BioMedLib Search Engine [ goto HOMEPAGE ]

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Transplantation.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18245655.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] Italy

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Hazardous Substances Data Bank. PREDNISONE .

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 = 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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

Genetic Alliance. consumer health - Hodgkin lymphoma.

Genetic Alliance. consumer health - Hodgkin lymphoma, childhood.

Genetic Alliance. consumer health - Lymphoblastic lymphoma.

Genetic Alliance. consumer health - Non-Hodgkin lymphoma, childhood.

Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.

MedlinePlus Health Information. consumer health - Endocrine Diseases.

MedlinePlus Health Information. consumer health - Metabolic Disorders.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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.

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

MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Hazardous Substances Data Bank. IMATINIB MESYLATE .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

SciCrunch. DrugBank: Data: Chemical .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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.

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.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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.

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

Genetic Alliance. consumer health - Childhood Cancer.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Hazardous Substances Data Bank. METHYLPHENIDATE .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Pediatr Neurol. 2002 Apr;26(4):261-6 [11992752.001]

[Cites] J Clin Oncol. 2001 Mar 15;19(6):1802-8 [11251012.001]

[Cites] Pediatr Rehabil. 2004 Jan-Mar;7(1):1-14; discussion 15-6 [14744668.001]

[Cites] J Am Acad Child Adolesc Psychiatry. 2004 May;43(5):559-67 [15100562.001]

[Cites] J Child Psychol Psychiatry. 1977 Apr;18(2):137-65 [326801.001]

[Cites] Pediatrics. 1990 Aug;86(2):184-92 [2196520.001]

[Cites] J Child Psychol Psychiatry. 1992 Jan;33(1):153-95 [1371122.001]

[Cites] J Child Neurol. 1992 Oct;7(4):462-3 [1469256.001]

[Cites] Pediatrics. 1993 Jun;91(6):1101-6 [8502509.001]

[Cites] Child Psychiatry Hum Dev. 1993 Fall;24(1):25-30 [8404241.001]

[Cites] J Clin Exp Neuropsychol. 1994 Feb;16(1):21-42 [8150888.001]

[Cites] Pediatrics. 1997 Oct;100(4):662-6 [9310521.001]

[Cites] J Clin Oncol. 2004 Dec 1;22(23):4795-803 [15570081.001]

[Cites] Ann Pharmacother. 2006 Jun;40(6):1134-42 [16735655.001]

[Cites] Drug Saf. 2007;30(1):17-26 [17194168.001]

[Cites] Expert Rev Neurother. 2007 Feb;7(2):195-201 [17286552.001]

[Cites] J Pediatr Psychol. 2007 Oct;32(9):1127-39 [17569711.001]

[Cites] Hematol Oncol Clin North Am. 2008 Apr;22(2):211-31, v-vi [18395146.001]

[Cites] J Consult Clin Psychol. 2008 Jun;76(3):367-78 [18540731.001]

[Cites] Clin Psychol Rev. 2002 Nov;22(8):1107-31 [12436807.001]

(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

   

[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] 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

MedlinePlus Health Information. consumer health - Melanoma.

MedlinePlus Health Information. consumer health - Skin Cancer.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

Advertisement

[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] 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.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

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

[Cites] Blood. 1995 Apr 15;85(8):2025-37 [7718875.001]

[Cites] Leukemia. 1998 Apr;12(4):463-73 [9557602.001]

[Cites] N Engl J Med. 1998 Jun 4;338(23):1663-71 [9614257.001]

[Cites] Blood. 1998 Sep 1;92(5):1556-64 [9716583.001]

[Cites] Blood. 1999 Jun 1;93(11):3983-93 [10339508.001]

[Cites] Leukemia. 2004 Dec;18(12):2032-5 [15483674.001]

[Cites] Eur J Haematol. 2005 Jun;74(6):466-80 [15876250.001]

[Cites] Br J Haematol. 2005 Jun;129(6):734-45 [15952999.001]

[Cites] Br J Haematol. 2005 Jul;130(2):166-73 [16029445.001]

[Cites] Dan Med Bull. 2006 Feb;53(1):76-9 [16761337.001]

[Cites] Cancer. 2006 Oct 1;107(7):1551-61 [16955505.001]

[Cites] Hematology Am Soc Hematol Educ Program. 2006;:128-32 [17124051.001]

[Cites] Pediatr Blood Cancer. 2007 Mar;48(3):254-61 [16421910.001]

[Cites] Blood. 2007 May 15;109(10):4164-7 [17264295.001]

[Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]

[Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]

[Cites] J Clin Oncol. 2003 Mar 1;21(5):760-1 [12610169.001]

