[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 16 of about 16
1. Sgarbieri UR, Fisberg M, Tone LG, Latorre Mdo R: Nutritional assessment and serum zinc and copper concentration among children with acute lymphocytic leukemia: a longitudinal study. Sao Paulo Med J; 2006 Nov 7;124(6):316-20
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] Nutritional assessment and serum zinc and copper concentration among children with acute lymphocytic leukemia: a longitudinal study.
  • CONTEXT AND OBJECTIVE: When undergoing chemotherapy and/or radiotherapy, children with acute lymphocytic leukemia may present important nutritional disorders because of the gastrointestinal toxicity of most chemotherapy agents or the effects of radiation on the organism.
  • The present study aimed to follow anthropometric parameters and serum levels of zinc and copper in a group of children under treatment for acute lymphocytic leukemia.
  • DESIGN AND SETTING: Longitudinal study, at the Pediatric Section of Hospital das Clínicas, Ribeirão Preto, Brazil.
  • METHODS: Forty-five children with acute lymphocytic leukemia were studied.
  • Anthropometric parameters such as weight and height and the daily intakes and serum levels of copper and zinc were recorded at diagnosis and during the treatment.
  • RESULTS: During the initial phase of the treatment, there was an increase in energy intake accompanied by weight gain.
  • However, during the later phases of treatment there was a reduction in energy intake with accompanying weight loss.
  • Decreased growth rate during treatment was more pronounced in children with high-risk acute lymphocytic leukemia, probably due to radiation therapy.
  • Serum zinc levels remained basically unaltered during the treatment, whereas copper levels decreased dramatically with the beginning of treatment.
  • CONCLUSIONS: The treatment given to children with acute lymphocytic leukemia has an important effect on their linear growth rate and nutritional status, and also on their serum copper levels.
  • [MeSH-major] Copper / blood. Growth / drug effects. Nutrition Assessment. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Zinc / blood
  • [MeSH-minor] Anthropometry. Antineoplastic Combined Chemotherapy Protocols. Body Size / physiology. Child. Child, Preschool. Energy Intake. Female. Humans. Infant. Longitudinal Studies. Male. Nutritional Status. Risk Factors. Time Factors

  • Hazardous Substances Data Bank. COPPER, ELEMENTAL .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17322951.001).
  • [ISSN] 1516-3180
  • [Journal-full-title] São Paulo medical journal = Revista paulista de medicina
  • [ISO-abbreviation] Sao Paulo Med J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 789U1901C5 / Copper; J41CSQ7QDS / Zinc
  •  go-up   go-down


2. Schwemmlein M, Stieglmaier J, Kellner C, Peipp M, Saul D, Oduncu F, Emmerich B, Stockmeyer B, Lang P, Beck JD, Fey GH: A CD19-specific single-chain immunotoxin mediates potent apoptosis of B-lineage leukemic cells. Leukemia; 2007 Jul;21(7):1405-12
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.
  • It is present at high surface density on chronic B-lymphocytic leukemia (B-CLL) cells and cells of other B-cell malignancies, and is a prime target for therapy with antibody-derived agents.
  • Many attempts have been made to target malignant cells via CD19, but to date none of these agents have received drug approval.
  • This fusion protein induced efficient antigen-restricted apoptosis of several human leukemia- and lymphoma-derived cell lines including Nalm-6, which it eliminated at an effective concentration (EC(50)) of 2.5 nM.
  • It induced apoptosis of primary malignant cells in 12/12 samples from B-CLL patients, including patients responding poorly to fludarabine, and of cells from one pediatric acute lymphoblastic leukemia patient.
  • [MeSH-major] Antigens, CD19 / drug effects. Apoptosis / drug effects. Immunotoxins / pharmacology. Leukemia, B-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Drug Synergism. Exotoxins. Humans. Immunoglobulin Fragments. Mice. Mice, SCID. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Pseudomonas. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / therapeutic use. Survival Rate. Tumor Burden / drug effects. Tumor Cells, Cultured

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17495978.001).
  • [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 / Antigens, CD19; 0 / Exotoxins; 0 / Immunoglobulin Fragments; 0 / Immunotoxins; 0 / Recombinant Fusion Proteins
  •  go-up   go-down


