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[Title] Assessment of nutritional status in children with acute lymphoblastic leukemia in Northern México: A 5-year experience.

Nutritional status is an important variable when planning the treatment of children with acute lymphoblastic leukemia (ALL).

The majority of children with ALL in Northern Mexico are well nourished at diagnosis and have a normal body composition.

[MeSH-major] Nutrition Assessment. Nutritional Status. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 18064642.001).

[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; Review

[Publication-country] United States

[Number-of-references] 19

   

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[Title] Atypical pyoderma gangrenosum as a manifestation of childhood acute lymphoblastic leukemia.

Although the association of this entity with myeloid malignancies is well known, its association with lymphoid malignancy is extremely rare.

We describe atypical pyoderma gangrenosum in association with acute lymphoblastic leukemia in a 2-year-old child, an occurrence not reported before.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyoderma Gangrenosum / drug therapy. Pyoderma Gangrenosum / pathology

[MeSH-minor] Anti-Bacterial Agents / therapeutic use. Asparaginase / therapeutic use. Biopsy, Needle. Child, Preschool. Daunorubicin / therapeutic use. Diagnosis, Differential. Follow-Up Studies. Humans. Immunohistochemistry. Male. Prednisone / therapeutic use. Risk Assessment. Severity of Illness Index. Treatment Outcome. Vincristine / therapeutic use

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(PMID = 16354258.001).

[ISSN] 0736-8046

[Journal-full-title] Pediatric dermatology

[ISO-abbreviation] Pediatr Dermatol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin

   

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[Title] Reduced intensity conditioning allogeneic stem cell transplantation for adult patients with acute lymphoblastic leukemia: a retrospective study from the European Group for Blood and Marrow Transplantation.

This retrospective study reported the outcome of 97 adult acute lymphoblastic leukemia patients who received a reduced-intensity conditioning allogeneic stem cell transplantation.

With a median follow-up of 2.8 years, two year overall-survival, leukemia-free survival and non-relapse mortality were significantly better in patients transplanted in first complete remission (CR1, 52+/-9%; 42+/-10%; and 18+/-7% respectively) compared with those transplanted in more advanced phase (p=0.003, p=0.002 and p=0.01 respectively).

In multivariate analysis, disease status (CR1 vs. advanced; p=0.001) and chronic graft-vs-host disease (p=0.01) were associated with an improved overall-survival, suggesting that reduced-intensity conditioning allogeneic stem cell transplantation is feasible in patients with high risk lymphoblastic leukemia in remission at transplantation.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Stem Cell Transplantation. Transplantation Conditioning

[MeSH-minor] Adolescent. Adult. Aged. Chronic Disease. Disease-Free Survival. Europe. Female. Follow-Up Studies. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Neoplasm Staging. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous

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(PMID = 18245655.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] Italy

   

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[Title] The impact of acute lymphoblastic leukemia treatment on central nervous system results in Bogota, Colombia.

To improve the outcome of children with acute lymphoblastic leukemia (ALL) treated at the National Cancer Institute, Bogota, Colombia, a protocol based on the BFM-90 (Berlin, Frankfurt, Munster study) and the LSA2L2 regimens was implemented in the year 1993.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Central Nervous System Neoplasms / prevention & control. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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(PMID = 18776755.001).

[ISSN] 1536-3678

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

[Chemical-registry-number] VB0R961HZT / Prednisone

   

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[Title] A single amino acid change A91V in perforin: a novel, frequent predisposing factor to childhood acute lymphoblastic leukemia?

We screened 100 children with acute lymphoblastic leukemia (ALL) to assess the incidence of single amino acid change A91V in perforin.

[MeSH-major] Amino Acid Substitution. Membrane Glycoproteins / genetics. Mutation, Missense. Pore Forming Cytotoxic Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Child. Child, Preschool. DNA Mutational Analysis. DNA, Neoplasm / genetics. Female. Genetic Predisposition to Disease. Genetic Testing. Genotype. Humans. Incidence. Infant. Infant, Newborn. Lymphohistiocytosis, Hemophagocytic / genetics. Male. Perforin. Polymorphism, Single Nucleotide

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(PMID = 15921391.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Letter; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Membrane Glycoproteins; 0 / Pore Forming Cytotoxic Proteins; 126465-35-8 / Perforin

   

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[Title] Endocrine and metabolic disorders in young adult survivors of childhood acute lymphoblastic leukaemia (ALL) or non-Hodgkin lymphoma (NHL).

BACKGROUND: Treatments of acute lymphoblastic leukaemia (ALL) and non-Hodgkin lymphoma (NHL), involving various combinations of chemotherapy (chemo), cranial irradiation (CI) and/or bone marrow transplantation after total body irradiation (BMT/TBI), are often successful but may have several long-term harmful effects.

[MeSH-major] Endocrine System Diseases / epidemiology. Lymphoma, Non-Hodgkin / epidemiology. Metabolic Diseases / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Survivors / statistics & numerical data

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(PMID = 18429947.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

[ISO-abbreviation] Clin. Endocrinol. (Oxf)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I

   

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BACKGROUND: Resistance to imatinib mesylate can occur in chronic myelogenous leukemia (CML).

METHODS: In a phase 1 dose-escalation study, we assigned 119 patients with imatinib-resistant CML or acute lymphoblastic leukemia (ALL) to receive nilotinib orally at doses of 50 mg, 100 mg, 200 mg, 400 mg, 600 mg, 800 mg, and 1200 mg once daily and at 400 mg and 600 mg twice daily.

Of 33 patients with the blastic phase of disease, 13 had a hematologic response and 9 had a cytogenetic response; of 46 patients with the accelerated phase, 33 had a hematologic response and 22 had a cytogenetic response; 11 of 12 patients with the chronic phase had a complete hematologic remission.

[MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage

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[Copyright] Copyright 2006 Massachusetts Medical Society.

[CommentIn] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]

(PMID = 16775235.001).

[ISSN] 1533-4406

[Journal-full-title] The New England journal of medicine

[ISO-abbreviation] N. Engl. J. Med.

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00109707

[Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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CLINICAL RELEVANCE: The early diagnosis and management of dental conditions that affect athletes will ensure sound dental health is preserved for these high risk patients.

The clinician needs to be aware of a variety of dental conditions that can prevent significant dental trauma and acute manifestations at the time of competition.

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[ReprintOf] Dent Update. 2009 Apr;36(3):135-8, 141-4 [19480101.001]

(PMID = 19725331.001).

