. Mitoxantrone / administration & dosage. Prognosis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. TREOSULFAN .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18630483.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] BZ114NVM5P / Mitoxantrone; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  •  go-up   go-down


51. Xu XJ, Shi SW, Tang YM, Song H, Yang SL, Wei J, Xu WQ, Pan BH, Chen YH, Zhao FY, Shen HQ, Qian BQ, Zhang LY, Ning BT: [Long-term follow-up of treatment outcome and prognosis on 46 children with acute promyelocytic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2007 Feb;9(1):28-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Long-term follow-up of treatment outcome and prognosis on 46 children with acute promyelocytic leukemia].
  • OBJECTIVE: Acute promyelocytic leukemia (APL) is a specific type of hematopoietic malignancy, accounting for 10% of the de novo acute myeloid leukemia (AML).
  • The aim of this study was to investigate the clinical biological features, diagnosis, prognosis and long-term survival of childhood APL.
  • CONCLUSIONS: Remission induction therapy with ATRA + DNR or THP is effective and safe for newly diagnosed childhood APL.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Male. Oncogene Proteins, Fusion / genetics. Prognosis. Survival Rate. Treatment Outcome. Tretinoin / administration & dosage

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17306073.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
  •  go-up   go-down


52. McGrath P, Suppiah R, Patton MA: Re-entering life: paediatric acute myeloid leukaemia at one year post treatment. Aust J Holist Nurs; 2005 Oct;12(2):23-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Re-entering life: paediatric acute myeloid leukaemia at one year post treatment.
  • To date, there is scant psychosocial research on the experience of childhood AML.
  • This article presents findings from the perspective of the child patients, their parents and siblings at one year post-treatment.
  • [MeSH-major] Attitude to Health. Holistic Health. Leukemia, Myelomonocytic, Acute / psychology. Parent-Child Relations. Parenting / psychology

  • MedlinePlus Health Information. consumer health - Parenting.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19175261.001).
  • [ISSN] 1322-8803
  • [Journal-full-title] The Australian journal of holistic nursing
  • [ISO-abbreviation] Aust J Holist Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  •  go-up   go-down


53. Ho PA, Zeng R, Alonzo TA, Gerbing RB, Miller KL, Pollard JA, Stirewalt DL, Heerema NA, Raimondi SC, Hirsch B, Franklin JL, Lange B, Meshinchi S: Prevalence and prognostic implications of WT1 mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group. Blood; 2010 Aug 05;116(5):702-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and prognostic implications of WT1 mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.
  • Recent studies of WT1 mutations in acute myeloid leukemia (AML) mostly report an association with unfavorable clinical outcome.
  • We screened 842 patients treated on 3 consecutive pediatric AML trials for WT1 zinc-finger mutations.
  • In current risk stratification schemes incorporating cytogenetics and FLT3/ITD status, the presence of WT1 mutations has no independent prognostic significance in predicting outcome in pediatric AML.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid / genetics. Mutation
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons / genetics. Female. Humans. Infant. Infant, Newborn. Kaplan-Meier Estimate. Karyotyping. Male. Prevalence. Prognosis. Proportional Hazards Models. Retrospective Studies. Tandem Repeat Sequences / genetics. Treatment Outcome. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Leukemia. 2007 May;21(5):868-76 [17361230.001]
  • [Cites] Br J Haematol. 2004 Jun;125(5):590-600 [15147374.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4140-6 [15483024.001]
  • [Cites] Leukemia. 1992 May;6(5):405-9 [1317488.001]
  • [Cites] Hum Mol Genet. 1994 Sep;3(9):1633-7 [7833922.001]
  • [Cites] Hum Mol Genet. 1995 Mar;4(3):351-8 [7795587.001]
  • [Cites] Biochemistry. 1996 Sep 17;35(37):12070-6 [8810912.001]
  • [Cites] Hum Mutat. 1997;9(3):209-25 [9090524.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Curr Opin Hematol. 2007 Mar;14(2):106-14 [17255787.001]
  • [Cites] Leukemia. 2007 Mar;21(3):550-1; author reply 552 [17205055.001]
  • [Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):346-55 [18692685.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Blood. 2009 May 7;113(19):4505-11 [19221039.001]
  • [Cites] Blood. 2009 Jun 4;113(23):5951-60 [19171881.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]
  • [Cites] Cancer. 2009 Aug 15;115(16):3719-27 [19536888.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1472-9 [19322206.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1136-9 [19618455.001]
  • [Cites] Blood. 2010 Mar 25;115(12):2372-9 [20056794.001]
  • [Cites] Gene. 2001 Aug 8;273(2):141-61 [11595161.001]
  • (PMID = 20413658.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002798/ NCT00070174
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R21CA10262-01; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2918327
  •  go-up   go-down


54. Laningham FH, Kun LE, Reddick WE, Ogg RJ, Morris EB, Pui CH: Childhood central nervous system leukemia: historical perspectives, current therapy, and acute neurological sequelae. Neuroradiology; 2007 Nov;49(11):873-88
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood central nervous system leukemia: historical perspectives, current therapy, and acute neurological sequelae.
  • INTRODUCTION: During the past three decades, improvements in the treatment of childhood leukemia have resulted in high cure rates, particularly for acute lymphoblastic leukemia (ALL).
  • METHODS AND RESULTS: In this review we discuss the poignant, historical aspects of CNS leukemia therapy, outline current methods of systemic and CNS leukemia therapy, and present imaging findings we have encountered in childhood leukemia patients with a variety of acute neurological conditions.
  • A major objective of our research is to understand the neuroimaging correlates of acute and chronic effects of cancer and therapy.
  • Specific features related to CNS leukemia and associated short-term toxicities, both disease- and therapy-related, are emphasized in this review with the specific neuroimaging findings.
  • Specific CNS findings are similarly important when treating acute myelogenous leukemia (AML), and details of leukemic involvement and toxicities are also presented in this entity.
  • CONCLUSION: Despite contemporary treatment approaches which favor the use of chemotherapy (including intrathecal therapy) over radiotherapy in the treatment of CNS leukemia, children still occasionally experience morbid neurotoxicity.
  • It is important to appreciate that intrathecal and high doses of systemic chemotherapy are not innocuous and are associated with acute, specific, recognizable, and often serious neurological consequences.

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for central nervous system leukemia .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Invest. 1993;11(5):534-53 [8402223.001]
  • [Cites] Pediatr Blood Cancer. 2007 Feb;48(2):152-9 [16317748.001]
  • [Cites] Neuroradiology. 1994 Nov;36(8):652-5 [7862289.001]
  • [Cites] N Engl J Med. 1996 May 30;334(22):1428-34 [8618581.001]
  • [Cites] Neuroradiology. 1996 Apr;38(3):264-8 [8741199.001]
  • [Cites] J Natl Cancer Inst. 1996 Oct 16;88(20):1483-8 [8841024.001]
  • [Cites] AJNR Am J Neuroradiol. 1996 Feb;17(2):295-310 [8938302.001]
  • [Cites] Cancer. 1997 Dec 1;80(11 Suppl):2191-8 [9395033.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1712-22 [9586883.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):438-40 [10080582.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] Leukemia. 2001 Mar;15(3):348-54 [11237056.001]
  • [Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]
  • [Cites] Neuroradiology. 2001 Jun;43(6):492-5 [11465764.001]
  • [Cites] Neuroradiology. 2002 Jul;44(7):559-67 [12136356.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):184-8 [12525508.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] Cleve Clin J Med. 2004 Aug;71(8):633-7 [15449758.001]
  • [Cites] J Pediatr. 1970 Dec;77(6):1089-91 [4922336.001]
  • [Cites] Neuroradiology. 1978;16:543-6 [284200.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1979 Spring;1(1):21-30 [396790.001]
  • [Cites] Neuroradiology. 1981;22(2):79-84 [6946301.001]
  • [Cites] Blood. 1985 Nov;66(5):1062-7 [3840394.001]
  • [Cites] J Natl Cancer Inst. 1992 Feb 19;84(4):252-6 [1734087.001]
  • [Cites] Blood. 1992 Feb 15;79(4):871-5 [1737097.001]
  • [Cites] Neurology. 1993 Mar;43(3 Pt 1):618-20 [8451012.001]
  • [Cites] N Engl J Med. 1993 Jul 29;329(5):314-9 [8321259.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] AJNR Am J Neuroradiol. 2004 Nov-Dec;25(10):1688-95 [15569732.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jul;45(1):10-5 [15547931.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2030-42 [16304570.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2216-22 [16804111.001]
  • [Cites] J Natl Cancer Inst. 2006 Nov 1;98(21):1528-37 [17077355.001]
  • [Cites] AJNR Am J Neuroradiol. 1994 Feb;15(2):300-1 [8192076.001]
  • (PMID = 17924103.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090246-05; United States / NCI NIH HHS / CA / R01 CA090246; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / R01 CA090246-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 39
  • [Other-IDs] NLM/ NIHMS49119; NLM/ PMC2386669
  •  go-up   go-down


55. Rubnitz JE: Childhood acute myeloid leukemia. Curr Treat Options Oncol; 2008 Feb;9(1):95-105
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood acute myeloid leukemia.
  • OPINION STATEMENT: Despite the use of intensive chemotherapy and hematopoietic stem cell transplantation, approximately one-third of children with acute myeloid leukemia (AML) still suffer relapse of their disease.
  • Instead, advances in the treatment of children with AML will require a greater understanding of the biology of the disease, with particular attention to the genetic abnormalities underlying leukemogenesis and drug resistance.
  • More important, we must develop alternative treatment approaches, such as agents that target specific leukemia-associated abnormalities and agents that selectively eradicate leukemic stem cells.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Child. Humans


56. Kadan-Lottick NS, Dinu I, Wasilewski-Masker K, Kaste S, Meacham LR, Mahajan A, Stovall M, Yasui Y, Robison LL, Sklar CA: Osteonecrosis in adult survivors of childhood cancer: a report from the childhood cancer survivor study. J Clin Oncol; 2008 Jun 20;26(18):3038-45
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osteonecrosis in adult survivors of childhood cancer: a report from the childhood cancer survivor study.
  • PURPOSE: Osteonecrosis (ON) is a potentially serious complication of therapy in survivors of childhood cancer.
  • PATIENTS AND METHODS: The rate of self-reported ON was determined for 9,261 patients enrolled onto the Childhood Cancer Survivor Study, a cohort of 5-year survivors of childhood cancer diagnosed from 1970 to 1986, and compared with the rate in a random sample of 2,872 siblings of survivors.
  • The RR was greatest among survivors of stem-cell transplantation for acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (RR = 26.9, 66.5, and 93.1, respectively).
  • Nontransplantation patients with ALL (RR = 6.5; 95% CI, 2.2 to 19.4), AML (RR = 11.2; 95% CI, 2.1 to 61.2), and bone sarcoma (RR = 7.3; 95% CI, 2.0 to 26.2) were at higher risk for ON.
  • CONCLUSION: ON among long-term survivors of childhood cancer is rare.
  • However, compared with siblings, childhood cancer survivors have a significantly increased relative rate of ON, particularly those who were older at diagnosis and who received dexamethasone or radiation therapy.