3. Lu Y, Sun LR, Pang XY, Lu ZH, Sui AH: [Infection status and clinical significance of Epstein-Barr virus in pediatric leukemia---a report of 35 cases]. Ai Zheng; 2007 Jan;26(1):54-7
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] [Infection status and clinical significance of Epstein-Barr virus in pediatric leukemia---a report of 35 cases].
  • This study was to detect EBV infection in pediatric leukemia, and to explore its clinical significance.
  • METHODS: EBV DNA in peripheral blood mononuclear cells in 35 pediatric leukemia patients, including 26 cases of acute lymphoblastic leukemia (ALL) (24 received initial treatment and 2 received retreatment), 8 cases of acute non-lymphocytic leukemia (ANLL) and 1 case of chronic lymphocytic leukemia (CLL), and in 14 healthy children was detected by fluorescent quantitative polymerase chain reaction (FQ-PCR).
  • Its clinical significance was analyzed according to the clinical manifestations, prednisone sensitivity test, and complete remission (CR) rate after induction chemotherapy.
  • RESULTS: EBV DNA was detected in 8 (22.86%) of the 35 pediatric leukemia patients.
  • The positive rate of EBV DNA was 26.92% (7/26) in ALL with quantity of (5.144+/-6.91)x10(5) copies/ml, and 12.5% (1/8) in ANLL patients with quantity of 4.031x10(3) copies/ml.
  • In ALL, the rate of no response to prednisone was significantly higher in the patients with EBV infection than in the patients without EBV infection (100% vs. 26.32%, P =0.001); CR rate after induction chemotherapy was significantly lower in the patients with EBV infection than in the patients without EBV infection (28.57% vs. 84.21%, P=0.003).
  • In ANLL, the differences of CR rate and relapse rate were not significant between the patients with and without EBV infection (P=0.5).
  • CONCLUSIONS: Pediatric leukemia patients with EBV infection have higher incidence of peripheral leukocytosis and hepatosplenomegaly.
  • [MeSH-major] Epstein-Barr Virus Infections. Leukemia, Myeloid, Acute / virology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / virology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Child. Child, Preschool. DNA, Viral / blood. Female. Hepatomegaly / etiology. Herpesvirus 4, Human / genetics. Humans. Infant. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / virology. Leukocytosis / etiology. Male. Prednisone / therapeutic use. Remission Induction. Splenomegaly / etiology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17222368.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / DNA, Viral; VB0R961HZT / Prednisone
  •  go-up   go-down


Advertisement
4. Kendall HE, Vacek PM, Rivers JL, Rice SC, Messier TL, Finette BA: Analysis of genetic alterations and clonal proliferation in children treated for acute lymphocytic leukemia. Cancer Res; 2006 Sep 1;66(17):8455-61
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] Analysis of genetic alterations and clonal proliferation in children treated for acute lymphocytic leukemia.
  • The development of risk-directed treatment protocols over the last 25 years has resulted in an increase in the survival rates of children treated for cancer.
  • As a consequence, there is a growing population of pediatric cancer survivors in which the long-term genotoxic effects of chemotherapy is unknown.
  • We previously reported that children treated for acute lymphocytic leukemia have significantly elevated somatic mutant frequencies at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene in their peripheral T cells.
  • To understand the molecular etiology of the increase in mutant frequencies following chemotherapy, we investigated the HPRT mutation spectra and the extent of clonal proliferation in 562 HPRT T cell mutant isolates of 87 blood samples from 47 subjects at diagnosis, during chemotherapy, and postchemotherapy.
  • We observed a significant increase in the proportion of CpG transitions following treatment (13.6-23.3%) compared with healthy controls (4.0%) and a significant decrease in V(D)J-mediated deletions following treatment (0-6.8%) compared with healthy controls (17.0%).
  • There was also a significant change in the class type percentage of V(D)J-mediated HPRT deletions following treatment.
  • These data indicate that unique genetic alterations and extensive clonal proliferation are occurring in children following treatment for acute lymphocytic leukemia that may influence long-term risks for multifactorial diseases, including secondary cancers.
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Cloning, Molecular. Female. Humans. Male. Polymerase Chain Reaction. Receptors, Antigen, T-Cell / genetics