[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] Journal Article

[Publication-country] South Africa

   

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OBJECTIVES: To investigate the frequency and severity of side effects of methylphenidate among childhood survivors of acute lymphoblastic leukemia and brain tumors and identify predictors of higher adverse effect levels.

[MeSH-major] Brain Neoplasms / epidemiology. Central Nervous System Stimulants / adverse effects. Cognition Disorders / drug therapy. Cognition Disorders / epidemiology. Methylphenidate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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(PMID = 19564304.001).

[ISSN] 1098-4275

[Journal-full-title] Pediatrics

[ISO-abbreviation] Pediatrics

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00576472

[Grant] United States / NCI NIH HHS / CA / R01 CA078957-05; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NCI NIH HHS / CA / P30CA21765; United States / NCI NIH HHS / CA / R01 CA078957; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / U01 CA081445-05; United States / NCI NIH HHS / CA / R01CA078957; United States / NCI NIH HHS / CA / U01 CA81445

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Central Nervous System Stimulants; 207ZZ9QZ49 / Methylphenidate

[Other-IDs] NLM/ NIHMS78776; NLM/ PMC2705008

   

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[Title] Detection and functional analysis of CD8+ T cells specific for PRAME: a target for T-cell therapy.

PURPOSE: Preferentially expressed antigen on melanomas (PRAME) is an interesting antigen for T-cell therapy because it is frequently expressed in melanomas (95%) and other tumor types.

Moreover, due to its role in oncogenic transformation, PRAME-negative tumor cells are not expected to easily arise and escape from T-cell immunity.

The purpose of this study is to investigate the usefulness of PRAME as target for anticancer T-cell therapies.

EXPERIMENTAL DESIGN: HLA-A*0201-subtyped healthy individuals and advanced melanoma patients were screened for CD8+ T cells directed against previously identified HLA-A*0201-binding PRAME peptides by IFN-gamma enzyme-linked immunosorbent spot assays and tetramer staining.

PRAME-specific T-cell clones were isolated and tested for recognition of melanoma and acute lymphoid leukemia (ALL) cell lines.

PRA(100-108)-tetramer+ T-cell clones were shown to recognize and lyse HLA-A*0201+ and PRAME+ melanoma but not ALL cell lines.

Quantitative real-time reverse transcription-PCR showed significantly lower PRAME mRNA levels in ALL than in melanoma cell lines, suggesting that PRAME expression in ALL is below the recognition threshold of our PRA(100-108)-tetramer+ T cells.

CONCLUSION: These data support the usefulness of PRAME and in particular the PRA(100-108) epitope as target for T-cell therapy of PRAME-overexpressing cancers.

[MeSH-minor] Enzyme-Linked Immunosorbent Assay. Epitopes. HLA-A Antigens / immunology. HLA-A2 Antigen. Humans. Immunotherapy / methods. Tumor Cells, Cultured

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(PMID = 16707612.001).

[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

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Epitopes; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / PRAME protein, human

   

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[Title] New approaches to the management of Philadelphia-chromosome-positive acute lymphocytic leukemia.

The discovery of targeted ABL tyrosine kinase inhibitors has allowed significant advances in the treatment of de novo Philadelphia chromosome (Ph)-positive ALL.

Whereas the outcome with standard chemotherapy was previously dismal, the use of imatinib in front-line therapy has improved relapse-free survival and overall survival, even in the absence of allogeneic stem cell transplantation in first complete remission (particularly for those with comorbidities or lack of a suitable donor).

Optimal use of these novel agents in the treatment schema of Ph-positive ALL will be paramount in ensuring continued success in the eradication of this disease.

[MeSH-major] Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

[MeSH-minor] Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Clinical Trials as Topic / statistics & numerical data. Combined Modality Therapy. Disease-Free Survival. Drug Delivery Systems. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Multicenter Studies as Topic / statistics & numerical data. Recurrence. Remission Induction. Stem Cell Transplantation. Survival Analysis. Treatment Outcome

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(PMID = 20425368.001).

[ISSN] 1558-822X

[Journal-full-title] Current hematologic malignancy reports

[ISO-abbreviation] Curr Hematol Malig Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

[Number-of-references] 59

   

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[Title] What determines the outcomes for adolescents and young adults with acute lymphoblastic leukemia treated on cooperative group protocols? A comparison of Children's Cancer Group and Cancer and Leukemia Group B studies.

We performed a retrospective comparison of presenting features, planned treatment, complete remission (CR) rate, and outcome of 321 adolescents and young adults (AYAs) ages 16 to 20 years with newly diagnosed acute lymphoblastic leukemia (ALL) who were treated on consecutive trials in either the Children's Cancer Group (CCG) or the Cancer and Leukemia Group B (CALGB) from 1988 to 2001.

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[Cites] J Clin Oncol. 1997 Jun;15(6):2222-30 [9196134.001]

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[CommentIn] Blood. 2009 Feb 19;113(8):1861; author reply 1862 [19228933.001]

(PMID = 18502832.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA 31946; United States / NCI NIH HHS / CA / CA 98543

[Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ PMC2518876

   

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[Title] Expression of two markers of germinal center T cells (SAP and PD-1) in angioimmunoblastic T-cell lymphoma.

BACKGROUND AND OBJECTIVES: In the present paper we report that SAP, an intracytoplasmic molecule that is involved in cell signaling, is an immunohistologic marker for germinal center T cells in paraffin-embedded tissue.

We document its expression, and also that of PD-1 (another recently described marker of germinal center T cells to which a new antibody has been raised), in normal and neoplastic lymphoid tissue to evaluate the suggestion that helper T cells within the germinal centers of human lymphoid tissue are the cell of origin of angioimmunoblastic T-cell lymphoma (AITL), and to assess the diagnostic value of these two markers.

DESIGN AND METHODS: Expression of SAP and PD-1 was investigated by immunohistochemistry in paraffin-embedded tissue sections and in cell lines.

Western blotting was performed on cell lines, and antibody specificity was confirmed by immunostaining of transfected cells.

RESULTS Screening on more than 500 lymphoma biopsies showed that 95% (40/42) of cases of AITL expressed at least one of these markers.

SAP was also expressed on many cases (15/21) of acute T lymphoblastic leukemia, in keeping with its presence in cortical thymocytes.

However, PD-1 and SAP were also found in a minority of cases of peripheral T-cell lymphoma other than AITL, in contrast to a report that the former marker is specific for AITL.