  • Genetic Alliance. consumer health - Childhood Cancer.
  • Genetic Alliance. consumer health - Osteonecrosis.
  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • MedlinePlus Health Information. consumer health - Osteonecrosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18565890.001).
  • [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 / U24 CA055727; United States / NCRR NIH HHS / RR / KL2 RR024138; United States / NCI NIH HHS / CA / U24-CA-55727
  • [Publication-type] Journal Article; Multicenter Study; 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
  •  go-up   go-down


57. Bierings M, Nachman JB, Zwaan CM: Stem cell transplantation in pediatric leukemia and myelodysplasia: state of the art and current challenges. Curr Stem Cell Res Ther; 2007 Jan;2(1):53-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell transplantation in pediatric leukemia and myelodysplasia: state of the art and current challenges.
  • The role of stem cell transplantation in the treatment of leukemia and myelodysplasia (MDS) in children has changed over the past decade.
  • In pediatric acute lymphoblastic leukemia (ALL), the overall cure-rate is high with conventional chemotherapy.
  • In pediatric acute myeloid leukemia (AML) the role of allo-HSCT in CR1 is declining, due to better outcome with modern multi-agent chemotherapy.
  • In relapsed AML patients, allo-HSCT still seems indispensable.
  • Targeted therapy may change the role of HSCT, in particular in chronic myeloid leukemia, where the role of allografting is changing in the imatinib era.
  • [MeSH-major] Leukemia / therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation / trends
  • [MeSH-minor] Child. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy


58. Balamurugan S, Sugapriya D, Shanthi P, Thilaka V, Venkatadesilalu S, Pushpa V, Madhavan M: Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias. Indian J Hematol Blood Transfus; 2007 Dec;23(3-4):73-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias.
  • We have studied MDR1 expression and AgNORS in 41 cases of acute leukemia in children.
  • In this study, AgNOR counts in patients with acute lymphoblastic leukemia (ALL) L2 subtype (FAB classification) were significantly higher as compared to the ALL L1 subtype.
  • Similarly, mean AgNOR count in the acute myeloid Leukemia (AML) M2 subtype was significantly higher as compared to the ALL L1 subtype.
  • However, there was no correlation between AgNOR and treatment outcome or between AgNOR counts and MDR1 expression in any of the subtypes of acute leukemia included in this series.
  • In AML, MDR1 gene expression was found to be related to reduced remission induction rates and hence poorer prognosis.
  • This would suggest that factors other than MDR1 may be of relevance in Pediatric ALL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Blood. 1992 Jan 15;79(2):295-8 [1346094.001]
  • [Cites] Blood. 1992 Jan 15;79(2):473-6 [1370388.001]
  • [Cites] Br J Haematol. 1991 Jan;77(1):50-3 [1671821.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1237-47 [8644864.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1202-10 [12663440.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1201-7 [15547738.001]
  • [Cites] J Pathol. 1989 Jul;158(3):185-8 [2475599.001]
  • [Cites] Br J Haematol. 1981 Apr;47(4):553-61 [6938236.001]
  • [Cites] Blood. 1993 May 1;81(9):2394-8 [8097634.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3480-1 [8507883.001]
  • [Cites] Leuk Lymphoma. 1995 Sep;19(1-2):135-40 [8574159.001]
  • [Cites] Cancer Lett. 1996 Nov 12;108(1):87-91 [8950214.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1673-80 [9324288.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1512-8 [9552060.001]
  • [Cites] Am J Hematol. 1999 Jun;61(2):149-52 [10367797.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):309-14 [11999562.001]
  • [Cites] Mol Cancer Res. 2004 Jun;2(6):339-47 [15235109.001]
  • [Cites] Best Pract Res Clin Haematol. 2004 Dec;17(4):641-51 [15494300.001]
  • (PMID = 23100919.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453125
  • [Keywords] NOTNLM ; Acute leukemia / AgNOR / Multidrug Resistance 1 / P-glycoprotein
  •  go-up   go-down


59. Shih LY, Liang DC, Huang CF, Chang YT, Lai CL, Lin TH, Yang CP, Hung IJ, Liu HC, Jaing TH, Wang LY, Yeh TC: Cooperating mutations of receptor tyrosine kinases and Ras genes in childhood core-binding factor acute myeloid leukemia and a comparative analysis on paired diagnosis and relapse samples. Leukemia; 2008 Feb;22(2):303-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cooperating mutations of receptor tyrosine kinases and Ras genes in childhood core-binding factor acute myeloid leukemia and a comparative analysis on paired diagnosis and relapse samples.
  • c-KIT mutations have been described in core-binding factor (CBF) acute myeloid leukemia (AML) at diagnosis.
  • The role of c-KIT mutations in the relapse of CBF-AML is not clear.
  • The role of CSF1R mutation in the pathogenesis of AML remains to be determined.
  • We analyzed receptor tyrosine kinases (RTKs) and Ras mutations on 154 children with AML.
  • Also, we examined the paired diagnosis and relapse samples in CBF-AML.
  • CBF-AML accounted for 27% (41/154).
  • c-KIT mutations were detected in 41.5% of CBF-AML at diagnosis (6 in exon 8, 10 in exon 17 and 1 in both exons 8 and 17) , FLT3-TKD 2.7%, N-Ras mutations 7.3% and K-Ras mutations 4.9%.
  • FLT3-LM and CSF1R mutations were not found in CBF-AML.
  • Eight of the 41 CBF-AML patients relapsed; four patients retained the identical c-KIT mutation patterns as those at diagnosis, the remaining four without c-KIT mutations at diagnosis did not acquire c-KIT mutations at relapse.
  • Our study showed that 54% of childhood CBF-AML had RTKs and/or Ras mutations; c-KIT but not CSF1R mutations play a role in the leukemogenesis of childhood CBF-AML.
  • [MeSH-major] Core Binding Factors. Genes, ras / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics. Receptor Protein-Tyrosine Kinases / genetics. Receptor, Macrophage Colony-Stimulating Factor / genetics
  • [MeSH-minor] Adolescent. Bone Marrow / pathology. Child. Child, Preschool. DNA Mutational Analysis. Humans. Recurrence. Time Factors

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17960171.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  •  go-up   go-down


60. Kaspers GJ, Creutzig U: Pediatric acute myeloid leukemia: international progress and future directions. Leukemia; 2005 Dec;19(12):2025-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric acute myeloid leukemia: international progress and future directions.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Child. Forecasting. Humans. Prognosis. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16304569.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Number-of-references] 30
  •  go-up   go-down


61. Ortiz MI, Hernández-Rubio I, Cortés-Alva D, Romo-Hernández G, López-Cadena JM, Copca-García JA: Treatment of acute myelogenous leukemia in a Mexican pediatric hospital. Proc West Pharmacol Soc; 2010;53:37-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute myelogenous leukemia in a Mexican pediatric hospital.
  • Acute leukemia is the most common malignancy in children, and accounts for nearly 35% of all childhood cancers.
  • Acute myelogenous leukemia (AML) constitutes about 20% of acute leukemias.
  • Initially, treatment of AML involves the immediate management of emergencies associated as hyperleukocytosis, tumor lysis syndrome, hemorrhages and infections.
  • Therefore we performed a retrospective, descriptive and transversal study to investigate the drugs used in patients with AML who were admitted at the Hospital del Niño DIF from 2007 to 2008.
  • We conclude that AML is common in our hospital with a high mortality rate.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Female. Humans. Infant. Male. Mexico. Retrospective Studies

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 22128449.001).
  • [ISSN] 0083-8969
  • [Journal-full-title] Proceedings of the Western Pharmacology Society
  • [ISO-abbreviation] Proc. West. Pharmacol. Soc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