  • 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 = 16951156.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K01CA77737; United States / NCI NIH HHS / CA / 1R01CA09094013; United States / NICHD NIH HHS / HD / 1R29HD35309; United States / NCI NIH HHS / CA / P30CA22435
  • [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 / Antineoplastic Agents; 0 / Receptors, Antigen, T-Cell; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase
  •  go-up   go-down


5. Talano JM, Casper JT, Camitta BM, Keever-Taylor CA, Murray KJ, Eapen M, Pierce KL, Margolis DA: Alternative donor bone marrow transplant for children with Philadelphia chromosome ALL. Bone Marrow Transplant; 2006 Jan;37(2):135-41
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.
  • Children with Philadelphia chromosome positive (Ph+) acute lymphocytic leukemia (ALL) have only a 20% event-free survival when treated with chemotherapy alone.
  • Four developed grades III-IV acute GVHD.
  • Three of 24 evaluable patients developed extensive chronic GVHD.
  • Five of six patients in >CR2 or relapse at the time of transplant died.
  • [MeSH-major] Bone Marrow Transplantation. Donor Selection. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Conditioning

  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16273115.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine; 8N3DW7272P / Cyclophosphamide
  •  go-up   go-down


6. Rice SC, Vacek PM, Homans AH, Kendall H, Rivers J, Messier T, Finette BA: Comparative analysis of HPRT mutant frequency in children with cancer. Environ Mol Mutagen; 2003;42(1):44-9
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.
  • To gain insight into somatic mutational mechanisms in children who develop cancer, we determined the background mutant frequency (Mf) in the hypoxanthine phosphoribosyl transferase (HPRT) reporter gene of peripheral blood lymphocytes from pediatric cancer patients at the time of diagnosis and prior to therapeutic intervention.
  • We studied 23 children with hematologic malignancies and 31 children with solid tumors prior to initial therapeutic intervention.
  • Children with solid tumors, specifically sarcomas, and Hodgkin's disease were significantly older and had elevated HPRT Mfs (6.1 x 10(-6) and 3.7 x 10(-6), respectively) at the time of diagnosis, compared to normal controls (2.3 x 10(-6)) and other pediatric tumor groups including children with acute lymphocytic leukemia and non-Hodgkin's lymphoma (ALL/NHL, 1.7 x 10(-6)), central nervous system tumors (CNS, 3.6 x 10(-6)), and neuroblastoma (1.9 x 10(-6)).
  • In addition, these data demonstrate the importance of correcting for the effect of age when comparing the frequency of somatic mutations in children and should provide baseline data for future longitudinal biomonitoring studies on the genetic effects of chemotherapy in children treated for cancer.

  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • 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 2003 Wiley-Liss, Inc.
  • (PMID = 12874812.001).
  • [ISSN] 0893-6692
  • [Journal-full-title] Environmental and molecular mutagenesis
  • [ISO-abbreviation] Environ. Mol. Mutagen.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 1F32ES058701ZRG4; United States / NCI NIH HHS / CA / 1K01CA77737; United States / NICHD NIH HHS / HD / 1K11HD01010; United States / NICHD NIH HHS / HD / 1R29HD35309-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase
  •  go-up   go-down


7. Moe PJ, Holen A, Nygaard R, Glomstein A, Madsen B, Hellebostad M, Stokland T, Wefring KW, Steen-Johnsen J, Nielsen B, Hapnes C, Børsting S: Methotrexate infusions as central nervous system prophylaxis in children with acute lymphocytic leukemia: the Norwegian experience. Pediatr Hematol Oncol; 2003 Apr-May;20(3):187-200
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] Methotrexate infusions as central nervous system prophylaxis in children with acute lymphocytic leukemia: the Norwegian experience.
  • This study included all 690 children in Norway diagnosed as having acute lymphocytic leukemia (ALL) from July 1975 till the end of 1997.
  • From 1992, systemic therapy was considerably intensified, and, in addition, patients in a subgroup of the high-risk and very high-risk groups were given prophylactic cranial irradiation.
  • The overall findings showed that MTX significantly reduced central nervous system (CNS)-related relapses, and, in general, reinforced systemic therapy reduced significantly non-CNS relapses and deaths.
  • Forty patients (6%) developed isolated CNS relapse, 27 (4%) had combined CNS relapse, whereas 180 (26%) had non-CNS relapse.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Central Nervous System Neoplasms / prevention & control. Methotrexate / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Clinical Trials as Topic. Combined Modality Therapy. Cranial Irradiation. Drug Administration Schedule. Humans. Infant. Infusion Pumps. Injections, Spinal. Neoplasm Recurrence, Local. Norway / epidemiology. Prospective Studies. Risk Factors. Survival Analysis. Time Factors. Treatment Outcome