They may also prove of value in the diagnosis of this disease since a negative reaction was rarely observed in this disorder.

[MeSH-major] Adaptor Proteins, Signal Transducing / analysis. Antigens, CD / analysis. Antigens, Differentiation, T-Lymphocyte / analysis. Apoptosis Regulatory Proteins / analysis. Germinal Center / pathology. Immunoblastic Lymphadenopathy / pathology. Intracellular Signaling Peptides and Proteins / analysis. Lymphoma, T-Cell / pathology. Neoplasm Proteins / analysis. T-Lymphocytes / chemistry

[MeSH-minor] Hodgkin Disease / metabolism. Hodgkin Disease / pathology. Humans. Lymphocytes, Tumor-Infiltrating / chemistry. Lymphocytes, Tumor-Infiltrating / pathology. Lymphoma, B-Cell / chemistry. Lymphoma, B-Cell / pathology. Palatine Tonsil / pathology. Programmed Cell Death 1 Receptor. Spleen / pathology. Thymus Gland / pathology

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(PMID = 17640856.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Apoptosis Regulatory Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / PDCD1 protein, human; 0 / Programmed Cell Death 1 Receptor; 0 / SH2D1A protein, human

   

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[Title] Total-body irradiation--role and indications: results from the German Registry for Stem Cell Transplantation (DRST).

BACKGROUND AND PURPOSE: Total-body irradiation (TBI) is a key part of the conditioning regimen before hematopoietic stem cell transplantation (HSCT).

MATERIAL AND METHODS: 14,371 patients (1998-2002) documented in the German Stem Cell Transplantation Registry (DRST) were analyzed regarding TBI utilization prior to autologous or allogeneic transplantation, underlying disorder, type of donor, stem cell source, and size of the treatment center.

RESULTS: For autologous HSCT approximately 10% of the patients (873/8,167) received TBI, with chronic lymphocytic leukemia (CLL, approximately 80%, 171/214) and low-grade non-Hodgkin's lymphoma (l-NHL, approximately 35%, 330/929) being the most important disorders.

In the allogeneic setting 50% of the patients (2,399/4,904) received TBI, with acute lymphocytic leukemia (ALL, 85%, 794/930), acute myeloid leukemia (AML, 45%, 662/1,487) and chronic myeloid leukemia (CML, 49%, 561/1,156) being the key indications.

The type of donor, stem cell source and center size did not strongly influence the use of TBI.

[MeSH-major] Registries. Stem Cell Transplantation. Transplantation Conditioning. Whole-Body Irradiation

[MeSH-minor] Acute Disease. Germany. Histocompatibility Testing. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid / therapy. Lymphoma, Non-Hodgkin / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Tissue Donors. Transplantation, Autologous. Transplantation, Homologous

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(PMID = 16622624.001).

[ISSN] 0179-7158

[Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]

[ISO-abbreviation] Strahlenther Onkol

[Language] eng

[Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

   

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[Title] [High dose methotrexate induced acute renal insufficiency in a patient with acute lymphoblastic leukemia].

[MeSH-major] Acute Kidney Injury / chemically induced. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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(PMID = 17349162.001).

[ISSN] 0578-1310

[Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics

[ISO-abbreviation] Zhonghua Er Ke Za Zhi

[Language] chi

[Publication-type] Case Reports; Journal Article

[Publication-country] China

[Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate

   

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[Title] Haploinsufficiency of the IKZF1 (IKAROS) tumor suppressor gene cooperates with BCR-ABL in a transgenic model of acute lymphoblastic leukemia.

[MeSH-major] Fusion Proteins, bcr-abl / physiology. Genes, Tumor Suppressor / physiology. Ikaros Transcription Factor / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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(PMID = 20393504.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Letter; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] Inhibition of the Akt/survivin pathway synergizes the antileukemia effect of nutlin-3 in acute lymphoblastic leukemia cells.

The phosphatidylinositol 3-kinase (PI3K)/Akt and p53 pathways play antiapoptotic and proapoptotic roles in cell death, respectively.

Cancer cell growth and progression are associated with high levels of PI3K/Akt activation by loss of PTEN expression and the inactivation of p53 by MDM2 overexpression.

We report that inhibition of PI3K/Akt, either by the PI3K inhibitor Ly294002 or by expression of PTEN, synergized the ability of the MDM2 antagonist nutlin-3 to induce apoptosis in acute lymphoblastic leukemia (ALL).

We used a set of ALL cell lines with wild-type p53 and MDM2 overexpression, but different status of PTEN expression/PI3K/Akt activation, to test the ability of nutlin-3 to induce p53 and apoptosis.

Nutlin-3 activated p53 in all the ALL cell lines; however, induction of apoptosis was dependent on PTEN status.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Imidazoles / pharmacology. Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / metabolism. Microtubule-Associated Proteins / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. Piperazines / pharmacology. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Signal Transduction / drug effects

[MeSH-minor] Acute Disease. Apoptosis. Cell Death. Chromones / pharmacology. Drug Synergism. Humans. Inhibitor of Apoptosis Proteins. Morpholines / pharmacology. PTEN Phosphohydrolase / metabolism. RNA, Small Interfering. Transfection. Tumor Cells, Cultured

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(PMID = 18483299.001).

[ISSN] 1535-7163

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA123490

[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 / BIRC5 protein, human; 0 / Chromones; 0 / Imidazoles; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Morpholines; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / RNA, Small Interfering; 0 / nutlin 3; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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[Title] Intravenous busulfan and melphalan, tacrolimus, and short-course methotrexate followed by unmodified HLA-matched related or unrelated hematopoietic stem cell transplantation for the treatment of advanced hematologic malignancies.

Results of allogeneic hematopoietic stem cell transplantation (HCT) to treat advanced leukemia or myelodysplastic syndrome (MDS) remain poor due to excessive relapse and transplant-related mortality.

To improve transplant outcome in this patient population, 43 patients (median age, 46.1 years) with high-risk or advanced lymphoid (n = 5) or myeloid malignancy (n = 38) were prospectively enrolled on a pilot trial of cytoreduction with intravenous busulfan and melphalan followed by an unmodified HLA-A, -B, and -DRbeta1-matched related (n = 18) or unrelated (n = 25) HCT.

Graft-versus-host disease (GVHD) prophylaxis consisted of tacrolimus and methotrexate.

Seventeen patients had unfavorable cytogenetics, 8 patients underwent transplantation for secondary MDS or acute myelogenous leukemia, and 4 patients had relapsed after a previous allogeneic transplantation.