[Cites] J Clin Oncol. 2003 Mar 1;21(5):774-80 [12610173.001]

[Cites] Cancer. 2003 Mar 15;97(6):1471-80 [12627512.001]

[Cites] Blood. 2003 May 15;101(10):3809-17 [12531809.001]

[Cites] Leukemia. 1998 Feb;12(2):144-9 [9519775.001]

[Cites] Cancer Treat Rev. 2004 Feb;30(1):37-51 [14766125.001]

[Cites] Ann Hematol. 2004;83 Suppl 1:S127-8 [15124704.001]

[Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]

[Cites] Med Pediatr Oncol. 1990;18(4):273-9 [2355886.001]

[Cites] Cancer. 1991 Aug 15;68(4):751-8 [1855175.001]

[Cites] Blood. 1994 Nov 1;84(9):3122-33 [7949185.001]

[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

   

[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] 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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] Statistical processing: not so implausible after all.

Myczek and Simons (2008) have shown that findings attributed to a statistical mode of perceptual processing can, instead, be explained by focused attention to samples of just a few items.

Some new findings raise questions about this claim. (1) Participants, given conditions that would require different focused attention strategies, did no worse when the conditions were randomly mixed than when they were blocked. (2) Participants were significantly worse at estimating the mean size when given small samples than when given the whole display. (3) One plausible suggested strategy--comparing the largest item in each display, rather than the mean size--was not, in fact, used.

Distributed attention to sets of similar stimuli, enabling a statistical-processing mode, provides a coherent account of these and other phenomena.

[MeSH-major] Cognition. Data Interpretation, Statistical

[MeSH-minor] Humans

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentOn] Percept Psychophys. 2008 Jul;70(5):772-88 [18613626.001]

(PMID = 18927015.001).

[ISSN] 0031-5117

[Journal-full-title] Perception & psychophysics

[ISO-abbreviation] Percept Psychophys

[Language] eng

[Grant] United States / NIMH NIH HHS / MH / 2R01 MH 058383-04A1

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

[Publication-country] United States

   

[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] Plant endocytosis: it is clathrin after all.

Endocytosis occurs in plants, but the involvement of clathrin-coated vesicles has been unclear; a new study provides strong evidence that, as in animal cells, clathrin-coated vesicles are a major means of internalisation by plant cells.

[MeSH-major] Arabidopsis / metabolism. Clathrin / physiology. Clathrin-Coated Vesicles / physiology. Endocytosis / physiology

[MeSH-minor] Protoplasts / metabolism

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentOn] Curr Biol. 2007 Mar 20;17(6):520-7 [17306539.001]

(PMID = 17371763.001).

[ISSN] 0960-9822

[Journal-full-title] Current biology : CB

[ISO-abbreviation] Curr. Biol.

[Language] eng

[Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBS/B/09562

[Publication-type] Comment; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Clathrin

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Jackson Laboratory JAX®Mice Database. culture/stock collections - B6.Cg-Tg(BCR/ABL)623Hkp/J (subscription/membership/fee required).

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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 = 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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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 = 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

   

[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] 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

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. MELPHALAN .

Hazardous Substances Data Bank. BUSULFAN .

Hazardous Substances Data Bank. METHOTREXATE .

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 = 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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

Genetic Alliance. consumer health - Transplantation.

Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .

Hazardous Substances Data Bank. METHOTREXATE .

Hazardous Substances Data Bank. CYCLOSPORIN A .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] 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

   

[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] 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

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

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 = 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

   

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

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

[Title] The association between atopy and childhood/adolescent leukemia: a meta-analysis.

Atopic disease is hypothesized to be protective against several malignancies, including childhood/adolescent leukemia.

To summarize the available epidemiologic evidence, the authors performed a meta-analysis of associations between atopy/allergies, asthma, eczema, hay fever, and hives and childhood/adolescent leukemia, acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML).

Odds ratios for atopy/allergies were 1.42 (95% confidence interval (CI): 0.60, 3.35) for 3 studies of leukemia overall, 0.69 (95% CI: 0.54, 0.89) for 6 studies of ALL, and 0.87 (95% CI: 0.62, 1.22) for 2 studies of AML, with high levels of heterogeneity detected for leukemia overall and ALL.