62. Belson M, Kingsley B, Holmes A: Risk factors for acute leukemia in children: a review. Environ Health Perspect; 2007 Jan;115(1):138-45
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors for acute leukemia in children: a review.
  • Although overall incidence is rare, leukemia is the most common type of childhood cancer.
  • Within this population, acute lymphocytic leukemia (ALL) occurs approximately five times more frequently than acute myelogenous leukemia (AML) and accounts for approximately 78% of all childhood leukemia diagnoses.
  • Epidemiologic studies of acute leukemias in children have examined possible risk factors, including genetic, infectious, and environmental, in an attempt to determine etiology.
  • Only one environmental risk factor (ionizing radiation) has been significantly linked to ALL or AML.
  • Most environmental risk factors have been found to be weakly and inconsistently associated with either form of acute childhood leukemia.
  • Our review focuses on the demographics of childhood leukemia and the risk factors that have been associated with the development of childhood ALL or AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Child. Communicable Diseases / complications. Environmental Exposure. Genetic Predisposition to Disease. Humans. Risk Factors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1989 Jul 15;49(14):4030-7 [2736544.001]
  • [Cites] BMJ. 1990 Feb 17;300(6722):423-9 [2107892.001]
  • [Cites] Am J Hum Genet. 1990 Jun;46(6):1041-52 [2160192.001]
  • [Cites] Pediatr Hematol Oncol. 1987;4(1):63-72 [3152913.001]
  • [Cites] Br J Cancer. 1990 Dec;62(6):1008-14 [2257204.001]
  • [Cites] Environ Health Perspect. 1990 Aug;88:325-37 [2272330.001]
  • [Cites] Med J Aust. 1991 Apr 1;154(7):483-7 [2005848.001]
  • [Cites] BMJ. 1991 Mar 23;302(6778):681-7 [2021741.001]
  • [Cites] BMJ. 1991 Mar 23;302(6778):687-92 [2021742.001]
  • [Cites] Cancer. 1991 Sep 15;68(6):1351-5 [1873786.001]
  • [Cites] Br J Cancer. 1991 Sep;64(3):549-54 [1911197.001]
  • [Cites] Br J Cancer. 2001 Feb 2;84(3):406-12 [11161408.001]
  • [Cites] Int J Epidemiol. 2001 Feb;30(1):125-9 [11171872.001]
  • [Cites] Am J Epidemiol. 2001 Mar 15;153(6):615-7 [11257071.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2542-6 [11289128.001]
  • [Cites] Am J Public Health. 2001 Apr;91(4):564-7 [11291366.001]
  • [Cites] Cancer Causes Control. 2001 Aug;12(6):483-90 [11519756.001]
  • [Cites] Paediatr Perinat Epidemiol. 2001 Oct;15(4):338-45 [11703681.001]
  • [Cites] Radiat Res. 2001 Dec;156(6):718-23 [11741495.001]
  • [Cites] Environ Health Perspect. 1991 Aug;94:5-7 [1954939.001]
  • [Cites] Eur J Cancer. 1992;29A(1):87-95 [1445751.001]
  • [Cites] BMJ. 1993 Jan 9;306(6870):89-94 [8435648.001]
  • [Cites] Leukemia. 1993 Mar;7(3):349-60 [8445941.001]
  • [Cites] BMJ. 1993 Mar 6;306(6878):615-21 [8461811.001]
  • [Cites] BMJ. 1993 May 1;306(6886):1153-8 [8499814.001]
  • [Cites] Leukemia. 1993 Aug;7 Suppl 2:S146-7 [8361221.001]
  • [Cites] BMJ. 1993 Oct 16;307(6910):959-66 [8241906.001]
  • [Cites] Med Pediatr Oncol. 1994;22(2):78-83 [8259105.001]
  • [Cites] Nature. 1994 Feb 24;367(6465):678-80 [8107860.001]
  • [Cites] BMJ. 1994 Jul 16;309(6948):154-7 [8044093.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Sep;3(6):457-60 [8000294.001]
  • [Cites] Br J Cancer. 1995 Jan;71(1):1-5 [7819022.001]
  • [Cites] Am J Public Health. 1995 Feb;85(2):249-52 [7856787.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):645-53 [7881337.001]
  • [Cites] Cancer. 1995 Apr 15;75(8):2186-95 [7697611.001]
  • [Cites] Epidemiol Rev. 1994;16(2):243-72 [7713179.001]
  • [Cites] Environ Health Perspect. 1995 Jun;103(6):550-4 [7556005.001]
  • [Cites] Eur J Cancer Prev. 1995 Sep;4 Suppl 1:3-107 [7496333.001]
  • [Cites] J Natl Cancer Inst. 1996 Jan 3;88(1):24-31 [8847721.001]
  • [Cites] Ann Epidemiol. 1995 Sep;5(5):354-9 [8653207.001]
  • [Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:177-84 [8549470.001]
  • [Cites] Epidemiology. 1999 Sep;10(5):481-7 [10468419.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]
  • [Cites] Curr Opin Pediatr. 2004 Feb;16(1):9-14 [14758108.001]
  • [Cites] Environ Mol Mutagen. 2004;43(2):100-9 [14991750.001]
  • [Cites] Cancer Detect Prev. 2004;28(2):83-7 [15068830.001]
  • [Cites] Cancer Res. 1967 Dec;27(12):2420-3 [4230121.001]
  • [Cites] J Natl Cancer Inst. 1968 May;40(5):1079-85 [5648133.001]
  • [Cites] Nature. 1971 Apr 9;230(5293):370-3 [4927726.001]
  • [Cites] Lancet. 1971 Apr 3;1(7701):699-701 [4101637.001]
  • [Cites] Science. 1973 Dec 28;182(4119):1355-6 [4586464.001]
  • [Cites] J Med Genet. 1977 Apr;14(2):81-90 [856959.001]
  • [Cites] Cancer Res. 1978 Mar;38(3):485-93 [203382.001]
  • [Cites] Cancer. 1980 Apr 1;45(7):1675-8 [6929216.001]
  • [Cites] J Pediatr. 1981 Sep;99(3):425-8 [7264801.001]
  • [Cites] Am J Ind Med. 1981;2(3):217-45 [7345926.001]
  • [Cites] J Occup Med. 1984 Sep;26(9):679-82 [6207280.001]
  • [Cites] Leuk Res. 1985;9(6):817-23 [3159943.001]
  • [Cites] Am J Epidemiol. 1985 Feb;121(2):216-24 [3860001.001]
  • [Cites] Nature. 1987 Jan 22-28;325(6102):355-7 [3808031.001]
  • [Cites] Br J Cancer. 1987 Feb;55(2):179-90 [3814487.001]
  • [Cites] J Natl Cancer Inst. 1987 Jul;79(1):39-46 [3474448.001]
  • [Cites] Prog Clin Biol Res. 1987;246:19-32 [2958880.001]
  • [Cites] Am J Epidemiol. 1988 Apr;127(4):713-25 [3354538.001]
  • [Cites] Int J Epidemiol. 2001 Dec;30(6):1428-37 [11821358.001]
  • [Cites] BMJ. 2002 Feb 2;324(7332):283-7 [11823363.001]
  • [Cites] Lancet. 2002 Feb 2;359(9304):431-4 [11844534.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Feb;11(2):177-85 [11867505.001]
  • [Cites] Environ Health Perspect. 2002 Mar;110(3):319-24 [11882484.001]
  • [Cites] Rev Environ Health. 2001 Jul-Sep;16(4):263-79 [12041882.001]
  • [Cites] Lancet Oncol. 2002 May;3(5):269-79 [12067803.001]
  • [Cites] Environ Health Perspect. 2002 Sep;110(9):955-60 [12204832.001]
  • [Cites] Br J Cancer. 2002 Sep 23;87(7):740-5 [12232757.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6 [12415113.001]
  • [Cites] Pharmacogenetics. 2002 Nov;12(8):655-8 [12439226.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13950-4 [9391133.001]
  • [Cites] Br J Cancer. 1998 Mar;77(5):842-9 [9514068.001]
  • [Cites] Epidemiology. 1998 May;9(3):234-45 [9583414.001]
  • [Cites] Leukemia. 1998 May;12(5):645-51 [9593260.001]
  • [Cites] Environ Health Perspect. 1998 Jun;106 Suppl 3:893-908 [9646054.001]
  • [Cites] Br J Cancer. 1998 Jul;78(1):119-24 [9662261.001]
  • [Cites] Radiat Environ Biophys. 1998 Jul;37(2):87-93 [9728740.001]
  • [Cites] Radiat Res. 1998 Nov;150(5 Suppl):S30-41 [9806607.001]
  • [Cites] Cancer. 1999 Mar 15;85(6):1380-8 [10189146.001]
  • [Cites] Teratology. 1999 Apr;59(4):227-33 [10331524.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 16;91(12):1051-8 [10379968.001]
  • [Cites] Int J Radiat Biol. 1999 Jul;75(7):801-10 [10489891.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):783-91 [10498397.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):793-9 [10498398.001]
  • [Cites] Br J Cancer. 1999 Oct;81(3):549-53 [10507784.001]
  • [Cites] N Engl J Med. 1955 Jul 21;253(3):88-90 [14394332.001]
  • [Cites] Lancet. 1956 Sep 1;271(6940):447 [13358242.001]
  • [Cites] Arch Intern Med. 1961 Jul;108:86-90 [13720079.001]
  • [Cites] N Engl J Med. 1965 Apr 29;272:882-7 [14274439.001]
  • [Cites] N Engl J Med. 1959 Sep 17;261:585-9 [14425443.001]
  • [Cites] J Epidemiol Community Health. 2005 Feb;59(2):101-5 [15650139.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):651-5 [15767345.001]
  • [Cites] Environ Health. 2004;3(1):12 [15533260.001]
  • [Cites] Occup Environ Med. 2006 Feb;63(2):131-4 [16421392.001]
  • [Cites] Environ Health Perspect. 2003 Apr;111(4):663-8 [12676632.001]
  • [Cites] Hematol Oncol. 2003 Jun;21(2):51-5 [12802809.001]
  • [Cites] Environ Health Perspect. 2003 Jun;111(7):962-70 [12782499.001]
  • [Cites] Epidemiology. 2003 Jul;14(4):437-41 [12843769.001]
  • [Cites] Epidemiology. 2003 Sep;14(5):569-77 [14501272.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]
  • [Cites] Lancet. 1988 Sep 17;2(8612):665-9 [2901525.001]
  • [Cites] Lancet. 1988 Dec 10;2(8624):1323-7 [2904050.001]
  • [Cites] Cancer. 1989 May 15;63(10):1904-11 [2649219.001]
  • [Cites] Radiat Res. 1996 May;145(5):595-601 [8619025.001]
  • [Cites] Br J Cancer. 1996 Apr;73(8):1006-12 [8611419.001]
  • [Cites] Med Pediatr Oncol Suppl. 1996;1:29-34 [8643045.001]
  • [Cites] Nature. 1996 Jul 25;382(6589):352-3 [8684463.001]
  • [Cites] Int J Cancer. 1996 Jul 29;67(3):343-52 [8707407.001]
  • [Cites] Cancer. 1995 Apr 1;75(7):1718-27 [8826933.001]
  • [Cites] Cancer Causes Control. 1996 Nov;7(6):581-90 [8932918.001]
  • [Cites] J Natl Cancer Inst. 1997 Feb 5;89(3):238-44 [9017004.001]
  • [Cites] Br J Cancer. 1997;75(3):457-63 [9020498.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):3-16 [9045302.001]
  • [Cites] Occup Environ Med. 1996 Nov;53(11):773-81 [9038803.001]
  • [Cites] Br J Radiol. 1997 Feb;70:130-9 [9135438.001]
  • [Cites] Ann Epidemiol. 1997 Apr;7(3):172-9 [9141639.001]
  • [Cites] Cancer. 1997 May 15;79(10):2045-51 [9149034.001]
  • [Cites] Nature. 1997 May 15;387(6630):246 [9153387.001]
  • [Cites] Occup Environ Med. 1997 Mar;54(3):152-66 [9155776.001]
  • [Cites] N Engl J Med. 1997 Jul 3;337(1):1-7 [9203424.001]
  • [Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):939-47 [9214673.001]
  • [Cites] Pediatr Clin North Am. 1997 Aug;44(4):831-46 [9286287.001]
  • [Cites] Environ Health Perspect. 1997 Oct;105(10):1068-77 [9349828.001]
  • [Cites] J Natl Cancer Inst. 1999 Oct 20;91(20):1765-72 [10528028.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(4):813-23 [10673523.001]
  • [Cites] Curr Opin Oncol. 2000 Jan;12(1):3-12 [10687723.001]
  • [Cites] Am J Epidemiol. 2000 Mar 1;151(5):512-5 [10707920.001]
  • [Cites] CA Cancer J Clin. 2000 Jan-Feb;50(1):7-33 [10735013.001]
  • [Cites] Br J Cancer. 2000 Sep;83(5):692-8 [10944614.001]
  • [Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]
  • [Cites] Epidemiology. 2000 Nov;11(6):624-34 [11055621.001]
  • [CommentIn] Environ Health Perspect. 2007 Aug;115(8):A395-6 [17687418.001]
  • [CommentIn] Environ Health Perspect. 2007 Aug;115(8):A395 [17687419.001]
  • [ErratumIn] Environ Health Perspect. 2010 Sep;118(9):A380
  • (PMID = 17366834.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 145
  • [Other-IDs] NLM/ PMC1817663
  •  go-up   go-down


63. Mantadakis E, Samonis G, Kalmanti M: A comprehensive review of acute promyelocytic leukemia in children. Acta Haematol; 2008;119(2):73-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comprehensive review of acute promyelocytic leukemia in children.
  • The outcome of patients with acute promyelocytic leukemia (APL) has substantially improved since the successful introduction of tretinoin, and nowadays combining tretinoin with chemotherapy is potentially curative for at least 70-75% of patients with newly diagnosed APL.
  • In most pediatric series, APL represents < or = 10% of childhood acute myelogenous leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Child. Humans. Prognosis. Risk Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2008 S. Karger AG, Basel
  • (PMID = 18285695.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 70
  •  go-up   go-down


64. Mizushima Y, Taki T, Shimada A, Yui Y, Hiraumi Y, Matsubara H, Watanabe M, Watanabe K, Kamitsuji Y, Hayashi Y, Tsukimoto I, Kobayashi R, Horibe K, Tawa A, Nakahata T, Adachi S: Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group. Int J Hematol; 2010 Jun;91(5):831-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group.
  • High BAALC (brain and acute leukemia, cytoplasmic) gene expression may indicate an adverse prognosis for adults who have acute myeloid leukemia (AML) and a normal karyotype, but its prognostic significance for pediatric AML cases is unclear.
  • Newly diagnosed AML patients with normal karyotype who were treated by the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed in terms of their BAALC expression levels (n = 29), BAALC isoforms (n = 29), and CEBPA mutations (n = 49).
  • Thus, 1-5-6-8 isoform expression may be associated with an adverse prognosis in pediatric AML with normal karyotype.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. CCAAT-Enhancer-Binding Proteins. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Mutation. Neoplasm Proteins
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Prognosis. Protein Isoforms / genetics


65. Wang J, Ouyang J, Zhou R, Chen B, Yang Y: Autologous hematopoietic stem cell transplantation for acute myeloid leukemia in first complete remission: a meta-analysis of randomized trials. Acta Haematol; 2010;124(2):61-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous hematopoietic stem cell transplantation for acute myeloid leukemia in first complete remission: a meta-analysis of randomized trials.
  • METHODS: A meta-analysis evaluating autologous SCT versus further chemotherapy or no treatment for acute myeloid leukemia (AML) in first complete remission (CR1) was completed.
  • Four studies were in pediatric patients and 9 were in adults.
  • For adults, AML in CR1 compared with non-SCT, lower relapse and higher transplantation-related mortality were associated with autologous SCT, a significant disease-free survival benefit of autologous SCT was documented, and there was no difference in overall survival when studies were pooled.
  • For pediatric AML in CR1, there were no differences in relapse, transplantation-related mortality, disease-free survival and overall survival.
  • CONCLUSION: Our results support the conclusion that autologous SCT should not be considered as the first-line post-remission therapy for AML patients in CR1.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / mortality. Hematopoietic Stem Cell Transplantation / statistics & numerical data. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy


66. Al-Tonbary Y, Mansour AK, Ghazy H, Elghannam DM, Abd-Elghaffar HA: Prognostic significance of foetal-like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia. Int J Lab Hematol; 2009 Jun;31(3):320-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of foetal-like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia.
  • In children with acute myelogenous leukaemia (AML), internal tandem duplication of the Flt3 gene (Flt3/ITD) was previously reported and correlated to poor prognosis.
  • Limited data are available about childhood acute lymphoblastic leukaemia (ALL).
  • We analysed bone marrow specimens from 55 newly diagnosed acute leukaemia cases including 30 AML and 25 ALL by genomic PCR for the presence of Flt3/ITD and correlated its presence with clinical outcome.
  • Tandem duplication was found in 6/30(20%) AML cases: 2/8 M1, 1/8 M2, 2/6 M3, 1/6 M4 with loss of heterozygosity (LOH) in two cases.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Egypt / epidemiology. Female. Gene Duplication. Gene Frequency / genetics. Humans. Infant. Male. Multivariate Analysis. Mutation / genetics. Prognosis. Remission Induction. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18336585.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


67. van Delft FW, Bellotti T, Luo Z, Jones LK, Patel N, Yiannikouris O, Hill AS, Hubank M, Kempski H, Fletcher D, Chaplin T, Foot N, Young BD, Hann IM, Gammerman A, Saha V: Prospective gene expression analysis accurately subtypes acute leukaemia in children and establishes a commonality between hyperdiploidy and t(12;21) in acute lymphoblastic leukaemia. Br J Haematol; 2005 Jul;130(1):26-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective gene expression analysis accurately subtypes acute leukaemia in children and establishes a commonality between hyperdiploidy and t(12;21) in acute lymphoblastic leukaemia.
  • We have prospectively analysed and correlated the gene expression profiles of children presenting with acute leukaemia to the Royal London and Great Ormond Street Hospitals with morphological diagnosis, immunophenotype and karyotype.
  • Total RNA extracted from freshly sorted blast cells was obtained from 84 lymphoblastic [acute lymphoblastic leukaemia (ALL)], 20 myeloid [acute myeloid leukaemia (AML)] and three unclassified acute leukaemias and hybridised to the high density Affymetrix U133A oligonucleotide array.
  • A novel 50-gene set accurately identified all patients with ALL and AML and predicted for a diagnosis of AML in three patients with unclassified acute leukaemia.
  • A unique gene set was derived for each of eight subtypes of acute leukaemia within our data set.
  • Our analyses demonstrate that not only is microarray analysis the single most effective tool for the diagnosis of acute leukaemias of childhood but it has the ability to identify unique biological pathways.
  • To further evaluate its prognostic value it needs to be incorporated into the routine diagnostic analysis for large-scale clinical trials in childhood acute leukaemias.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Analysis of Variance. Child. Chromosome Banding. Core Binding Factor Alpha 2 Subunit. DNA-Binding Proteins / genetics. Diagnosis, Differential. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia / genetics. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics. Ploidies. Principal Component Analysis. Prospective Studies. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-ets. Repressor Proteins / genetics. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Telomeric Repeat Binding Protein 2 / genetics. Transcription Factors / genetics. Translocation, Genetic

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15982341.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 14840
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Telomeric Repeat Binding Protein 2; 0 / Transcription Factors
  •  go-up   go-down


68. Meyer S, Fergusson WD, Whetton AD, Moreira-Leite F, Pepper SD, Miller C, Saunders EK, White DJ, Will AM, Eden T, Ikeda H, Ullmann R, Tuerkmen S, Gerlach A, Klopocki E, Tönnies H: Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption. Genes Chromosomes Cancer; 2007 Apr;46(4):359-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption.
  • Fanconi anemia (FA) is an inherited disease with congenital abnormalities and an extreme risk of acute myeloid leukemia (AML).
  • Genetic events occurring during malignant transformation in FA and the biology of FA-associated AML are poorly understood, but are often preceded by the development of chromosomal aberrations involving 3q26-29 in bone marrow of FA patients.
  • We report here the molecular cytogenetic characterization of FA-derived AML cell lines SB1685CB and SB1690CB by conventional and array comparative genomic hybridization, fluorescence in situ hybridization, and SKY.
  • We identified gains of a 3.7 MB chromosomal region on 3q26.2-26.31, which preceded transformation to overt leukemia.
  • Rearrangements of 3q, which are rare in childhood AML, commonly result in overexpression of EVI1, which determines specific gene expression patterns and confers poor prognosis.
  • We detected overexpression of EVI1 in all three FA-derived AML.
  • We hypothesize that constitutional or acquired FA defects might be a common factor for the development of 3q abnormalities in AML.
  • In addition, cryptic imbalances as detected here might account for overexpression of EVI1 in AML without overt 3q26 rearrangements.
  • [MeSH-major] BRCA2 Protein / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Fanconi Anemia / genetics. Gene Amplification. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line. Child. Humans


69. Entz-Werle N, Suciu S, van der Werff ten Bosch J, Vilmer E, Bertrand Y, Benoit Y, Margueritte G, Plouvier E, Boutard P, Vandecruys E, Ferster A, Lutz P, Uyttebroeck A, Hoyoux C, Thyss A, Rialland X, Norton L, Pages MP, Philippe N, Otten J, Behar C, EORTC Children Leukemia Group: Results of 58872 and 58921 trials in acute myeloblastic leukemia and relative value of chemotherapy vs allogeneic bone marrow transplantation in first complete remission: the EORTC Children Leukemia Group report. Leukemia; 2005 Dec;19(12):2072-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of 58872 and 58921 trials in acute myeloblastic leukemia and relative value of chemotherapy vs allogeneic bone marrow transplantation in first complete remission: the EORTC Children Leukemia Group report.
  • The first EORTC (European Organization of Research and Treatment of Cancer) acute myeloblastic leukemia (AML) pilot study (58872) was conducted between January 1988 and December 1991.
  • It indicated that mitoxantrone could be substituted for conventional anthracyclines in the treatment of childhood AML without inducing cardiotoxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Idarubicin / therapeutic use. Infant. Infant, Newborn. Male. Mitoxantrone / therapeutic use. Remission Induction. Survival Rate. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16136166.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U10-CA11488-18; United States / NCI NIH HHS / CA / 5U10-CA11488-35
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
  •  go-up   go-down


70. Tan RM, Quah TC, Aung L, Liang S, Kirk RC, Yeoh AE: Improved outcome in childhood acute myeloid leukemia in Singapore with the MRC AML 10 protocol. Pediatr Blood Cancer; 2007 Mar;48(3):262-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved outcome in childhood acute myeloid leukemia in Singapore with the MRC AML 10 protocol.
  • BACKGROUND: The introduction of the United Kingdom Medical Research Council's 10th AML trial (MRC AML 10) protocol incorporating high-dose anthracycline therapy has improved outcome of children with acute myeloid leukemia (AML).
  • In this study, we review the results of childhood AML therapy in a Singapore university hospital over the last 17 years emphasizing toxicity and outcome.
  • PROCEDURE: Retrospective analysis revealed 34 children with AML between 1988 and 2003.
  • From September 1996, all but one of 15 children received MRC AML 10 treatment.
  • MRC AML 10-treated patients (n = 14) had significantly better 3-year overall, event-free, and disease-free survival (74% vs. 35%, 77% vs. 20%, 83% vs. 31%; P = 0.019, P = 0.002, and P = 0.010, respectively) and were likelier to achieve complete remission (CR) than non-MRC AML 10 patients (P = 0.102).
  • Among patients who achieved CR, MRC AML 10-treated patients were significantly more likely to achieve CR after only one cycle of chemotherapy (P = 0.016).
  • CONCLUSIONS: These findings suggest that MRC AML 10 treatment results in significantly superior survival, without excess toxicity.
  • Future studies should attempt to elucidate the relative importance of individual MRC AML 10 components and reduce the high cumulative anthracycline dose without compromising outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. 6-Mercaptopurine / adverse effects. Acute Disease. Amsacrine / administration & dosage. Amsacrine / adverse effects. Azacitidine / administration & dosage. Azacitidine / adverse effects. Child. Child, Preschool. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Developing Countries. Disease-Free Survival. Drug Evaluation. Drug-Induced Liver Injury / etiology. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Gastrointestinal Diseases / chemically induced. Heart Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Infant. Infection / etiology. Kaplan-Meier Estimate. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Prednisone / administration & dosage. Prednisone / adverse effects. Remission Induction. Retrospective Studies. Singapore / epidemiology. Survival Analysis. Thioguanine / administration & dosage. Thioguanine / adverse effects. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. AMSACRINE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16602120.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 00DPD30SOY / Amsacrine; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; E7WED276I5 / 6-Mercaptopurine; FTK8U1GZNX / Thioguanine; M801H13NRU / Azacitidine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; MRC AML 10 protocol; POG-8498 protocol
  •  go-up   go-down


71. Xie C, Edwards H, Xu X, Zhou H, Buck SA, Stout ML, Yu Q, Rubnitz JE, Matherly LH, Taub JW, Ge Y: Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia. Clin Cancer Res; 2010 Nov 15;16(22):5499-510
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia.
  • PURPOSE: To determine the possibility of synergistic antileukemic activity and the underlying molecular mechanisms associated with cytarabine combined with valproic acid (VPA; a histone deacetylase inhibitor and a Food and Drug Administration-licensed drug for treating both children and adults with epilepsy) in pediatric acute myeloid leukemia (AML).
  • EXPERIMENTAL DESIGN: The type and extent of antileukemic interactions between cytarabine and VPA in clinically relevant pediatric AML cell lines and diagnostic blasts from children with AML were determined by MTT assays and standard isobologram analyses.
  • RESULTS: We showed synergistic antileukemic activities between cytarabine and VPA in four pediatric AML cell lines and nine diagnostic AML blast samples. t(8;21) AML blasts were significantly more sensitive to VPA and showed far greater sensitivities to combined cytarabine and VPA than non-t(8;21) AML cases.
  • CONCLUSIONS: Our results establish global synergistic antileukemic activity of combined VPA and cytarabine in pediatric AML and provide compelling evidence to support the use of VPA in the treatment of children with this deadly disease.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] Blood. 2008 Mar 1;111(5):2505-15 [18299451.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Sep;298(3):865-72 [11504778.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4500-10 [18628465.001]
  • [Cites] Blood. 2009 Sep 24;114(13):2744-52 [19638627.001]
  • [Cites] Mol Cell Biol. 2009 Dec;29(23):6149-69 [19805519.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):6969-78 [11742974.001]
  • [Cites] Leuk Res. 2002 May;26(5):495-502 [11916526.001]
  • [Cites] Leukemia. 2003 Jan;17(1):120-4 [12529668.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):425-9 [14706334.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1246-51 [15116123.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1266-9 [15155466.001]
  • [Cites] Br J Haematol. 2004 Nov;127(3):264-79 [15491285.001]
  • [Cites] Adv Cancer Res. 1998;72:197-233 [9338077.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1393-400 [10438727.001]
  • [Cites] Nat Med. 2005 Jan;11(1):71-6 [15619634.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):226-31 [15687366.001]
  • [Cites] Leuk Res. 2005 Jul;29(7):739-48 [15927669.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3923-31 [15897550.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1335-42 [15936818.001]
  • [Cites] Trends Mol Med. 2005 Oct;11(10):442-4 [16150641.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):16090-5 [16243973.001]
  • [Cites] Blood. 2006 Jan 1;107(1):241-9 [16141349.001]
  • [Cites] Cancer. 2006 Jan 1;106(1):112-9 [16323176.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1174-82 [16675713.001]
  • [Cites] Mol Cancer Res. 2006 Aug;4(8):563-73 [16877702.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8903-11 [16951208.001]
  • [Cites] Nat Rev Drug Discov. 2006 Sep;5(9):769-84 [16955068.001]
  • [Cites] Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Seizure. 2006 Dec;15(8):630-2 [17070075.001]
  • [Cites] Leukemia. 2007 Feb;21(2):248-52 [17122863.001]
  • [Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1979-85 [17513804.001]
  • [Cites] Blood. 2007 Jul 1;110(1):267-77 [17356134.001]
  • [Cites] Curr Drug Targets. 2007 Jun;8(6):727-37 [17584028.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2302-8 [17596541.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1519-32 [18024401.001]
  • [Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):886-95 [10959836.001]
  • [Cites] Cancer Treat Rev. 2008 May;34(3):206-22 [18226465.001]
  • (PMID = 20889917.001).
  • [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 / NCI NIH HHS / CA / CA120772-01A2; United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / CA120772; United States / NCI NIH HHS / CA / R01 CA120772-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ NIHMS238223; NLM/ PMC3018695
  •  go-up   go-down