  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12637215.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


8. da Costa Moraes CA, Trompieri NM, Cavalcante Felix FH: Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital. J Pediatr Hematol Oncol; 2008 May;30(5):387-90
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 promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital.
  • Acute promyelocytic leukemia (APL) is an uncommon form of pediatric acute nonlymphocytic leukemia.
  • The introduction of all-transretinoic acid (ATRA) or tretinoin, a biologic response modifier, in its therapy was followed by dramatic improvement in its outcome.
  • To show the results of APL treatment in our hospital, we reviewed the information about 15 patients less than 18 years old, newly diagnosed with APL between November 2002 and November 2006.
  • The clinical charts were searched for data regarding clinical presentation, diagnosis, initial response with induction therapy, toxicity of ATRA, and antracyclic drug (daunorubicin).
  • Fourteen patients received induction chemotherapy.
  • There was a death owing to sepsis before the beginning of the therapy and 2 relapses with death associated with the therapy discontinuation.
  • Preliminary results are encouraging and confirm that ATRA is safe and efficacious as first choice therapy for APL.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Brazil. Female. Hospitals, Pediatric. Humans. Male. Retrospective Studies

  • 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 = 18458575.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  •  go-up   go-down


9. Sonabend RY, McKay SV, Okcu MF, Yan J, Haymond MW, Margolin JF: Hyperglycemia during induction therapy is associated with increased infectious complications in childhood acute lymphocytic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):387-92
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] Hyperglycemia during induction therapy is associated with increased infectious complications in childhood acute lymphocytic leukemia.
  • BACKGROUND: Children with acute lymphocytic leukemia (ALL) are at high risk for developing hyperglycemia.
  • We hypothesized that children with ALL who become hyperglycemic during induction chemotherapy have an increased risk for infection during their first year of treatment.
  • PROCEDURE: We conducted a retrospective chart review of 135 patients diagnosed with ALL during 1999-2001 at Texas Children's Hospital.
  • Infectious outcomes during the first year of therapy were compared in three groups patients based on blood glucose concentrations during induction therapy: euglycemic (<140 mg/dl), mild hyperglycemic (MH) (140-199 mg/dl) and overt hyperglycemic (OH) (blood glucose >200 mg/dl).
  • Patients with MH and OH were 2.5 times (95% CI 1.0-6.2) and 2.1 times (95% CI 1.0-4.6) more likely to have documented infections, respectively.
  • Patients with OH were 4.2 times (95% CI 1.5-12) more likely to have bacteremia/fungemia, 3.8 times (95% CI 1.2-11.6) more likely to have cellulitis, and 4.0 times (95% CI 1.7-9.3) more likely to be admitted for fever and neutropenia than the euglycemia group.
  • CONCLUSION: Hyperglycemia, especially when overt, may be a previously unrecognized risk factor of infectious complications in children with ALL during the first year of treatment.
  • [MeSH-major] Hyperglycemia / complications. Infection / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

  • MedlinePlus Health Information. consumer health - Hyperglycemia.
  • 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 = 18523991.001).
  • [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] 0 / Blood Glucose
  •  go-up   go-down