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Obstet Gynaecol. 1987 Aug;94(8):721-3 [3311129.001]

[Cites] Int J Cancer. 2009 Jun 1;124(11):2658-70 [19173295.001]

[Cites] Pediatr Infect Dis J. 1988 May;7(5 Suppl):S10-2 [2840629.001]

[Cites] Lancet. 1988 Dec 10;2(8624):1323-7 [2904050.001]

[Cites] BMJ. 1989 Nov 18;299(6710):1259-60 [2513902.001]

[Cites] J Epidemiol Community Health. 1989 Dec;43(4):352-5 [2614325.001]

[Cites] Tumori. 1990 Oct 31;76(5):413-9 [2256184.001]

[Cites] J Autoimmun. 1992 Apr;5 Suppl A:363-71 [1503633.001]

[Cites] Cancer Causes Control. 1993 Jul;4(4):361-8 [8347786.001]

[Cites] Leukemia. 1994 May;8(5):856-64 [8182942.001]

[Cites] Cancer Detect Prev. 1994;18(4):241-52 [7982234.001]

[Cites] Arch Pediatr Adolesc Med. 1995 May;149(5):553-8 [7735412.001]

[Cites] BMJ. 1997 Sep 13;315(7109):629-34 [9310563.001]

[Cites] Br J Cancer. 1997;76(9):1241-7 [9365177.001]

[Cites] Cancer Causes Control. 1998 May;9(3):285-98 [9684709.001]

[Cites] Klin Padiatr. 1998 Jul-Aug;210(4):185-91 [9743951.001]

[Cites] BMJ. 1998 Dec 5;317(7172):1562-3 [9836655.001]

[Cites] Clin Exp Allergy. 1998 Nov;28 Suppl 5:39-44; discussion 50-1 [9988446.001]

[Cites] Curr Probl Dermatol. 1999;28:1-8 [10374044.001]

[Cites] Br J Cancer. 1999 May;80(3-4):585-90 [10408870.001]

[Cites] Crit Rev Oncog. 1999;10(3):247-60 [10468184.001]

[Cites] J Natl Cancer Inst. 1957 Dec;19(6):1087-94 [13502763.001]

[Cites] Cancer Causes Control. 2000 Apr;11(4):303-7 [10843442.001]

[Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]

[Cites] J Paediatr Child Health. 2001 Aug;37(4):397-9 [11532063.001]

[Cites] Br J Cancer. 2002 Feb 1;86(3):350-5 [11875698.001]

[Cites] Nat Rev Immunol. 2001 Oct;1(1):69-75 [11905816.001]

[Cites] Stat Med. 2002 Jun 15;21(11):1539-58 [12111919.001]

[Cites] Int J Cancer. 2003 Jun 10;105(2):255-60 [12673688.001]

[Cites] Chem Immunol. 2000;78:50-61 [12847718.001]

[Cites] J Allergy Clin Immunol. 2003 Aug;112(2):252-62 [12897728.001]

[Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]

[Cites] Br J Cancer. 2004 Jan 12;90(1):139-45 [14710221.001]

[Cites] Eur J Cancer. 2004 Mar;40(4):579-84 [14962726.001]

[Cites] N Engl J Med. 1972 Jul 20;287(3):107-10 [5032269.001]

[Cites] Br Med J. 1973 May 26;2(5864):482-3 [4736507.001]

[Cites] J Med. 1973;4(5):276-81 [4520972.001]

[Cites] Prev Med. 1974 Mar;3(1):165-70 [4815275.001]

[Cites] Prev Med. 1974 Sep;3(3):361-9 [4415641.001]

[Cites] J Natl Cancer Inst. 1976 May;56(5):891-8 [994201.001]

[Cites] Control Clin Trials. 1986 Sep;7(3):177-88 [3802833.001]

[Cites] Br Med J. 1958 Jun 28;1(5086):1495-508 [13546604.001]

[Cites] J Chronic Dis. 1965 Feb;18:113-32 [14258467.001]

[Cites] JAMA. 1964 May 4;188:459 [14125221.001]

[Cites] J Am Acad Dermatol. 2004 Nov;51(5 Suppl):S151-5 [15577757.001]

[Cites] Paediatr Perinat Epidemiol. 2005 Mar;19(2):152-64 [15787890.001]

[Cites] Immunol Allergy Clin North Am. 2005 Nov;25(4):621-39 [16257629.001]

[Cites] J Investig Allergol Clin Immunol. 2005;15(3):161-6 [16261950.001]

[Cites] Haematologica. 2006 Feb;91(2):240-3 [16461310.001]

[Cites] Int J Cancer. 2006 Jun 15;118(12):3124-32 [16395696.001]

[Cites] Lancet. 2006 Aug 26;368(9537):733-43 [16935684.001]

[Cites] Eur J Cancer. 2006 Nov;42(17):3028-33 [16945522.001]

[Cites] Int J Cancer. 2007 Aug 15;121(4):819-24 [17390373.001]

[Cites] Cancer. 2008 Jan 15;112(2):416-32 [18074355.001]

[Cites] Eur J Pediatr. 2008 Jun;167(6):697-8 [17619899.001]

[Cites] Br J Cancer. 2008 Nov 18;99(10):1668-72 [19002185.001]

[Cites] Blood Cells Mol Dis. 2009 Mar-Apr;42(2):99-104 [19049852.001]

[Cites] Vital Health Stat 10. 2009 Jan;(239):1-80 [19326838.001]

[Cites] Leukemia. 1988 Feb;2(2):120-5 [3278171.001]

(PMID = 20228139.001).