The cumulative incidence of grade II-IV acute GVHD was 24%, and that of extensive chronic GVHD was 7%.

With a minimum follow-up of 18 months, the estimated 3-year overall survival is 37% and the estimated disease-free survival (DFS) is 33%.

For 18 patients with MDS (< or = RAEB-2) or high-risk myeloproliferative disorder, the estimated 3 year DFS is 61%.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Conditioning / methods

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(PMID = 17241929.001).

[ISSN] 1083-8791

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Immunosuppressive Agents; G1LN9045DK / Busulfan; Q41OR9510P / Melphalan; WM0HAQ4WNM / Tacrolimus; YL5FZ2Y5U1 / Methotrexate

   

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[Title] Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement.

The fusion transcripts of MLL rearrangement [MLL(+)] in acute myeloid leukemia (AML) and their clinicohematologic correlation have not be well characterized in the previous studies.

We used Southern blot analysis to screen MLL(+) in de novo AML.

[MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic / genetics

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child, Preschool. Female. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prospective Studies. Survival Rate. Treatment Outcome

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(PMID = 16341046.001).

[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 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

   

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[Title] T-Cell activation by t(9;22) acute lymphoblastic leukemia-derived dendritic-like cells is associated with increased tapasin expression.

Dendritic-like cells from t(9;22) acute lymphoblastic leukemia (ALL) blasts can activate T cells, while the original unmodified leukemic blasts cannot.

Seven t(9;22) ALL patient samples and one cell line were studied for APM component expression utilizing a unique panel of recently developed monoclonal antibodies and a recently developed intracellular staining technique.

In addition, the HLA class I antigen cell surface expression was measured.

These results provide a potential mechanism for the ability of t(9;22) ALL-derived dendritic-like cells to induce T-cell activation and, suggest that tapasin upregulation may serve as a marker to standardize and monitor the quality of the dendritic-like cells used in immunotherapy.

[MeSH-major] Antiporters / biosynthesis. Dendritic Cells / immunology. Immunoglobulins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. T-Lymphocytes / immunology

[MeSH-minor] Antibodies, Monoclonal / immunology. Antigen Presentation / immunology. Antigens, CD / biosynthesis. Antigens, CD / immunology. Cell Line, Tumor. Histocompatibility Antigens Class I / biosynthesis. Histocompatibility Antigens Class I / immunology. Humans. In Situ Hybridization, Fluorescence / methods. Membrane Transport Proteins. Translocation, Genetic / immunology

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(PMID = 16010586.001).

[ISSN] 0340-7004

[Journal-full-title] Cancer immunology, immunotherapy : CII

[ISO-abbreviation] Cancer Immunol. Immunother.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 16056; United States / NCI NIH HHS / CA / CA 67108

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antiporters; 0 / Histocompatibility Antigens Class I; 0 / Immunoglobulins; 0 / Membrane Transport Proteins; 0 / tapasin

   

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[Title] Cyclosporine A and mycophenolate mofetil vs cyclosporine A and methotrexate for graft-versus-host disease prophylaxis after stem cell transplantation from HLA-identical siblings.

The combination of Cyclosporin A (CSA) and Methotrexate (MTX) is considered to be the standard regimen for the prevention of graft-versus-host disease (GVHD) after stem cell transplantation (SCT) from HLA-identical siblings.

We retrospectively compared CSA/MTX and CSA/MMF in 93 patients (median age 35 years, range 17-59 years, male subjects 48, female subjects 45) with acute myeloid leukemia (n=33), myelodysplastic syndrome (MDS) (n=3), acute lymphoblastic leukemia (ALL) (n=20) or chronic myeloid leukemia (n=37) who received CSA/MMF (n=26) or CSA/MTX (n=67) as GVHD prophylaxis following high-dose therapy and allogeneic SCT from HLA-identical siblings.

No statistically significant differences were found in overall survival, relapse rate, treatment-related mortality and acute or chronic GVHD.

[MeSH-major] Cyclosporine / administration & dosage. Graft vs Host Disease / prevention & control. Immunosuppressive Agents / administration & dosage. Methotrexate / administration & dosage. Mycophenolic Acid / administration & dosage. Mycophenolic Acid / analogs & derivatives. Stem Cell Transplantation / methods

[MeSH-minor] Adolescent. Adult. Female. HLA Antigens. Histocompatibility. Histocompatibility Testing. Humans. Leukemia / mortality. Leukemia / therapy. Living Donors. Male. Middle Aged. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Recurrence. Retrospective Studies. Siblings. Time Factors. Transplantation Conditioning. Transplantation, Homologous / methods. Treatment Outcome

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[CommentIn] Bone Marrow Transplant. 2006 Jan;37(2):235-6; author reply 236-7 [16284607.001]

(PMID = 15821769.001).

[ISSN] 0268-3369

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / HLA Antigens; 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; YL5FZ2Y5U1 / Methotrexate

   

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[Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.

The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.

The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.

Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.

Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.

[MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology

[MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

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(PMID = 15875082.001).

[ISSN] 0028-2685

[Journal-full-title] Neoplasma

[ISO-abbreviation] Neoplasma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Slovakia

[Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase

   

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[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.

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(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

   

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PROCEDURE: A retrospective chart review of all children with leukemia/lymphoma diagnosed between November 2002 and April 2004 who received sevelamer during their initial admission was conducted.

Nine children had acute lymphoblastic leukemia, one had acute myeloid leukemia and 3 had non-Hodgkin's lymphoma.

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[Copyright] (c) 2008 Wiley-Liss, Inc.

(PMID = 18240167.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Calcium Phosphates; 0 / Chelating Agents; 0 / Phosphates; 0 / Polyamines; 97Z1WI3NDX / calcium phosphate; 9YCX42I8IU / Sevelamer

   

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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

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[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

   

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Because folate is the cornerstone in DNA synthesis, we analysed herein if the polymorphisms in MTHFR gene can alter the susceptibility of lymphoproliferative disease risk and if it has an effect on chemotherapy response.

One hundred fifty-six patients with lymphoid malignancies and 82 healthy controls were included into the study.

Neither gene frequencies nor allel frequencies were found to increase lymphoproliferative disease risk significantly in both overall group and subgroups.