10. Zhang JB, Sun Y, Dong J, Liu LX, Ning F: [Expression of lung resistance protein and multidrug resistance-associated protein in naive childhood acute leukemia and their clinical significance]. Ai Zheng; 2005 Aug;24(8):1015-7
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 lung resistance protein and multidrug resistance-associated protein in naive childhood acute leukemia and their clinical significance].
  • BACKGROUND & OBJECTIVE: Previous studies revealed that lung resistance protein (LRP) and multidrug resistance-associated protein (MRP) relate to drug resistance of childhood leukemia, which is not caused by only one mechanism.
  • This study was to evaluate the expression of LRP and MRP genes in childhood leukemia and their correlation.
  • METHODS: The expression of LRP and MRP in 38 children with acute leukemia and 6 healthy children were measured with reverse transcription-polymerase chain reaction (RT-PCR); their clinical significance was analyzed according to complete remission (CR) rate of the patients after chemotherapy.
  • The positive rate of LRP was significantly lower in acute lymphoblastic leukemia (ALL) than in acute nonlymphocytic leukemia (ANLL) [18.5% (5/27) vs. 45.5% (6/11), P < 0.05]; however, the positive rate of MRP was 59.3% (16/27) in ALL, and 45.5% (5/11) in ANLL (P > 0.05).
  • CONCLUSION: Childhood acute leukemia patients with overexpression of LRP and MRP suffer severe disease and achieve low remission rateû lower remission rate of childhood ANLL patients may relate to LRP expression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Multidrug Resistance-Associated Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vault Ribonucleoprotein Particles / metabolism

  • 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 = 16086885.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
  •  go-up   go-down


11. Hou Y, Hu Q, Liu AG, Zhang LQ, Liu SY: [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy]. Zhongguo Dang Dai Er Ke Za Zhi; 2006 Apr;8(2):101-4
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] [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy].
  • This study aimed to investigate the expression of survivin and its location as well as the relationship between cellular location and expression of survivin and the therapeutic efficacy at the cellular level.
  • METHODS: The expression of survivin protein was detected by immunohistochemical assay in bone marrow cells from 62 children with acute leukemia and 40 hospitalized children who did not have leukemia (Control group), and in a human acute T lymphocytic leukemia cell line (Molt-4 cells) treated in vitro with daunorubicin (DNR).
  • RESULTS: Survivin protein was expressed in 41.9% of the 62 children with acute leukemia but in only 5.0% of the Control group (chi(2)=16.66; P < 0.01).
  • The expression rate of survivin was 46.2% in cytoplasm and 53.9% in nucleus in the children with acute leukemia (chi(2)0.3077; P> 0.05).
  • However, the remission rate of patients in whom survivin expression was seen in the nucleus was significantly higher than that in patients in whom survivin was expressed in cytoplasm after chemotherapy.
  • The survivin expression in Molt-4 cells decreased remarkably by DNR treatment in a time and dosage-dependent manner.
  • DNR treatment also induced survivin transllocation from cytoplasm to nucleus and cell apoptosis in a time and dosage-dependent manner.
  • CONCLUSIONS: Survivin may play an important role in the development and prognosis of childhood acute leukemia.
  • The different expression pattern of survivin in the cytoplasm and the nucleus may be associated with therapeutic efficacy and prognosis in acute leukemia.
  • [MeSH-major] Bone Marrow Cells / chemistry. Daunorubicin / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Apoptosis / drug effects. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Inhibitor of Apoptosis Proteins. Male

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16613699.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


12. Kreitman RJ: Recombinant immunotoxins for the treatment of chemoresistant hematologic malignancies. Curr Pharm Des; 2009;15(23):2652-64
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] Recombinant immunotoxins for the treatment of chemoresistant hematologic malignancies.
  • Recombinant immunotoxins which have been tested in patients with chemotherapy-pretreated hematologic malignancies include LMB-2 (anti-CD25), BL22 (CAT-3888, anti-CD22) and HA22 (CAT-8015, anti-CD22), each containing an Fv fragment fused to truncated Pseudomonas exotoxin.
  • Major responses were observed with LMB-2 in adult T-cell leukemia, chronic lymphocytic leukemia (CLL), cutaneous T-cell lymphoma, Hodgkin's disease, and hairy cell leukemia (HCL).
  • HA22, an improved version of BL22 with higher affinity to CD22, is now undergoing phase I testing in HCL, CLL, non-Hodgkin's lymphoma, and pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Drug Discovery / methods. Drug Resistance, Neoplasm / drug effects. Hematologic Neoplasms / drug therapy. Immunotoxins / therapeutic use. Recombinant Proteins / therapeutic use