72. Elgendi HM, Mekawy MA, Abdel Wahab SE, Tawfik LM, Ismail EA, Adly AA: AC133 expression in egyptian children with acute leukemia: impact on treatment response and disease outcome. J Pediatr Hematol Oncol; 2010 May;32(4):286-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AC133 expression in egyptian children with acute leukemia: impact on treatment response and disease outcome.
  • Hence, it is expected to be a valuable prognostic marker in acute leukemia.
  • Sixty Egyptian children with acute leukemia were enrolled into this prospective study divided into 2 groups: 30 acute myeloblastic leukemia (AML) and 30 acute lymphoblastic leukemia (ALL) patients.
  • AC133 was expressed in 66.7% and 40% of AML and ALL patients, respectively.
  • In AML, 80% of patients with poor clinical outcome (relapse or death) were positive for AC133 expression, whereas, all ALL patients who developed resistance as well as those who displayed poor clinical outcome had AC133-positive expression (P<0.05).
  • Patients with positive AC133 expression had significantly shorter overall and disease-free survival times compared with AC133-negative patients in both ALL (P<0.001) and AML (P<0.05) groups.
  • AC133-positive expression is an independent poor prognostic factor in childhood acute leukemia and could characterize a group of patients with resistance to standard chemotherapy, as well as high incidence of relapse and death.
  • [MeSH-major] Antigens, CD / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glycoproteins / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Peptides / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Immunophenotyping. Infant. Karyotyping. Male. Prospective Studies. Survival Rate. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20224439.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides
  •  go-up   go-down


73. Perkins JL, Kunin-Batson AS, Youngren NM, Ness KK, Ulrich KJ, Hansen MJ, Petryk A, Steinberger J, Anderson FS, Baker KS: Long-term follow-up of children who underwent hematopoeitic cell transplant (HCT) for AML or ALL at less than 3 years of age. Pediatr Blood Cancer; 2007 Dec;49(7):958-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term follow-up of children who underwent hematopoeitic cell transplant (HCT) for AML or ALL at less than 3 years of age.
  • BACKGROUND: Hematopoeitic cell transplantation (HCT) in childhood has been associated with late complications including endocrine, neurocognitive, and cardiopulmonary abnormalities.
  • PROCEDURE: Eligible subjects underwent HCT for acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML) at less than 3 years of age.
  • Eleven patients had AML, 11 were female.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Conditioning
  • [MeSH-minor] Child, Preschool. Dyslipidemias / pathology. Female. Follow-Up Studies. Humans. Infant. Male. Metabolic Syndrome X / diagnosis. Quality of Life. Risk Factors. Survival Rate. Time. Transplantation, Homologous. Treatment Outcome. Whole-Body Irradiation


74. Castagnola E, Rossi MR, Cesaro S, Livadiotti S, Giacchino M, Zanazzo G, Fioredda F, Beretta C, Ciocchello F, Carli M, Putti MC, Pansini V, Berger M, Licciardello M, Farina S, Caviglia I, Haupt R: Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study. Pediatr Blood Cancer; 2010 Dec 1;55(6):1103-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study.
  • BACKGROUND: Data on the epidemiology of bacteremias and invasive fungal diseases (IFD) in children with acute myeloid leukemia (AML) are scarce.
  • DESIGN AND METHODS: In a multi-center, retrospective study, we analyzed proportion, rate per 1,000 person-days at risk, and cumulative risk of bacteremias and IFD in children with AML.
  • RESULTS: Between January 1998 and December 2005, 240 children were treated for AML at 8 Italian Centers, for a total of 521 treatment courses and 63,232 person-days at risk.
  • The epidemiology of bacteremias and IFD was different during front-line therapy for M3 as compared to other types of AML, but the differences were not statistically significant.
  • CONCLUSIONS: Severe infectious complications are frequent during the treatment of pediatric AML, especially during relapse treatment, and bacteremias are more frequent than IFD.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bacteremia / etiology. Leukemia, Myeloid, Acute / microbiology. Mycoses / etiology
  • [MeSH-minor] Child. Female. Follow-Up Studies. Humans. Incidence. Italy. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / microbiology. Retrospective Studies


75. Cloos J, Goemans BF, Hess CJ, van Oostveen JW, Waisfisz Q, Corthals S, de Lange D, Boeckx N, Hählen K, Reinhardt D, Creutzig U, Schuurhuis GJ, Zwaan ChM, Kaspers GJ: Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples. Leukemia; 2006 Jul;20(7):1217-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples.
  • In acute myeloid leukemia (AML), activating mutations in the fms-like tyrosine kinase 3 (FLT3) gene predict poor prognosis.
  • We determined FLT3 internal tandem duplications (FLT3/ITD) and D835 point mutations in paired initial and relapse samples from 80 pediatric and adult AML patients.
  • One D835 point mutation was found in an initial pediatric AML sample.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Point Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Female. Genetic Markers. Genetic Predisposition to Disease / epidemiology. Humans. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Neoplasm, Residual / epidemiology. Neoplasm, Residual / genetics. Prognosis. Recurrence. Risk Factors. Tandem Repeat Sequences

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16642044.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


76. Andreeva SV, Drozdova VD, Kavardakova NV: [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia]. Tsitol Genet; 2010 May-Jun;44(3):41-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia].
  • Analysis of chromosomal abnormalities in bone marrow cells in 116 children with diagnosis of acute myeloid leukemia (AML) was performed.
  • Frequency of evolution of clonal chromosome abnormalities in AML constituted 42,3%.
  • Identity of abnormal chromosome structure at diagnosis and relapse of disease can be an evidence of the influence of chemical agent on establishment of some types of evolution of chromosome abnormalities in leukemic cells in AML in children.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosome Deletion. Clone Cells. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Monosomy. Translocation, Genetic. Trisomy


77. Zhang H, Luo XQ, Zhang P, Huang LB, Zheng YS, Wu J, Zhou H, Qu LH, Xu L, Chen YQ: MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in pediatric acute leukemia. PLoS One; 2009;4(11):e7826
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in pediatric acute leukemia.
  • BACKGROUND: Recent reports have indicated that microRNAs (miRNAs) play a critical role in malignancies, and regulations in the progress of adult leukemia.
  • The role of miRNAs in pediatric leukemia still needs to be established.
  • The purpose of this study was to investigate the aberrantly expressed miRNAs in pediatric acute leukemia and demonstrate miRNA patterns that are pediatric-specific and prognostic parameter-associated.
  • METHODOLOGY/PRINCIPAL FINDINGS: A total of 111 pediatric bone marrow samples, including 99 patients and 12 normal donors, were enrolled in this study.
  • Of those samples, 36 patients and 7 normal samples were used as a test cohort for the evaluation of miRNA profiling; 63 pediatric patients and 5 normal donors were used as a validation cohort to confirm the miRNA differential expression.
  • Pediatric ALL- and AML-specific microRNA expression patterns were identified in this study.
  • The most highly expressed miRNAs in pediatric ALL were miR-34a, miR-128a, miR-128b, and miR-146a, while the highly expressed miRNAs in pediatric AML were miR-100, miR-125b, miR-335, miR-146a, and miR-99a, which are significantly different from those reported for adult CLL and AML. miR-125b and miR-126 may serve as favorable prognosticators for M3 and M2 patients, respectively.
  • CONCLUSIONS/SIGNIFICANCE: There are existing pediatric-associated and prognostic parameter-associated miRNAs that are independent of cell lineage and could provide therapeutic direction for individual risk-adapted therapy for pediatric leukemia patients.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Leukemia / diagnosis. Leukemia / pathology. MicroRNAs
  • [MeSH-minor] Child. Child, Preschool. Cohort Studies. Female. Gene Expression Profiling. Gene Expression Regulation. Humans. Infant. Male. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk

  • MedlinePlus Health Information. consumer health - Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2003 Apr 4;113(1):25-36 [12679032.001]
  • [Cites] Genes Dev. 2003 Feb 15;17(4):438-42 [12600936.001]
  • [Cites] J Pediatr (Rio J). 2003 Mar-Apr;79(2):149-58 [14502336.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Feb;39(2):167-9 [14695998.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 [14973191.001]
  • [Cites] Genes Dev. 2004 Mar 1;18(5):504-11 [15014042.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11755-60 [15284443.001]
  • [Cites] N Engl J Med. 2004 Aug 26;351(9):893-901 [15329427.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):769-73 [15685193.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] Nature. 2005 Mar 17;434(7031):338-45 [15735639.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1768-71 [16251533.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Nucleic Acids Res. 2005;33(20):e179 [16314309.001]
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):167-73 [16616063.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7390-4 [16885332.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19971-6 [18056805.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2825-32 [18089852.001]
  • [Cites] Blood. 2008 Mar 15;111(6):3183-9 [18187662.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15535-40 [18832181.001]
  • [Cites] J Exp Med. 2008 Oct 27;205(11):2499-506 [18936236.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]
  • [Cites] Leukemia. 2009 Feb;23(2):313-22 [18923441.001]
  • [Cites] Dev Biol. 1999 Dec 15;216(2):671-80 [10642801.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):179-81 [12525506.001]
  • [Cites] N Engl J Med. 2003 May 1;348(18):1764-75 [12724482.001]
  • (PMID = 19915715.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2773830
  •  go-up   go-down


78. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


79. Kömür M, Erbey F, Bayram I, Tanyeli A: Incidence and prognostic importance of molecular genetic defects in children with acute myeloblastic leukemia. Asian Pac J Cancer Prev; 2010;11(5):1393-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence and prognostic importance of molecular genetic defects in children with acute myeloblastic leukemia.
  • INTRODUCTION: Acute myeloblastic leukemia (AML) accounts for 15 to 25 percent of childhood acute leukemias.
  • The most common genetic abnormalities seen in pediatric AML patients are AML1-ETO, PML-RARα and CBFB-MYH11 genes resulting in t(8;21), t(15;17) and inv(16).
  • These genetic defects are seen in approximately 20-25% of AML patients.
  • OBJECTIVE: We investigated in this study, incidence and prognostic significance of the AML1-ETO, PML-RARα and CBFB-MYH11 genes in children with AML.
  • MATERIALS AND METHODS: The authors analyzed 34 children with AML using the real time-polymerase chain reaction for AML1-ETO, PML-RARα and CBFB-MYH11 genes.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction. Prognosis. Survival Rate

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21198299.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  •  go-up   go-down


80. Biswas S, Chakrabarti S, Chakraborty J, Paul PC, Konar A, Das S: Childhood acute leukemia in West Bengal, India with an emphasis on uncommon clinical features. Asian Pac J Cancer Prev; 2009;10(5):903-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood acute leukemia in West Bengal, India with an emphasis on uncommon clinical features.
  • Leukemias are the commonest childhood malignancy in West Bengal.
  • This study was undertaken on 75 children at NRS Medical College, West Bengal to determine the distribution of signs and symptoms of leukemia and to identify unusual clinical features.
  • Acute lymphoblastic leukaemia (ALL, 72%) was the commonest followed by acute myeloid leukaemia (AML, 18.7%).
  • Awareness of uncommon signs and symptoms of childhood leukemia together with laboratory tests may help in earlier diagnosis and proper management of the patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Abdominal Pain / etiology. Adolescent. Arthralgia / etiology. Child. Child, Preschool. Female. Fever / etiology. Humans. Incidence. India / epidemiology. Infant. Infant, Newborn. Male. Risk Factors. Survival Rate