Although it was not statistically significant, we found a 2.7-fold increased risk in acute lymphocytic leukaemia (ALL)/Burkitt lymphoma patients with TT genotype [odds ratio (OR), 2.7; 95% confidence interval (CI), 0.88-8.2] than CC genotype but a 1.7-fold decreased risk with TT genotype in diffuse large B-cell lymphoma (DLBCL; OR, 0.58; 95% CI, 0.17-1.88) and a 1.8-fold decreased risk in Hodgkin's lymphoma with TT genotype (OR, 0.55; 95% CI, 0.10-2.87) than CC genotype.

The chemotherapy response was analysed in DLBCL, Hodgkin's lymphoma and ALL/Burkitt's lymphoma because these patients received standard chemotherapy protocols.

As a conclusion, MTHFR C677T polymorphism does not increase the risk of lymphoproliferative disease, and it does not have an effect on chemotherapy response significantly; however, the patients with TT genotype have a slightly increased risk for ALL, and they also respond worse than CC genotype.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / genetics. Female. Genetic Predisposition to Disease. Genotype. Hodgkin Disease / drug therapy. Hodgkin Disease / genetics. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / genetics. Male. Middle Aged. Risk. Treatment Outcome

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[CommentIn] Ann Hematol. 2007 May;86(5):389 [17211521.001]

(PMID = 16944145.001).

[ISSN] 0939-5555

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)

   

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[Title] Nutritional status at initial presentation in childhood acute lymphoblastic leukemia and its effect on induction of remission.

This prospective study was aimed to evaluate the nutritional status at initial presentation in childhood acute lymphoblastic leukemia (ALL) and to ascertain the effects of nutrition on induction of remission.

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(PMID = 18946451.001).

[ISSN] 1022-4742

[Journal-full-title] Mymensingh medical journal : MMJ

[ISO-abbreviation] Mymensingh Med J

[Language] ENG

[Publication-type] Journal Article

[Publication-country] Bangladesh

   

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[Title] Specific viruses were not detected in Guthrie cards from children who later developed leukemia.

There are hypotheses concerning infectious mechanism in the development of acute lymphoblastic leukemia (ALL).

[MeSH-major] DNA Tumor Viruses. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / virology. Tumor Virus Infections / virology

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(PMID = 18092251.001).

[ISSN] 1521-0669

[Journal-full-title] Pediatric hematology and oncology

[ISO-abbreviation] Pediatr Hematol Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] The specificity of memory for a highly trained finger movement sequence: Change the ending, change all.

How are highly trained movement sequences represented in long-term memory?

Here we show that the gains attained in the performance of a well-trained sequence of finger movements can be expressed only when the order of the movements is exactly as practiced.

Ten young adults were trained to perform a given 5-element sequence of finger-to-thumb opposition movements with their left hand.

Movements were analyzed using video based tracking.

Three weeks of training resulted, along with improved accuracy, in robustly shortened movement times as well as shorter finger-to-thumb touch times.

However, there was little transfer of these gains in speed to the execution of the same component movements arranged in a new order.

Moreover, even when the only change was the omission of the one before final movement of the trained sequence (Omit sequence), the initial movements of the sequence were significantly slowed down, although these movements were identical to the initial movements of the trained sequence.

Our results support the notion that a well-trained sequence of finger movements can be represented, in the adult motor system, as a singular, co-articulated, unit of movement, in which even the initial component movements are contingent on the subsequent, anticipated, ones.

Because of co-articulation related anticipatory effects, gains in fluency and accuracy acquired in training on a specific movement sequence cannot be expressed in full in the execution of the trained component movements or of a full segment of the trained sequence, if followed by a different ending segment.

[MeSH-major] Memory / physiology. Motor Skills / physiology

[MeSH-minor] Adult. Female. Fingers / innervation. Fingers / physiology. Humans. Male. Young Adult

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[Copyright] Copyright 2010. Published by Elsevier B.V.

(PMID = 20298683.001).

[ISSN] 1872-6240

[Journal-full-title] Brain research

[ISO-abbreviation] Brain Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

   

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We found a statistically significantly increased incidence of hematological malignancies (SIR 1.12, 95% confidence interval [CI]: 1.05, 1.19), mainly due to high rates for non-Hodgkin lymphoma (SIR 1.22, 95% CI: 1.12, 1.33) and acute lymphoblastic leukemia (SIR 1.34, 95% CI: 0.95, 1.83).

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(PMID = 16332253.001).

[ISSN] 1471-2458

[Journal-full-title] BMC public health

[ISO-abbreviation] BMC Public Health

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Air Pollutants; 0 / Vehicle Emissions

[Other-IDs] NLM/ PMC1325225

   

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[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.

[MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

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(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

   

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[Title] How similar are those molecules after all? Use two descriptors and you will have three different answers.

IMPORTANCE OF THE FIELD: Molecular similarity searching (ligand-based virtual screening) is one of the routine computational techniques used in drug discovery and pharmacological research.

However, while a large number of descriptors exist, there are no general guidelines whatsoever which descriptors work better and which descriptors should be used in the different cases.

AREAS COVERED IN THIS REVIEW: This review provides a brief overview of current molecular descriptors and databases used for their evaluation, followed by a critical discussion of their differences.

WHAT THE READER WILL GAIN: After reading this review, the reader will be aware of how very differently molecular descriptors assess similarities of molecules, and the performance that can be realistically expected from them.

TAKE HOME MESSAGE: Molecular descriptors come in a variety of forms, and they show vast differences in assessing the similarity between molecules.

Virtual screening performance of many descriptors is often lower than expected, compared to 'dumb' descriptors while some simple methods such as circular fingerprints offer surprisingly good performance in many cases.

The choice of the right benchmark library is crucial, many of which are summarized in this review.

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(PMID = 22822717.001).

[ISSN] 1746-045X

[Journal-full-title] Expert opinion on drug discovery

[ISO-abbreviation] Expert Opin Drug Discov

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Acute hepatitis caused by a natural lipid-lowering product: when "alternative" medicine is no "alternative" at all.

The episode was regarded as an adverse drug reaction after exclusion of other possible causes of acute liver disease and the prompt normalization of liver function tests after Equisterol had been discontinued.

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[ErratumIn] J Hepatol. 2010 Mar;52(3):466

(PMID = 19398239.001).

[ISSN] 1600-0641

[Journal-full-title] Journal of hepatology

[ISO-abbreviation] J. Hepatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Biological Products; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Hypolipidemic Agents; 0 / Plant Extracts; 0 / Plant Gums; 0 / guggulu extract; 0 / red yeast rice; 9LHU78OQFD / Lovastatin; EC 2.3.2.2 / gamma-Glutamyltransferase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase

   

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[Title] Nilotinib: a second-generation tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia.