  • 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 = 19689336.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Immunotoxins; 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Recombinant Proteins; 0 / Toxins, Biological
  • [Number-of-references] 190
  •  go-up   go-down


13. Rice SC, Vacek P, Homans AH, Messier T, Rivers J, Kendall H, Finette BA: Genotoxicity of therapeutic intervention in children with acute lymphocytic leukemia. Cancer Res; 2004 Jul 1;64(13):4464-71
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] Genotoxicity of therapeutic intervention in children with acute lymphocytic leukemia.
  • The survival rates of children treated for cancer have dramatically increased after the development of standardized multiple-modality treatment protocols.
  • As a result, there is a rapidly growing population of pediatric cancer survivors in which the long-term genotoxic effects of chemotherapeutic intervention is unknown.
  • To study the genotoxic effects of antineoplastic treatment in children, we performed a comparative analysis of the changes in the frequency of somatic mutations (Mfs) at the hypoxanthine-guanine phosphoribosyltransferase (HPRT)-reporter gene in children treated for acute lymphocytic leukemia (ALL).
  • We measured HPRT Mfs from 130 peripheral blood samples from 45 children with ALL (13, low risk; 22, standard risk; and 10, high risk) from the time of diagnosis, as well as during and after the completion of therapy.
  • We observed a significant increase in mean HPRT Mfs during each phase of therapy (diagnosis, 1.4 x 10(-6); consolidation, 52.1 x 10(-6); maintenance, 93.2 x 10(-6); and off-therapy, 271.7 x 10(-6)) that were independent of the risk group treatment protocol used.
  • This 200-fold increase in mean somatic Mf remained elevated years after the completion of therapy.
  • We did not observe a significant difference in the genotoxicity of each risk group treatment modality despite differences in the compositional and clinical toxicity associated with these treatment protocols.
  • These findings suggest that combination chemotherapy used to treat children with ALL is quite genotoxic, resulting in an increased somatic mutational load that may result in an elevated risk for the development of multi-factorial diseases, in particular second malignancies.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / 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 = 15231655.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 1 P20RR16462; United States / NCI NIH HHS / CA / 1K01CA77737; United States / NCI NIH HHS / CA / 1R01CA09094013; United States / NICHD NIH HHS / HD / 1R29HD35309; United States / NCI NIH HHS / CA / P30CA22435
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase
  •  go-up   go-down


14. Adderson EE: Histoplasmosis in a pediatric oncology center. J Pediatr; 2004 Jan;144(1):100-6
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] Histoplasmosis in a pediatric oncology center.
  • OBJECTIVE: To understand the presentation and current management of histoplasmosis in a pediatric oncology center.
  • RESULTS: Between 1988 and 2001, 57 patients with cancer had 61 episodes of acute histoplasmosis.
  • Of these, 76% were male, and 64% had acute lymphocytic leukemia (ALL).
  • The most rapid and specific tests for histoplasmosis in patients with cancer were histopathologic examination of lung biopsy specimens in patients with localized pulmonary infection and Histoplasma sp. antigen detection in the urine of patients with disseminated histoplasmosis (DH).
  • The mean times to diagnosis were 20.6+/-15.2 days (pulmonary) and 18.6+/-8.2 days (disseminated) after the onset of symptoms.
  • Most patients were treated with amphotericin B (AmB) followed by azole drugs for a mean of 8.5+/-3.1 weeks (pulmonary) and 10.4+/-7.9 weeks (disseminated).
  • No patient died of histoplasmosis, but cancer therapy often was modified because of the infection.
  • Most received unnecessary antibacterial drugs.
  • No deaths were attributed to histoplasmosis; outcomes after treatment are good.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Child. Female. Humans. Lung Diseases, Fungal / complications. Lung Diseases, Fungal / diagnosis. Lung Diseases, Fungal / drug therapy. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Histoplasmosis.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14722526.001).
  • [ISSN] 0022-3476
  • [Journal-full-title] The Journal of pediatrics
  • [ISO-abbreviation] J. Pediatr.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
  •  go-up   go-down