[ISSN] 1476-6256

[Journal-full-title] American journal of epidemiology

[ISO-abbreviation] Am. J. Epidemiol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / T32 CA099936; United States / NCI NIH HHS / CA / T32CA099936

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

[Publication-country] United States

[Number-of-references] 67

[Other-IDs] NLM/ PMC2877483

   

[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.

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.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

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

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

It has been recognized that chromosomal abnormalities in childhood leukemia, are linked to both leukemogenesis and segregate patients into prognostic treatment groups.

This is best exemplified in cases of children with Down syndrome (DS), who have significantly higher risks of developing leukemia compared to non-DS children and distinctive treatment outcomes, particularly in cases of acute myeloid leukemia (AML).

The high event-free survival (EFS) rates of DS AML patients and in particular, patients with megakaryocytic leukemia (AMkL), at least in part reflects an increased sensitivity to cytosine arabinoside (ara-C) secondary to increased expression of the chromosome 21-localized gene, cystathionine-beta-synthase, and potentially global mechanisms which increase the susceptibility of cells to undergo apoptosis.

Hyperdiploid acute lymphoblastic leukemia (ALL) cells with extra copies of chromosome 21, generate higher levels of the active methotrexate (MTX) metabolite, MTX polyglutamates.

Microarray technology should lead to the identification of additional gene targets linked to the treatment response of specific cytogenetic leukemia subgroups.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 21. Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Myeloid / drug therapy

[MeSH-minor] Acute Disease. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / metabolism. Antineoplastic Agents, Alkylating / therapeutic use. Child. Disease-Free Survival. Humans. Methotrexate / adverse effects. Methotrexate / metabolism. Methotrexate / therapeutic use. Prognosis

Genetic Alliance. consumer health - Down Syndrome.

MedlinePlus Health Information. consumer health - Down Syndrome.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. METHOTREXATE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2004 Wiley-Liss, Inc.

(PMID = 15390307.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA92308

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; YL5FZ2Y5U1 / Methotrexate

[Number-of-references] 45

   

[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.

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

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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)

   

[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] 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.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

MedlinePlus Health Information. consumer health - Malnutrition.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

MedlinePlus Health Information. consumer health - Memory.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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.

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).

MedlinePlus Health Information. consumer health - Cancer in Children.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Ind Med. 1990;18(3):303-5 [2220835.001]

[Cites] Int J Cancer. 2004 Sep 20;111(5):647-52 [15252832.001]

[Cites] Anticancer Res. 1993 Mar-Apr;13(2):411-7 [8517656.001]

[Cites] Soc Sci Med. 1993 Sep;37(6):771-7 [8211293.001]

[Cites] Eur J Cancer. 1994;30A(4):469-73 [8018404.001]

[Cites] Occup Environ Med. 1995 Jun;52(6):374-9 [7627313.001]

[Cites] Eur J Cancer. 1995 Oct;31A(11):1822-9 [8541107.001]

[Cites] Environ Health Perspect. 1995 Nov;103 Suppl 8:219-24 [8741787.001]

[Cites] Int J Epidemiol. 1996 Aug;25(4):729-36 [8921449.001]

[Cites] Ned Tijdschr Geneeskd. 1997 Mar 8;141(10):468-73 [9173287.001]

[Cites] Scand J Work Environ Health. 1998 Aug;24(4):255-61 [9754856.001]

[Cites] Ned Tijdschr Geneeskd. 1983 Aug 20;127(34):1516-25 [6633686.001]

[Cites] Br Med J. 1976 Dec 25;2(6051):1525-36 [1009386.001]

[Cites] Environ Health Perspect. 1978 Feb;22:23-31 [648488.001]

[Cites] Scand J Work Environ Health. 1999 Oct;25(5):436-41 [10569464.001]

[Cites] Rev Environ Health. 2000 Jan-Jun;15(1-2):83-96 [10939086.001]

[Cites] Stat Med. 2000 Sep 15-30;19(17-18):2569-78 [10960872.001]

[Cites] Int J Epidemiol. 2001 Aug;30(4):839-45 [11511614.001]

[Cites] Occup Environ Med. 2001 Dec;58(12):769-73 [11706142.001]

[Cites] Environ Res. 2002 Mar;88(3):182-7 [12051796.001]

[Cites] Cancer Causes Control. 2002 Aug;13(6):563-71 [12195646.001]

[Cites] Toxicol Lett. 2004 Apr 1;149(1-3):295-300 [15093276.001]

[Cites] Int J Cancer. 1991 Apr 1;47(6):803-10 [2010224.001]

(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

   

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

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

[Title] Dedicated cytogenetics factor is critical for improving karyotyping results for childhood leukaemias - experience in the National University Hospital, Singapore 1989-2006.