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Asian Pac J Cancer Prev. 2010;11(1):267-8 [20593969.001]
  • (PMID = 20104987.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  •  go-up   go-down


81. Styczynski J, Czyzewski K, Wysocki M: Ex vivo activity of thalidomide in childhood acute leukemia. Leuk Lymphoma; 2006 Jun;47(6):1123-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ex vivo activity of thalidomide in childhood acute leukemia.
  • Thalidomide is a drug with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that were found to inhibit the production of TNF-alpha in vitro, stimulate reactive oxygen species production, and inhibit VEGFR in acute leukemias.
  • Ex vivo activity of thalidomide as a single agent and in combination with prednisolone or cytarabine in childhood acute leukemias was analyzed.
  • Forty samples of childhood acute lymphoblastic leukemia (ALL) and 13 acute myeloid leukemia (AML) were tested for cytotoxicity by the MTT assay and cell cycle phases by flow cytometry.
  • A weak anti-leukemic activity of thalidomide against childhood leukemic samples was observed.
  • However, in the presence of thalidomide, cytotoxicity of prednisolone or cytarabine, increased 3.3-fold and 2.7-fold, respectively, in childhood ALL but was not changed in AML.
  • Thalidomide increased apoptosis in lymphoblasts, and modulated cell cycle arrest caused by prednisolone but not cytarabine in childhood acute lymphoblastic leukemia samples.
  • Thalidomide potentiated ex vivo sensitivity of childhood ALL cells to prednisolone and cytarabine, while no sensitization effect was observed in AML cells.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / pharmacology
  • [MeSH-minor] Cell Cycle. Child. Child, Preschool. Cytarabine / pharmacology. Female. Humans. Immunophenotyping. Infant. Male. Prednisolone / pharmacology. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16840205.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; 4Z8R6ORS6L / Thalidomide; 9PHQ9Y1OLM / Prednisolone
  •  go-up   go-down


82. Ashfaq K, Yahaya I, Hyde C, Andronis L, Barton P, Bayliss S, Chen YF: Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review. Health Technol Assess; 2010 Dec;14(54):iii-iv, ix-xi, 1-141
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review.
  • BACKGROUND: Acute leukaemia is a group of rapidly progressing cancers of bone marrow and blood classified as either acute myeloid leukaemia (AML) or acute lymphoblastic leukaemia (ALL).
  • OBJECTIVES: A systematic overview of the best available evidence on the clinical effectiveness and cost-effectiveness of SCT in the treatment of acute leukaemia.
  • Included randomised controlled trials (RCTs) and donor versus no donor (DvND) studies were mapped to the evidence covered in existing systematic reviews and meta-analyses according to a framework of 12 decision problems (DPs): DP1 related to SCT in adults with AML in first complete remission (CR1); DP2 to adults with AML in second or subsequent remission or with refractory disease (CR2+); DP3 to children with AML in CR1; DP4 to children with AML in CR2+; DP5 to adults with ALL in CR1; DP6 to adults with ALL in CR2+; DP7 to children with ALL in CR1; DP8 to children with ALL in CR2+; DP9 to comparison of different sources of stem cells in transplantation; DP10 to different conditioning regimens; DP11 to the use of purging in autologous SCT; and DP12 to the use of T-cell depletion in allogeneic SCT.
  • Although there is a wealth of information on costs and some information on cost-effectiveness of allogeneic SCT in adults with AML (DPs 1 and 2), there is very limited evidence on relative costs and cost-effectiveness for other DPs.
  • CONCLUSIONS: Bearing in mind the limitations, existing evidence suggests that sibling donor allogeneic SCT may be more effective than chemotherapy in adult AML (except in good-risk patients) in CR1, childhood AML in CR1 and adult ALL in CR1, and that autologous SCT is equal to or less effective than chemotherapy.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery
  • [MeSH-minor] Adult. Child. Cost-Benefit Analysis. Humans


83. Urbanová D, Bubanská E, Hrebík M, Mladosievicová B: [Severe heart failure in consequence of late anthracycline-induced cardiotoxicity--case report]. Klin Onkol; 2009;22(1):34-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The patient was treated for childhood acute myeloid leukemia by chemotherapy containing anthracyclines.
  • [MeSH-minor] Adolescent. Heart Transplantation. Humans. Leukemia, Myeloid, Acute / drug therapy. Male

  • MedlinePlus Health Information. consumer health - Heart Failure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19534438.001).
  • [ISSN] 0862-495X
  • [Journal-full-title] Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
  • [ISO-abbreviation] Klin Onkol
  • [Language] slo
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic
  •  go-up   go-down


84. Meyer C, Kowarz E, Hofmann J, Renneville A, Zuna J, Trka J, Ben Abdelali R, Macintyre E, De Braekeleer E, De Braekeleer M, Delabesse E, de Oliveira MP, Cavé H, Clappier E, van Dongen JJ, Balgobind BV, van den Heuvel-Eibrink MM, Beverloo HB, Panzer-Grümayer R, Teigler-Schlegel A, Harbott J, Kjeldsen E, Schnittger S, Koehl U, Gruhn B, Heidenreich O, Chan LC, Yip SF, Krzywinski M, Eckert C, Möricke A, Schrappe M, Alonso CN, Schäfer BW, Krauter J, Lee DA, Zur Stadt U, Te Kronnie G, Sutton R, Izraeli S, Trakhtenbrot L, Lo Nigro L, Tsaur G, Fechina L, Szczepanski T, Strehl S, Ilencikova D, Molkentin M, Burmeister T, Dingermann T, Klingebiel T, Marschalek R: New insights to the MLL recombinome of acute leukemias. Leukemia; 2009 Aug;23(8):1490-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights to the MLL recombinome of acute leukemias.
  • Chromosomal rearrangements of the human MLL gene are associated with high-risk pediatric, adult and therapy-associated acute leukemias.
  • Genomic DNA was isolated from individual acute leukemia patients to identify and characterize chromosomal rearrangements involving the human MLL gene.
  • A total of 760 MLL-rearranged biopsy samples obtained from 384 pediatric and 376 adult leukemia patients were characterized at the molecular level.
  • The distribution of MLL breakpoints for clinical subtypes (acute lymphoblastic leukemia, acute myeloid leukemia, pediatric and adult) and fused translocation partner genes (TPGs) will be presented, including novel MLL fusion genes.
  • [MeSH-major] Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Recombination, Genetic. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Biopsy. Bone Marrow / chemistry. Bone Marrow / pathology. Child. Chromosome Breakage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Computational Biology. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19262598.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


85. Larson RA: Micro-RNAs and copy number changes: new levels of gene regulation in acute myeloid leukemia. Chem Biol Interact; 2010 Mar 19;184(1-2):21-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Micro-RNAs and copy number changes: new levels of gene regulation in acute myeloid leukemia.
  • Together with epigenetic alterations, these result in dysplasia, clonal expansion, and ultimately myeloid leukemia.
  • Combinations of lesions are required to induce overt leukemia.
  • Recent studies have shown that cytogenetically normal (CN-) AML is quite heterogeneous at the molecular level.
  • Patients with CN-AML harboring mutations in NPM1, FLT3, CEBPA, WT1 or expressing high levels of BAALC, ERG, or MN1 have distinctly different clinical outcomes.
  • NPM1 mutations are independently associated with higher remission rates and longer disease-free and overall survival in AML.
  • Fewer CNAs have been detected in AML than in pediatric ALL.
  • Distinctive genome-wide miR expression profiles have been associated with different subsets of AML.
  • A miR signature that is associated with clinical outcome in patients with high-risk molecular features of AML (those who have FLT3-ITD or wild-type NPM1) has been reported.
  • This subgroup constitutes approximately 65% of patients with CN-AML and one-third of all patients with AML <60 years old.
  • Down-regulation of the miR-181 family contributes to an aggressive leukemia phenotype through mechanisms associated with the activation of pathways of innate immunity mediated by toll-like receptors and interleukin-1beta.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):596-604 [20026798.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]
  • [Cites] Cell Cycle. 2006 Oct;5(19):2220-2 [17012846.001]
  • [Cites] Nature. 2006 Nov 23;444(7118):444-54 [17122850.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1552-9 [17940205.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2776-84 [17957027.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1919-28 [18450603.001]
  • [Cites] Leukemia. 2008 May;22(5):951-5 [18273044.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15535-40 [18832181.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1209-18 [19242497.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12950-5 [19651600.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1731-43 [19516275.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1224-32 [12149202.001]
  • (PMID = 19822134.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA014599-34; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / U10 CA031946-28; United States / NCI NIH HHS / CA / P30 CA014599-34; United States / NCI NIH HHS / CA / P01 CA040046-22; United States / NCI NIH HHS / CA / CA031946-28; United States / NCI NIH HHS / CA / CA040046-22; United States / NCI NIH HHS / CA / CA14599; United States / NCI NIH HHS / CA / CA31946
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ NIHMS156571; NLM/ PMC2846194
  •  go-up   go-down


86. Puhlmann U, Ziemann C, Ruedell G, Vorwerk H, Schaefer D, Langebrake C, Schuermann P, Creutzig U, Reinhardt D: Impact of the cyclooxygenase system on doxorubicin-induced functional multidrug resistance 1 overexpression and doxorubicin sensitivity in acute myeloid leukemic HL-60 cells. J Pharmacol Exp Ther; 2005 Jan;312(1):346-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of the cyclooxygenase system on doxorubicin-induced functional multidrug resistance 1 overexpression and doxorubicin sensitivity in acute myeloid leukemic HL-60 cells.
  • Multidrug resistance (MDR), a challenge in treating childhood acute myeloid leukemia (AML), is frequently associated with decreased drug accumulation caused by multidrug transporter MDR1.
  • Doxorubicin, an important anti-AML drug, is a known MDR1 substrate and inducer.
  • Our study focused on cyclooxygenase system's impact on drug-induced MDR1 overexpression in AML cells.
  • As a prerequisite, coexpression of MDR1 and cyclooxygenase-2 mRNA in HL-60 cells and primary AML blasts was demonstrated by Northern blot.
  • Interestingly, incubation of AML cells with doxorubicin not only induced functionally active MDR1 overexpression but also mediated increased cyclooxygenase-2 mRNA and protein expressions with subsequent PGE(2) release (determined by flow cytometry, rhodamine123 efflux assay, reverse transcription-polymerase chain reaction, and enzyme-linked immunosorbent assay).
  • After preincubation and subsequent parallel treatment with the cyclooxygenase-2-preferential inhibitor meloxicam, doxorubicin-induced MDR1 overexpression and function were reduced (maximally at 0.1-0.5 microM meloxicam), whereas cytostatic efficacy of doxorubicin in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assays was significantly increased by up to 78 (HL-60) and 30% (AML blasts) after 72 h of doxorubicin treatment.
  • In conclusion, the cyclooxygenase system, especially the cyclooxygenase-2 isoform, might be involved in regulating doxorubicin-induced MDR1 overexpression in AML cells, with PGE(2) seeming to be a mediating factor.
  • Cyclooxygenase inhibitors thus bear promise to overcome MDR in AML and improve therapy.
  • [MeSH-minor] Apoptosis. Biological Transport. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / pharmacology. Dinoprostone / metabolism. Drug Interactions. Drug Resistance, Multiple. Drug Screening Assays, Antitumor. Gene Expression / drug effects. HL-60 Cells. Humans. Leukemia, Myeloid, Acute. Membrane Proteins. Rhodamine 123 / pharmacology. Thiazines / pharmacology. Thiazoles / pharmacology

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. Meloxicam .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15501994.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Membrane Proteins; 0 / P-Glycoprotein; 0 / Thiazines; 0 / Thiazoles; 1N3CZ14C5O / Rhodamine 123; 71125-38-7 / meloxicam; 80168379AG / Doxorubicin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
  •  go-up   go-down