15. Horton TM, Sposto R, Brown P, Reynolds CP, Hunger SP, Winick NJ, Raetz EA, Carroll WL, Arceci RJ, Borowitz MJ, Gaynon PS, Gore L, Jeha S, Maurer BJ, Siegel SE, Biondi A, Kearns PR, Narendran A, Silverman LB, Smith MA, Zwaan CM, Whitlock JA, ALLNA 2008 Conference: Toxicity assessment of molecularly targeted drugs incorporated into multiagent chemotherapy regimens for pediatric acute lymphocytic leukemia (ALL): review from an international consensus conference. Pediatr Blood Cancer; 2010 Jul 1;54(7):872-8
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] Toxicity assessment of molecularly targeted drugs incorporated into multiagent chemotherapy regimens for pediatric acute lymphocytic leukemia (ALL): review from an international consensus conference.
  • One of the challenges of incorporating molecularly targeted drugs into multi-agent chemotherapy (backbone) regimens is defining dose-limiting toxicities (DLTs) of the targeted agent against the background of toxicities of the backbone regimen.
  • An international panel of 22 pediatric acute lymphocytic leukemia (ALL) experts addressed this issue (www.ALLNA.org).
  • (1) how toxicities can be best defined, assessed, and attributed; and (2) how effective dosing of new agents incorporated into multi-agent ALL clinical trials can be safely established in the face of disease- and therapy-related systemic toxicities.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • [Cites] J Clin Oncol. 2008 Aug 20;26(24):3971-8 [18711187.001]
  • [Cites] Clin Cancer Res. 2009 Feb 15;15(4):1126-32 [19228717.001]
  • [Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]
  • [Cites] J Pediatr Hematol Oncol. 1998 Sep-Oct;20(5):431-8 [9787315.001]
  • [Cites] Br J Haematol. 2005 Dec;131(5):579-87 [16351633.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Hematol Oncol. 2008 Jun;26(2):73-81 [18324639.001]
  • [Cites] Curr Drug Targets. 2007 Jun;8(6):703-14 [17584026.001]
  • [Cites] Curr Drug Targets. 2007 Jun;8(6):751-9 [17584030.001]
  • [Cites] Semin Oncol. 2007 Dec;34(6 Suppl 5):S13-20 [18086342.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):190-5 [18182661.001]
  • [Cites] Paediatr Drugs. 2008;10(2):85-92 [18345718.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3262-70 [16857985.001]
  • (PMID = 20127846.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113775-04; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / K23 CA113775; United States / NCI NIH HHS / CA / K23 CA113775-04
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Number-of-references] 14
  • [Other-IDs] NLM/ NIHMS163748; NLM/ PMC2857540
  •  go-up   go-down