BACKGROUND: Nilotinib, a second-generation tyrosine kinase inhibitor (TKI) formerly known as AMN107, was approved by the US Food and Drug Administration (FDA) on October 29, 2007, for the treatment of adult patients with chronic-phase (CP) and accelerated-phase (AP) Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) resistant to or intolerant of prior treatment that included imatinib.

OBJECTIVE: The purpose of this review was to evaluate the pharmacology, pharmacokinetic properties, and pharmacodynamic properties of nilotinib; results of clinical trials in patients with CML, Ph+ acute lymphoblastic leukemia (ALL), and gastrointestinal stromal tumors (GISTs); and potential drug interactions.

Search terms included, but were not limited to, nilotinib, AMN107, chronic myelogenous leukemia, acute lymphoblastic leukemia, bcr-abl, imatinib resistance, adverse events, pharmacology, and clinical trials.

RESULTS: Nilotinib is an orally bioavailable derivative of imatinib with improved specificity toward the breakpoint cluster region-Abelson murine leukemia (bcr-abl) viral protooncogene.

Of patients whose disease had progressed to AP, nilotinib was associated with major cytogenetic response in 32%; complete cytogenetic response in 19%; and CHR in 30%.

At 12 months, an estimated 56% of patients lacked progression of disease, and the estimated overall survival rate was 82%.

[MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use

[MeSH-minor] Animals. Clinical Trials as Topic. Fusion Proteins, bcr-abl. Gastrointestinal Stromal Tumors / drug therapy. Humans. Models, Biological. Molecular Structure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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(PMID = 19108785.001).

[ISSN] 0149-2918

[Journal-full-title] Clinical therapeutics

[ISO-abbreviation] Clin Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl

[Number-of-references] 91

   

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[Title] Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia.

Childhood acute lymphoblastic leukemia (ALL) is caused by malignant immature lymphocytes.

Given the high plasticity of cells, we searched for leukemia-associated genetic aberrations and immunoglobulin (IG) gene rearrangements in mesenchymal stem cells (MSC) from childhood B-cell precursor ALL patients.

MSC from all ten ALL patients analyzed presented the chromosomal translocations that had been detected in leukemia cells (TEL-AML1, E2A-PBX1, or MLL rearrangement).

Leukemia-specific IG gene rearrangements were detected in the MSC from three ALL patients.

The detection of leukemia-associated genetic aberrations in MSC indicates a clonal relationship between MSC and leukemia cells and suggests their involvement in the pathogenesis and/or pathophysiology of childhood ALL.

[MeSH-major] Mesenchymal Stromal Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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[CommentIn] J Mol Med (Berl). 2010 Mar;88(3):219-22 [20135087.001]

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(PMID = 20155409.001).

[ISSN] 1432-1440

[Journal-full-title] Journal of molecular medicine (Berlin, Germany)

[ISO-abbreviation] J. Mol. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein

   

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[Title] Influence of the polymorphism in candidate genes on late cardiac damage in patients treated due to acute leukemia in childhood.

The hypothesis was tested in a cohort of 76 long-term survivals of acute lymphoblastic leukemia in childhood.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cardiomyopathies / genetics. Genetic Association Studies. Heart / drug effects. Myocardium / pathology. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Survivors

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(PMID = 19863340.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Anthracyclines; 0 / Reactive Oxygen Species; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.15.1.1 / superoxide dismutase 2; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1

   

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Reversible posterior leukoencephalopathy syndrome (RPLS) is recently described disorder with typical radiological findings in the posterior regions of the cerebral hemisphere and cerebellum.

We presented nine patients with RPLS who had primary diagnoses such as acute post-streptococcal glomerulonephritis, idiopathic hypertension, the performing of intravenous immunoglobulin for infection with crescentic glomerulonephritis, erythrocyte transfusion for severe iron deficiency, L: -asparaginase treatment for acute lymphoblastic leukemia and performing of granulocyte-colony stimulating factor for ulcerative colitis due to neutropenia.

Early recognition of RPLS as complication during different diseases and therapy in childhood may facilitate precise diagnosis and appropriate treatment.

[MeSH-major] Posterior Leukoencephalopathy Syndrome / diagnosis

[MeSH-minor] Adolescent. Brain / pathology. Child. Diagnosis, Differential. Early Diagnosis. Female. Humans. Magnetic Resonance Imaging. Male

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[ISSN] 1590-3478

[Journal-full-title] Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology

[ISO-abbreviation] Neurol. Sci.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] Italy

[Number-of-references] 42

   

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[Title] Pre-B cell receptor signaling in acute lymphoblastic leukemia.

B cell lineage ALL represents by far the most frequent malignancy in children and is also common in adults.

In a recent study on 111 cases of pre-B cell-derived human ALL, we found that ALL cells carrying a BCR-ABL1-gene rearrangement lack expression of a functional pre-B cell receptor in virtually all cases.

In a proof-of-principle experiment, we studied pre-B cell receptor function during progressive leukemic transformation of pre-B cells in BCR-ABL1-transgenic mice: Interestingly, signaling from the pre-B cell receptor and the oncogenic BCR-ABL1 kinase are mutually exclusive and only "crippled" pre-B cells that fail to express a functional pre-B cell receptor are permissive to transformation by BCR-ABL1.

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(PMID = 19901533.001).

[ISSN] 1551-4005

[Journal-full-title] Cell cycle (Georgetown, Tex.)

[ISO-abbreviation] Cell Cycle

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01CA137606; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / R21 CA152497; None / None / / R01 CA139032-01; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / R01 CA137060-01A1; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060

[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 / ABI1 protein, human; 0 / Abi1 protein, mouse; 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / Cytoskeletal Proteins; 0 / Pre-B Cell Receptors; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr

[Other-IDs] NLM/ NIHMS230959; NLM/ PMC4047560

   

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[Title] Treatment of childhood T-cell lymphoblastic lymphoma according to the strategy for acute lymphoblastic leukaemia, without radiotherapy: long term results of the EORTC CLG 58881 trial.

From June 1989 through to November 1998, 121 children with newly diagnosed T-cell lymphoblastic lymphoma (T-LBL) were included in the EORTC 58881 trial conducted by the Children's Leukaemia Group.

Cranial irradiation, prophylactic cranial and local, was omitted, even for patients with central nervous involvement at diagnosis.