87. Ghosh I, Thulkar S, Arora R, Bakhshi S: Multifocal osteomyelitis as a presenting manifestation of childhood acute myeloid leukemia. J Pediatr Hematol Oncol; 2009 Jan;31(1):75-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multifocal osteomyelitis as a presenting manifestation of childhood acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Osteomyelitis / diagnosis


88. Chen YM, Liu TF, Ruan M, Zou Y, Chen XJ, Guo Y, Wang SC, Zhu XF: [Prognosis and chromosomal abnormalities in 79 children with t (8;21) acute myeloid leukemia]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2009 Oct;31(5):542-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognosis and chromosomal abnormalities in 79 children with t (8;21) acute myeloid leukemia].
  • OBJECTIVE: To investigate the chromosomal abnormalities and evaluate the prognostic value of post-remission chemotherapy in children with t (8;21) acute myeloid leukemia (AML).
  • METHODS: The diagnosis of AML and its subtyping were performed using morphological, immunological, and cytogenetic methodologies in 79 children.
  • CONCLUSION: Most children with t (8;21) AML have additional chromosomal abnormalities, although they do not affect the prognosis and long-term survival.
  • Childhood t (8;21) AML usually has high CR rate with relatively good prognosis, and post-remission consolidation by HDAC can improve the survival.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Female. Humans. Karyotype. Male. Prognosis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19968066.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


89. von Neuhoff C, Reinhardt D, Sander A, Zimmermann M, Bradtke J, Betts DR, Zemanova Z, Stary J, Bourquin JP, Haas OA, Dworzak MN, Creutzig U: Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98. J Clin Oncol; 2010 Jun 1;28(16):2682-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98.
  • PURPOSE: Because cytogenetic data are essential for risk stratification of childhood acute myeloid leukemia (AML), the impact of chromosomal aberrations is crucial.
  • PATIENTS AND METHODS: Data of a large group of patients younger than 18 years treated according to study AML-Berlin-Frankfurt-Münster (BFM) 98 (n = 454), including their cytogenetics, were analyzed.
  • CONCLUSION: Because the prognostic value of rare recurrent chromosomal aberrations still has to be elucidated, these data will contribute to future risk stratification for the treatment of pediatric AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Combined Modality Therapy. Confidence Intervals. Cytarabine / administration & dosage. Cytogenetic Analysis. Disease-Free Survival. Etoposide / administration & dosage. Female. Follow-Up Studies. Humans. Idarubicin / administration & dosage. In Situ Hybridization, Fluorescence. Male. Probability. Proportional Hazards Models. Radiotherapy, Adjuvant. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Severity of Illness Index. Statistics, Nonparametric. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20439630.001).
  • [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] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
  •  go-up   go-down


90. Langebrake C, Brinkmann I, Teigler-Schlegel A, Creutzig U, Griesinger F, Puhlmann U, Reinhardt D: Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring. Cytometry B Clin Cytom; 2005 Jan;63(1):1-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring.
  • BACKGROUND: Determination of antigen expression patterns is, in addition to morphologic analysis, essential to the diagnosis of acute myeloid leukemia (AML).
  • The present study was performed to determine (a) the degree of changes in immunophenotype and their consequences on the monitoring of minimal residual disease (MRD) in childhood AML and (b) whether certain clusters of changes in antigen expression patterns exist between diagnosis and relapse.
  • METHODS: Bone marrow specimens of 48 children enrolled in the German AML-BFM-93/98 (Acute Myeloid Leukemia-Berlin-Frankfurt-Munster) studies were analyzed immunologically, morphologically, and genetically at diagnosis and at first relapse.
  • We did not observe significant changes for lineage specific markers, with comparable occurrences of loss or gain of myeloid and lymphoid antigens in the sample pairs.
  • The antibody panels used for MRD monitoring in childhood AML should therefore not be restricted to the immunophenotype detected at presentation but should include in particular markers of lineage immaturity.
  • [MeSH-major] Antigens, Neoplasm / immunology. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Bone Marrow / immunology. Bone Marrow / pathology. Child. Child, Preschool. Clone Cells. Flow Cytometry. Humans. Infant. Karyotyping. Recurrence

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15624201.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
  •  go-up   go-down


91. Goubin A, Auclerc MF, Auvrignon A, Patte C, Bergeron C, Hémon D, Clavel J: Survival in France after childhood acute leukaemia and non-Hodgkin's lymphoma (1990-2000). Eur J Cancer; 2006 Mar;42(4):534-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival in France after childhood acute leukaemia and non-Hodgkin's lymphoma (1990-2000).
  • This article describes the survival after childhood acute leukaemia (AL) and non-Hodgkin's lymphoma (NHL) of French population aged less than 15 years.
  • The French National Registry of Childhood Leukaemia and Lymphoma recorded 3995 cases of acute lymphoblastic leukaemia (ALL), 812 of acute myeloid leukaemia (AML) and 1137 of NHL over the period from 1990 to 2000.
  • Overall survival rates at 5 years were 82% (95% CI 80-83), 58% (95% CI 54-61) and 87% (95% CI 85-89) for ALL, AML and NHL, respectively.
  • Survival after AL increased from 77% (95% CI 75-80) in 1990-1992 to 85% (95% CI 83-87) in 1997-2000 for ALL and from 47% (95% CI 41-54) to 61% (95% CI 55-67) for AML.
  • [MeSH-major] Lymphoma, Non-Hodgkin / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Down Syndrome / mortality. Female. France / epidemiology. Humans. Infant. Infant, Newborn. Male. Survival Rate

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16412629.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


92. Kaspers GJ, Reinhardt D, Fleischhack G, Armendariz H, Stark B, Zwaan CM, Zimmermann M, Creutzig U: Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML. Pediatr Blood Cancer; 2006 Oct 15;47(5):539-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML.
  • BACKGROUND: The efficacy in pediatric acute myeloid leukemia (AML) of single-agent methotrexate (MTX) at a higher dose than previously applied, 1,000 mg/m2, given as a theoretically beneficial 36-hr continuous infusion, is unknown, but may be beneficial based on preclinical data.
  • PROCEDURE: We performed a therapeutic window study in children with first relapsed AML treated in four different countries.
  • By that time, another four patients had been enrolled, of which one patient with a late relapsed AML FAB type M7 showed a good response.
  • CONCLUSIONS: This study shows that single-agent MTX in the applied regimen in pediatric relapsed AML has limited efficacy.
  • However, it also demonstrates the feasibility of an international and therapeutic window phase II study in pediatric relapsed AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methotrexate / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Humans. Infant. Infusions, Intravenous. Male. Maximum Tolerated Dose. Recurrence. Treatment Outcome


93. Linabery AM, Blair CK, Gamis AS, Olshan AF, Heerema NA, Ross JA: Congenital abnormalities and acute leukemia among children with Down syndrome: a Children's Oncology Group study. Cancer Epidemiol Biomarkers Prev; 2008 Oct;17(10):2572-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Congenital abnormalities and acute leukemia among children with Down syndrome: a Children's Oncology Group study.
  • Children with Down syndrome, due to their heightened risk of leukemia and increased prevalence of congenital abnormalities, comprise a valuable population in which to study etiology.
  • A Children's Oncology Group study investigated the causes of childhood leukemia in children with Down syndrome diagnosed at ages 0 to 19 years during the period 1997-2002.
  • Telephone interviews were completed with mothers of 158 cases [n=97 acute lymphoblastic leukemia (ALL) and n=61 acute myeloid leukemia (AML)] and 173 controls.
  • Odds ratios (OR) and 95% confidence intervals (95% CI) were computed via unconditional logistic regression to evaluate the association between congenital abnormalities and acute leukemia overall, and ALL and AML analyzed separately.
  • The results do not provide evidence for an association among the index children (OR(Combined), 0.74; 95% CI, 0.45-1.23; OR(ALL), 0.67; 95% CI, 0.38-1.20; OR(AML),1.03; 95% CI, 0.49-2.16) or their siblings (OR(Combined), 1.23; 95% CI, 0.71-2.13; OR(ALL), 1.12; 95% CI, 0.60-2.09; OR(AML), 1.60; 95% CI, 0.66-3.86), suggesting congenital malformations do not confer additional risk of leukemia beyond the risk attributable to trisomy 21 in this population.

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Birth Defects.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pediatr Hematol Oncol. 1987;4(3):211-30 [2978961.001]
  • [Cites] Am J Hum Genet. 1990 Mar;46(3):478-85 [2309699.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Mar-Apr;23(3):175-8 [11305722.001]
  • [Cites] Int J Epidemiol. 2001 Apr;30(2):350-2 [11369741.001]
  • [Cites] Int J Pediatr Otorhinolaryngol. 2001 Dec 1;61(3):199-205 [11700189.001]
  • [Cites] Cancer. 2003 Mar 1;97(5):1339-45 [12599243.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Sep 1;199(2):162-74 [15313588.001]
  • [Cites] Cancer Res. 1991 Jul 15;51(14):3696-701 [2065325.001]
  • [Cites] Leukemia. 1992;6 Suppl 1:5-7 [1532221.001]
  • [Cites] Am J Epidemiol. 1993 Mar 15;137(6):629-38 [8470664.001]
  • [Cites] Br J Cancer. 1993 Aug;68(2):357-63 [8347491.001]
  • [Cites] Cancer. 1996 Jan 1;77(1):201-7 [8630931.001]
  • [Cites] Am J Hum Genet. 1997 Mar;60(3):474-85 [9042906.001]
  • [Cites] Am J Med Genet. 1998 Jan 6;75(1):22-7 [9450852.001]
  • [Cites] Am J Med Genet. 1998 Jun 5;77(5):431-8 [9632176.001]
  • [Cites] Br J Cancer. 1998 Nov;78(9):1244-9 [9820188.001]
  • [Cites] J Pediatr. 1998 Nov;133(5):617-23 [9821417.001]
  • [Cites] Arch Dis Child. 1999 Jan;80(1):1-3 [10325750.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):8-12 [15390275.001]
  • [Cites] Cancer. 2005 May 1;103(9):1939-48 [15770693.001]
  • [Cites] Cancer. 2005 Jul 15;104(2):405-10 [15952191.001]
  • [Cites] J Pediatr Health Care. 2006 Jan-Feb;20(1):47-54 [16399479.001]
  • [Cites] Nature. 2006 Jun 1;441(7093):595-600 [16554754.001]
  • [Cites] Pediatrics. 2006 Nov;118(5):e1499-508 [17030598.001]
  • [Cites] Curr Opin Pediatr. 2007 Feb;19(1):9-14 [17224656.001]
  • [Cites] JAMA. 2008 Jan 2;299(1):61-9 [18167407.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):500-6 [18296646.001]
  • [Cites] Lancet. 1981 Nov 7;2(8254):1020-2 [6118480.001]
  • [Cites] Dev Med Child Neurol. 1982 Dec;24(6):817-29 [6218002.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • (PMID = 18829445.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA016086-259036; United States / NIEHS NIH HHS / ES / P30 ES10126; United States / NCI NIH HHS / CA / T32 CA099936-01A1; United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / R01 CA075169-03; United States / NCI NIH HHS / CA / P30 CA016086; United States / NCI NIH HHS / CA / R01 CA075169; United States / NCI NIH HHS / CA / R01 CA75169; United States / NCI NIH HHS / CA / CA075169-03; United States / NCI NIH HHS / CA / T32 CA099936; United States / NCI NIH HHS / CA / P30 CA016086-259036; United States / NCI NIH HHS / CA / CA099936-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS78459; NLM/ PMC2610427
  •  go-up   go-down