16. Sorich MJ, Pottier N, Pei D, Yang W, Kager L, Stocco G, Cheng C, Panetta JC, Pui CH, Relling MV, Cheok MH, Evans WE: In vivo response to methotrexate forecasts outcome of acute lymphoblastic leukemia and has a distinct gene expression profile. PLoS Med; 2008 Apr 15;5(4):e83
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] In vivo response to methotrexate forecasts outcome of acute lymphoblastic leukemia and has a distinct gene expression profile.
  • BACKGROUND: Childhood acute lymphoblastic leukemia (ALL) is the most common cancer in children, and can now be cured in approximately 80% of patients.
  • Nevertheless, drug resistance is the major cause of treatment failure in children with ALL.
  • The drug methotrexate (MTX), which is widely used to treat many human cancers, is used in essentially all treatment protocols worldwide for newly diagnosed ALL.
  • Although MTX has been extensively studied for many years, relatively little is known about mechanisms of de novo resistance in primary cancer cells, including leukemia cells.
  • METHODS AND FINDINGS: We utilized measures of decreased circulating leukemia cells of 293 newly diagnosed children after initial "up-front" in vivo MTX treatment (1 g/m(2)) to elucidate interpatient differences in the antileukemic effects of MTX.
  • We identified 48 genes and two cDNA clones whose expression was significantly related to the reduction of circulating leukemia cells after initial in vivo treatment with MTX.
  • CONCLUSIONS: Together, these data provide new insights into the genomic basis of MTX resistance and interpatient differences in MTX response, pointing to new strategies to overcome MTX resistance in childhood ALL.
  • TRIAL REGISTRATIONS: Total XV, Therapy for Newly Diagnosed Patients With Acute Lymphoblastic Leukemia, http://www.ClinicalTrials.gov (NCT00137111); Total XIIIBH, Phase III Randomized Study of Antimetabolite-Based Induction plus High-Dose MTX Consolidation for Newly Diagnosed Pediatric Acute Lymphocytic Leukemia at Intermediate or High Risk of Treatment Failure (NCI-T93-0101D); Total XIIIBL, Phase III Randomized Study of Antimetabolite-Based Induction plus High-Dose MTX Consolidation for Newly Diagnosed Pediatric Acute Lymphocytic Leukemia at Lower Risk of Treatment Failure (NCI-T93-0103D).
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Drug Resistance, Neoplasm. Gene Expression Profiling. Methotrexate / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cohort Studies. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Neoplastic Cells, Circulating. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 2004 Aug 5;351(6):533-42 [15295046.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S124-6 [15124703.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Bioinformatics. 2004 Jan 1;20(1):93-9 [14693814.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Sep;25(9):688-95 [12972803.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]
  • [Cites] Vitam Horm. 2003;66:403-56 [12852262.001]
  • [Cites] Nat Genet. 2003 May;34(1):85-90 [12704389.001]
  • [Cites] Br J Cancer. 2003 Mar 10;88(5):775-81 [12618889.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1240-7 [12149204.001]
  • [Cites] Clin Cancer Res. 2002 Jul;8(7):2423-9 [12114448.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1271-7 [17456722.001]
  • [Cites] Mol Pharmacol. 2006 Nov;70(5):1832-9 [16936229.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):331-42 [17010674.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):117-29 [16491071.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4752-8 [15713801.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):375-86 [15837626.001]
  • [Cites] Blood. 2005 Jan 15;105(2):821-6 [15388585.001]
  • [Cites] J Clin Invest. 2005 Jan;115(1):110-7 [15630450.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Biochem Pharmacol. 1999 Aug 15;58(4):539-55 [10413291.001]
  • [Cites] Cancer Res. 1999 Jun 1;59(11):2532-5 [10363967.001]
  • [Cites] Blood. 1999 Feb 1;93(3):1067-74 [9920857.001]
  • [Cites] J Biol Chem. 1980 Jun 25;255(12):5776-88 [6892914.001]
  • [Cites] J Clin Invest. 1985 Sep;76(3):907-12 [2413074.001]
  • [Cites] Cancer Res. 1988 Oct 15;48(20):5638-44 [2458828.001]
  • [Cites] Blood. 1990 Jul 1;76(1):44-9 [1694703.001]
  • [Cites] Blood. 1990 Oct 15;76(8):1449-63 [2207320.001]
  • [Cites] Blood. 1994 Jul 15;84(2):564-9 [7517720.001]
  • [Cites] J Clin Invest. 1994 Nov;94(5):1996-2001 [7525652.001]
  • [Cites] J Clin Invest. 1996 Jan 1;97(1):73-80 [8550853.001]
  • [Cites] N Engl J Med. 1996 Oct 3;335(14):1041-8 [8793930.001]
  • [Cites] J Natl Cancer Inst. 1996 Sep 18;88(18):1255-6 [8797761.001]
  • [Cites] Nat Genet. 1996 Dec;14(4):457-60 [8944026.001]
  • [Cites] Nat Genet. 1999 Jan;21(1 Suppl):20-4 [9915496.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Haematologica. 2001 Feb;86(2):121-7 [11224479.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7225-32 [11585759.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54 [11742071.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3144-50 [12036927.001]
  • [Cites] Biochim Biophys Acta. 2002 Jul 18;1587(2-3):164-73 [12084458.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • (PMID = 18416598.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00137111
  • [Grant] United States / NCI NIH HHS / CA / R37 CA36401; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA78224; United States / NCI NIH HHS / CA / R01 CA51001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2292747
  •  go-up   go-down






Advertisement