An intensive acute lymphoblastic leukaemia type chemotherapy regimen without irradiation leads to a high cure and survival rate in childhood T-LBL without an increased CNS recurrence.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Recurrence. Treatment Outcome

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(PMID = 18342502.001).

[ISSN] 0959-8049

[Journal-full-title] European journal of cancer (Oxford, England : 1990)

[ISO-abbreviation] Eur. J. Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 5U10-CA11488-18; United States / NCI NIH HHS / CA / 5U10-CA11488-19; United States / NCI NIH HHS / CA / 5U10-CA11488-20; United States / NCI NIH HHS / CA / 5U10-CA11488-21; United States / NCI NIH HHS / CA / 5U10-CA11488-22; United States / NCI NIH HHS / CA / 5U10-CA11488-23; United States / NCI NIH HHS / CA / 5U10-CA11488-24; United States / NCI NIH HHS / CA / 5U10-CA11488-25; United States / NCI NIH HHS / CA / 5U10-CA11488-26; United States / NCI NIH HHS / CA / 5U10-CA11488-27; United States / NCI NIH HHS / CA / 5U10-CA11488-28; United States / NCI NIH HHS / CA / 5U10-CA11488-29; United States / NCI NIH HHS / CA / 5U10-CA11488-30; United States / NCI NIH HHS / CA / 5U10-CA11488-31; United States / NCI NIH HHS / CA / 5U10-CA11488-32; United States / NCI NIH HHS / CA / 5U10-CA11488-33; United States / NCI NIH HHS / CA / 5U10-CA11488-34; United States / NCI NIH HHS / CA / 5U10-CA11488-35; United States / NCI NIH HHS / CA / 5U10-CA11488-36

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Investigator] Philippet P; Otten J; Plouvier E; Béhar C; Boutard P; Millot F; Waterkeyn C; Velde IV; Solbu G

   

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[Title] TEL-AML1 corrupts hematopoietic stem cells to persist in the bone marrow and initiate leukemia.

The initial steps in the pathogenesis of acute leukemia remain incompletely understood.

The TEL-AML1 gene fusion, the hallmark translocation in Childhood Acute Lymphoblastic Leukemia and the first hit, occurs years before the clinical disease, most often in utero.

TEL-AML1 renders mice prone to malignancy after chemical mutagenesis when expressed in hematopoietic stem cells (HSCs), but not in early lymphoid progenitors.

We reveal that TEL-AML1 markedly increases the number of HSCs and predominantly maintains them in the quiescent (G(0)) stage of the cell cycle.

[MeSH-major] Bone Marrow Cells / metabolism. Core Binding Factor Alpha 2 Subunit / genetics. Hematopoietic Stem Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Oncogenes

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[CommentIn] Cell Stem Cell. 2009 Jul 2;5(1):5-6 [19570506.001]

(PMID = 19570513.001).

[ISSN] 1875-9777

[Journal-full-title] Cell stem cell

[ISO-abbreviation] Cell Stem Cell

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P01 CA68486

[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 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factors; 0 / Interleukin-7; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein

   

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Normally found in small quantities in primary and secondary lymphoid organs, PDCs accumulate in a variety of inflammatory conditions, including Kikuchi-Fujimoto lymphadenopathy, hyaline-vascular Castleman disease, and autoimmune diseases, and in certain malignancies such as classical Hodgkin lymphoma and carcinomas.

Demonstrating potential for neoplastic transformation reflective of varying stages of maturation, clonal proliferations range from PDC nodules most commonly associated with chronic myelomonocytic leukemia to the rare but highly aggressive malignancy now known as blastic plasmacytoid dendritic cell neoplasm (BPDCN).

Formerly called blastic natural killer cell lymphoma or CD4/CD56 hematodermic neoplasm, BPDCN, unlike natural killer cell lymphomas, is not associated with Epstein-Barr virus infection and is generally not curable with treatment regimens for non-Hodgkin lymphomas.

In fact, this entity is no longer considered to be a lymphoma and instead represents a unique precursor hematopoietic neoplasm.

Acute leukemia therapy regimens may lead to sustained clinical remission of BPDCN, with bone marrow transplantation in first complete remission potentially curative in adult patients.

[MeSH-minor] Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / pathology. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Male. Toll-Like Receptors / immunology

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(PMID = 19851130.001).

[ISSN] 1533-4031

[Journal-full-title] Advances in anatomic pathology

[ISO-abbreviation] Adv Anat Pathol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Toll-Like Receptors

[Number-of-references] 151

   

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[Title] Increased cardiometabolic traits in pediatric survivors of acute lymphoblastic leukemia treated with total body irradiation.

Survivors of childhood acute lymphoblastic leukemia (ALL) may face an increased risk of metabolic and cardiovascular late effects.

To determine the prevalence of and risk factors for adverse cardiometabolic traits in a contemporary cohort of pediatric ALL survivors, we recruited 48 off-therapy patients in remission treated with conventional chemotherapy and 26 treated with total body irradiation (TBI)-based hematopoietic cell transplantation (HCT) in this cross-sectional pilot study.

Other risk factors included any cranial radiation exposure and family history of cardiometabolic disease.

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[Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.

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(PMID = 20685399.001).

[ISSN] 1523-6536

[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

[Grant] United States / NCRR NIH HHS / RR / UL1 RR024975-01; United States / NCRR NIH HHS / RR / UL1 RR025014-01; United States / NCRR NIH HHS / RR / TL1 RR024978; United States / NCRR NIH HHS / RR / KL2 RR024977; None / None / / UL1 RR025014-01; United States / NCRR NIH HHS / RR / UL1RR025014; United States / NCRR NIH HHS / RR / UL1RR024975; United States / NCRR NIH HHS / RR / UL1 RR025014; United States / NCRR NIH HHS / RR / UL1 RR024975

[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 / Leptin; 9007-41-4 / C-Reactive Protein

[Other-IDs] NLM/ NIHMS211258; NLM/ PMC2975816

   

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[Title] MDR1 C3435T polymorphism in Mexican children with acute lymphoblastic leukemia and in healthy individuals.

To determine the influence of the MDR1 C3435T polymorphism on the development of childhood acute lymphoblastic leukemia (ALL), we studied 107 children with ALL and 111 healthy subjects.

[MeSH-major] P-Glycoprotein / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 19317599.001).