94. Tsai MH, Yang CP, Chung HT, Shih LY: Acute myeloid leukemia in a young girl presenting with mediastinal granulocytic sarcoma invading pericardium and causing superior vena cava syndrome. J Pediatr Hematol Oncol; 2009 Dec;31(12):980-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia in a young girl presenting with mediastinal granulocytic sarcoma invading pericardium and causing superior vena cava syndrome.
  • A 1-year-4-month-old girl who presented with pericardial effusion and superior vena cava (SVC) syndrome caused by a mediastinal mass was later proved to be a case of acute myeloid leukemia (AML) with mixed-lineage leukemia-gene translocation.
  • She developed progressive SVC syndrome, unresolved pericardial effusion, and extensive leukemia cutis after initial induction therapy.
  • To our knowledge, this is the first reported case of childhood acute myeloid leukemia presenting with mediastinal granulocytic sarcoma causing pericardium invasion and SVC syndrome.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Mediastinal Neoplasms / diagnosis. Pericardium / pathology. Sarcoma, Myeloid / diagnosis. Superior Vena Cava Syndrome / diagnosis


95. Barnard DR, Woods WG: Treatment-related myelodysplastic syndrome/acute myeloid leukemia in survivors of childhood cancer--an update. Leuk Lymphoma; 2005 May;46(5):651-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment-related myelodysplastic syndrome/acute myeloid leukemia in survivors of childhood cancer--an update.
  • Treatment-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/t-AML) is a devastating complication of treatment for childhood cancer.
  • The understanding of the presentation, incidence, predisposing risk factors and pathobiology of t-MDS/t-AML is increasing.
  • This increased understanding has not yet been translated into improved outcomes of therapy for t-MDS/t-AML.
  • [MeSH-major] Leukemia, Myeloid / etiology. Myelodysplastic Syndromes / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Child. Female. Humans. Male. Neoplasms / therapy. Survivors


96. Aguilera DG, Vaklavas C, Tsimberidou AM, Wen S, Medeiros LJ, Corey SJ: Pediatric therapy-related myelodysplastic syndrome/acute myeloid leukemia: the MD Anderson Cancer Center experience. J Pediatr Hematol Oncol; 2009 Nov;31(11):803-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric therapy-related myelodysplastic syndrome/acute myeloid leukemia: the MD Anderson Cancer Center experience.
  • Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is a long-term complication of pediatric cancer.
  • We retrospectively studied pediatric t-MDS/AML patients treated at MD Anderson from 1975 to 2007.
  • We also compared those patients to pediatric patients with de novo MDS/AML during this time interval.
  • Among 2589 children with cancer treated at MD Anderson, we identified 22 patients with t-MDS/AML.
  • Patients with t-MDS/AML had a median age of 14 years.
  • Group 2 (n=5) patients received AML-type chemotherapy and a stem cell transplant postremission (n=5).
  • Patients with de novo AML were younger (P=0.001) and higher rates of complete remission (P=0.03), and survival (P<0.0001).
  • Independent factors predicting shorter survival were poor/intermediate-risk cytogenetics (P=0.01), lower hemoglobin level (P=0.0001), and t-MDS/AML (vs. de novo) (P=0.003).
  • Childhood t-MDS/AML has a poor prognosis.
  • Although patients benefited from AML-type induction chemotherapy followed by stem cell transplantation as postremission therapy, effective therapies, and prevention are needed.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / mortality. Neoplasms, Second Primary / mortality
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Hodgkin Disease / mortality. Hodgkin Disease / therapy. Humans. Male. Osteosarcoma / mortality. Osteosarcoma / therapy. Retrospective Studies. Risk Factors. Sex Factors. Stem Cell Transplantation. Survival Rate. Transplantation, Homologous


97. Rudant J, Menegaux F, Leverger G, Baruchel A, Lambilliotte A, Bertrand Y, Patte C, Pacquement H, Vérité C, Robert A, Michel G, Margueritte G, Gandemer V, Hémon D, Clavel J: Childhood hematopoietic malignancies and parental use of tobacco and alcohol: the ESCALE study (SFCE). Cancer Causes Control; 2008 Dec;19(10):1277-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood hematopoietic malignancies and parental use of tobacco and alcohol: the ESCALE study (SFCE).
  • OBJECTIVES: Investigating the role of parental smoking and maternal alcohol consumption in the etiology of childhood hematopoietic malignancies.
  • RESULTS: A total of 765 cases of acute leukemia (AL), 130 of Hodgkin's lymphoma (HL), 165 of non-Hodgkin's lymphoma (NHL) and 1681 controls were included.
  • Paternal smoking was significantly associated with childhood ALL (OR = 1.4 [1.1-1.7]), AML (OR = 1.5 [1.0-2.3]), Burkitt (OR = 2.0 [1.2-3.2]), and anaplastic large cell (OR = 3.2 [1.2-9.1]) NHL.
  • CONCLUSION: The results support the hypothesis that only paternal smoking, and not maternal alcohol consumption or cigarette smoking, plays a role in childhood hematopoietic malignancies.
  • [MeSH-minor] Burkitt Lymphoma / epidemiology. Burkitt Lymphoma / pathology. Case-Control Studies. Child. Child, Preschool. Female. France / epidemiology. Hodgkin Disease / epidemiology. Hodgkin Disease / pathology. Humans. Incidence. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / pathology. Logistic Models. Lymphoma, Non-Hodgkin / epidemiology. Lymphoma, Non-Hodgkin / pathology. Male. Maternal Exposure / adverse effects. Odds Ratio. Paternal Exposure / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Pregnancy. Registries / statistics & numerical data. Surveys and Questionnaires

  • MedlinePlus Health Information. consumer health - Alcohol.
  • MedlinePlus Health Information. consumer health - Smoking.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18618277.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


98. Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA: Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol; 2005 Aug 07;206(2):237-45
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular biomarkers for the study of childhood leukemia.
  • Various specific chromosome rearrangements, including t(8;21), t(15;17), and inv(16), are found in acute myeloid leukemia (AML) and in childhood acute lymphocytic leukemia (ALL), t(12;21) and t(1;19) are common.
  • We sequenced the translocation breakpoints of 56 patients with childhood ALL or AML harboring t(12;21), t(8;21), t(15;17), inv(16), and t(1;19), and demonstrated, with the notable exception of t(1;19), that these rearrangements are commonly detected in the neonatal blood spots (Guthrie cards) of the cases.
  • These findings show that most childhood leukemias begin before birth and that maternal and perinatal exposures such as chemical and infectious agents are likely to be critical.
  • Indeed, we have reported that exposure to indoor pesticides during pregnancy and the first year of life raises leukemia risk, but that later exposures do not.
  • We have also examined aberrant gene methylation in different cytogenetic subgroups and have found striking differences between them, suggesting that epigenetic events are also important in the development of some forms of childhood leukemia.
  • Further, at least two studies now show that the inactivating NAD(P)H:quinone acceptor oxidoreductase (NQO1) C609T polymorphism is positively associated with leukemias arising in the first 1-2 years of life and polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have been associated with adult and childhood ALL.
  • Thus, low folate intake and compounds that are detoxified by NQO1 may be important in elevating leukemia risk in children.
  • Finally, we are exploring the use of proteomics to subclassify leukemia, because cytogenetic analysis is costly and time-consuming.
  • Several proteins have been identified that may serve as useful biomarkers for rapidly identifying different forms of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Biomarkers. Child. DNA Methylation. Folic Acid / metabolism. Gene Expression Profiling. Humans. NAD(P)H Dehydrogenase (Quinone) / genetics. Risk Factors. Translocation, Genetic

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. FOLIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15967214.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES0098137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 935E97BOY8 / Folic Acid; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  • [Number-of-references] 55
  •  go-up   go-down


99. Svirnovski AI, Shman TV, Serhiyenka TF, Savitski VP, Smolnikova VV, Fedasenka UU: ABCB1 and ABCG2 proteins, their functional activity and gene expression in concert with drug sensitivity of leukemia cells. Hematology; 2009 Aug;14(4):204-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABCB1 and ABCG2 proteins, their functional activity and gene expression in concert with drug sensitivity of leukemia cells.
  • Childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) cells and chronic lymphocytic leukemia (CLL) cells of adults were studied.
  • No differences between expression of P-gp and BCRP and genes in primary and relapsed acute leukemia (AL) cells as well as in de novo and treated CLL samples were established.
  • Doxorubicine, rubomycinum and L-asparaginase resistance correlates with P-gp overexpression and increased function in pediatric AL whereas vincristine resistance might be associated with P-gp protein expression in AL samples and impared P-gp function in CLL lymphocytes only.
  • A tendency for the decreased doxorubicin cytotoxic activity was shown in BCRP-overexpressing cells both in children and adults leukemia.
  • Multifactorial ANOVA showed that P-gp/MDR1 and BCRP as well as their function could not be used as unconditional and universal predictors of leukemia cell drug resistance in vitro.
  • These results suggest that studied MDR transporter-proteins have a limited role per se in vitro and admittedly in vivo drug resistance estimated in leukemia patients or it is not yet fully understood unless would not be studied in aggregate.
  • In any event, the expression and function studies of the proteins under investigation when singularly considered do not have a crucial significance for impact on drug resistance evaluation in all leukemia patients.
  • [MeSH-major] ATP-Binding Cassette Transporters / biosynthesis. ATP-Binding Cassette, Sub-Family B, Member 1 / biosynthesis. Leukemia / drug therapy. Leukemia / metabolism. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family B. ATP Binding Cassette Transporter, Sub-Family G, Member 2. Acute Disease. Adolescent. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Child, Preschool. Drug Resistance, Neoplasm. Gene Expression. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19635183.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Neoplasm Proteins
  •  go-up   go-down


100. Yuan J, McDonough C, Kulharya A, Ramalingam P, Manaloor E: Isolated trisomy 10 in an infant with acute myeloid leukemia: a case report and review of literature. Int J Clin Exp Pathol; 2010;3(7):718-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated trisomy 10 in an infant with acute myeloid leukemia: a case report and review of literature.
  • Trisomy 10 as the sole cytogenetic abnormality in AML is rare, with an incidence rate of < 0.5%.
  • It tends to affect the elderly and is extremely rare in pediatric patients.
  • Compared to the two other reported pediatric cases, our patient has some unique features such as much younger age and additional findings such as bilineage dysplasia and bone marrow fibrosis.
  • Both reported cases and our case were classified as AML-M2 indicating that this may be a common subtype in pediatric patients.
  • These findings suggest that isolated trisomy 10 may be associated with distinct clinicopathologic features in pediatric AML.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Trisomy / genetics. Trisomy / pathology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Genet Cytogenet. 1999 Nov;115(1):47-51 [10565299.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Jul 15;89(2):114-7 [8697414.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Jul 15;89(2):173-4 [8697428.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Jan 1;100(1):84-7 [9406587.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Feb;101(1):68-71 [9460504.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Jun;103(2):130-2 [9614911.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Jan 15;108(2):175 [9973950.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Feb;109(1):88-9 [9973969.001]
  • [Cites] Ann Genet. 1999;42(1):5-10 [10214501.001]
  • [Cites] Int J Hematol. 2008 Jul;88(1):123-4 [18566741.001]
  • [Cites] Clin Pediatr (Phila). 2009 May;48(4):444-8 [19224868.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Jul 15;120(2):141-3 [10942805.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Apr 1;134(1):81-3 [11996802.001]
  • [Cites] Leuk Res. 1990;14(6):515-23 [1695699.001]
  • [Cites] Leuk Res. 1992 Aug;16(8):789-96 [1528067.001]
  • [Cites] Leukemia. 1995 Jul;9(7):1167-72 [7630192.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Apr 15;118(2):148-50 [10748296.001]
  • (PMID = 20830243.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2933392
  • [Keywords] NOTNLM ; CD13 / CD33 / CD34 / CD7 / Trisomy 10 / acute myeloid leukemia / infant / review
  •  go-up   go-down






Advertisement