[ISSN] 0018-7143

[Journal-full-title] Human biology

[ISO-abbreviation] Hum. Biol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / ABCB1 protein, human; 0 / P-Glycoprotein; 0 / P-Glycoproteins

   

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A rapid liquid chromatography/positive ion electrospray mass spectrometric assay (LC/ESI-MS) was developed for the quantitation of methotrexate, folinic acid, folic acid and ondansetron in human serum.

The assay was based on 100microL serum samples, following acetonitrile precipitation of proteins and filtration that enabled direct injection into the LC/MS system.

The assay was found to be linear in the concentration range of 0.01-25.00microgmL(-1) for methotrexate and 0.01-5.00microgmL(-1) for folic acid, folinic acid and ondansetron.

The method can be used to quantify methotrexate, folinic acid, folic acid and ondansetron in human serum covering a variety of clinical studies and it was applied to the analysis of human serum samples obtained from children with acute lymphoblastic leukemia.

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(PMID = 19828383.001).

[ISSN] 1873-376X

[Journal-full-title] Journal of chromatography. B, Analytical technologies in the biomedical and life sciences

[ISO-abbreviation] J. Chromatogr. B Analyt. Technol. Biomed. Life Sci.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 4AF302ESOS / Ondansetron; 935E97BOY8 / Folic Acid; Q573I9DVLP / Leucovorin; YL5FZ2Y5U1 / Methotrexate

   

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[Title] Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia.

RESULTS: A total of 31 patients with acute leukemia who developed febrile neutropenia were enrolled in the study.

Underlying diseases consisted of acute myeloid leukemia (n=15) and acute lymphoblastic leukemia (n=3).

[MeSH-minor] Adolescent. Adult. Algorithms. Echinocandins. Female. Fever / etiology. Humans. Leukemia, Myeloid / complications. Lipopeptides. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Prospective Studies

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(PMID = 16595990.001).

[ISSN] 1349-7235

[Journal-full-title] Internal medicine (Tokyo, Japan)

[ISO-abbreviation] Intern. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Lipopeptides; 0 / Lipoproteins; 0 / Peptides, Cyclic; R10H71BSWG / micafungin

   

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[Title] Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35.

Adenovirus 5 (Ad5) virus or adeno-associated viral vectors have been used to study the tumor suppressor function of FHIT in solid tumors, but these tools have not been effective in leukemias.

EXPERIMENTAL DESIGN: Infection efficiency of Ad5/F35-FHIT and Ad5/F35-GFP viruses was tested in leukemia cell lines that lacked FHIT expression, and biological effects of successful infection were assessed.

An acute myelogenous leukemia, a chronic myelogenous leukemia, and four acute lymphoblastic leukemia human cell lines were examined as well as two EBV-transformed B lymphoblastoid cell lines that expressed endogenous FHIT.

RESULTS: Two of four acute lymphoblastic leukemia cell lines, Jurkat and MV4;11, which were efficiently infected with Ad5/F35-FHIT, underwent growth suppression and massive induction of apoptosis without apparent activation of caspase-8 or caspase-2 and late activation of caspase-3.

The two remaining infected acute lymphoblastic leukemia cell lines, Molt-3 and RS4;11, were apparently unaffected.

Restoration of FHIT expression in the chronic myelogenous leukemia K562 cell line and the acute myelogenous leukemia KG1a cell line also induced apoptosis but at later time points than seen in the acute lymphoblastic leukemia Jurkat and MV4;11 cell lines. I.v. injection of Ad5/F35-FHIT-infected Jurkat cells resulted in abrogation of tumorigenicity in the NOD/SCID xenogeneic engraftment model.

CONCLUSION: FHIT restoration in some FHIT-deficient leukemia cells induces both antiproliferative and proapoptotic effects involving the intrinsic caspase apoptotic pathway.

[MeSH-major] Acid Anhydride Hydrolases / genetics. Adenoviruses, Human / genetics. Gene Expression Regulation, Neoplastic / genetics. Genetic Therapy / methods. Leukemia / genetics. Neoplasm Proteins / genetics

[MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Cell Cycle. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Gene Transfer Techniques. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Humans. Kinetics. Mice. Mice, Inbred NOD. Mice, SCID. Structure-Activity Relationship. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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[ErratumIn] Clin Cancer Res. 2016 Dec 15;22(24):6304 [27856602.001]

(PMID = 16740775.001).

[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 / CA56036; United States / NCI NIH HHS / CA / CA77738; United States / NCI NIH HHS / CA / CA78890; United States / NCI NIH HHS / CA / CA89341

[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 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.6.- / Acid Anhydride Hydrolases

   

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[Title] Rituximab plus chemotherapy in children with relapsed or refractory CD20-positive B-cell precursor acute lymphoblastic leukemia.

We treated three children with relapsed or refractory CD20 positive B-cell precursor acute lymphoblastic leukemia with rituximab in combination with chemotherapy, which produced a decreasing or persistent low positive minimal residual disease load.

Two children subsequently underwent allogeneic stem cell transplantation and remain in complete remission at days +399 and +332.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy / methods

[MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, CD20. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Rituximab. Treatment Outcome

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(PMID = 16461321.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Italy

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab

   

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[Title] Limited redundancy in phosphorylation of retinoblastoma tumor suppressor protein by cyclin-dependent kinases in acute lymphoblastic leukemia.

In Nalm-6 acute lymphoblastic leukemia extracts, serine 608 is phosphorylated by CDK4/6 complexes but not by CDK2.

Serine 612 phosphorylation by CDK4 also occurred in extracts of childhood acute lymphoblastic leukemia cells but not in extracts of mobilized CD34+ hemopoietic progenitor cells.

This phenomenon could contribute to the commitment of childhood acute lymphocytic leukemia cells to proliferate and explain their refractoriness to differentiation-inducing agents.

[MeSH-major] Burkitt Lymphoma / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein Processing, Post-Translational. Retinoblastoma-Like Protein p107 / metabolism

[MeSH-minor] Antigens, CD34. Cell Differentiation / drug effects. Cell Line, Tumor. Cell-Free System / metabolism. Drug Resistance, Neoplasm / drug effects. G1 Phase / drug effects. Hematopoietic Stem Cells / metabolism. Humans. Indoles / pharmacology. Multiprotein Complexes / metabolism. Phosphorylation / drug effects

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(PMID = 16936279.001).

[ISSN] 0002-9440

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Indoles; 0 / Multiprotein Complexes; 0 / Retinoblastoma-Like Protein p107; 114719-57-2 / fascaplysine; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinase 4

[Other-IDs] NLM/ PMC1698824