INTRODUCTION: Childhood leukaemia accounts for more than 40% of new childhood cancer cases.

Unfortunately, karyotyping of childhood leukaemia is difficult, laborious and often unsuccessful.

Among them, 369 newly diagnosed and relapsed childhood acute leukaemia cases [281 acute lymphoblastic leukaemia (ALL) and 88 acute myeloid leukaemia (AML)] have been diagnosed at NUH.

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

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20237730.001).

[ISSN] 0304-4602

[Journal-full-title] Annals of the Academy of Medicine, Singapore

[ISO-abbreviation] Ann. Acad. Med. Singap.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Singapore

   

[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] 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.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

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

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

[Title] Acute 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.

Genetic Alliance. consumer health - Hepatitis.

MedlinePlus Health Information. consumer health - Complementary and Integrative Medicine.

MedlinePlus Health Information. consumer health - Drug Reactions.

Hazardous Substances Data Bank. LOVASTATIN .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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] 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

MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

COS Scholar Universe. author profiles.

Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827855505 for PMID:19108785 [PharmGKB] .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

SciCrunch. DrugBank: Data: Chemical .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

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

[Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]

[Cites] Cell Death Differ. 2009 May;16(5):749-57 [19219067.001]

[Cites] Leukemia. 1999 Jan;13(1):110-8 [10049045.001]

[Cites] Nature. 2007 Sep 27;449(7161):473-7 [17851532.001]

[Cites] Bone. 1996 Nov;19(5):421-8 [8922639.001]

[Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]

[Cites] Nature. 2004 Nov 18;432(7015):338-41 [15549096.001]

[Cites] Genes Dev. 1991 Mar;5(3):358-68 [1672117.001]

[Cites] Nat Rev Immunol. 2006 Feb;6(2):107-16 [16491135.001]

[Cites] Blood Rev. 2001 Mar;15(1):49-59 [11333138.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):449-54 [15626757.001]

[Cites] Eur J Cancer. 2008 Jan;44(2):257-68 [17981026.001]

[Cites] Cancer Res. 2007 Oct 1;67(19):9142-9 [17909019.001]

[Cites] Exp Hematol. 1996 Jan;24(1):1-10 [8536785.001]

[Cites] Hum Gene Ther. 1997 Sep 20;8(14 ):1695-700 [9322872.001]

[Cites] J Cell Physiol. 1996 Mar;166(3):618-30 [8600166.001]

[Cites] Cancer Res. 2005 Feb 15;65(4):1442-9 [15735032.001]

[Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]

[Cites] Science. 1997 Apr 4;276(5309):71-4 [9082988.001]

[Cites] Leukemia. 2007 Apr;21(4):604-11 [17287850.001]

[Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]

[Cites] Nature. 2002 Jul 4;418(6893):41-9 [12077603.001]

[Cites] Leuk Res. 2006 Aug;30(8):993-1003 [16448696.001]

[Cites] PLoS Biol. 2007 Mar;5(3):e43 [17298184.001]

[Cites] Stem Cells Dev. 2009 Apr;18(3):497-510 [18598159.001]

[Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]

[Cites] Cancer Genet Cytogenet. 2003 May;143(1):89-91 [12742162.001]

[Cites] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]

[Cites] Blood. 1999 Jun 1;93(11):3956-63 [10339505.001]

[Cites] Blood. 1994 Jun 1;83(11):3271-8 [8193362.001]

[Cites] Cell. 2008 Apr 18;133(2):250-64 [18423197.001]

[Cites] Blood. 2009 Apr 2;113(14 ):3287-96 [19147788.001]

[Cites] Leukemia. 2009 Aug;23(8):1515-27 [19357701.001]

[Cites] Science. 2008 Nov 28;322(5906):1377-80 [19039135.001]

[Cites] J Cell Sci. 2006 Apr 15;119(Pt 8):1477-82 [16551697.001]

[Cites] Leukemia. 2009 Apr;23(4):664-72 [19151777.001]

[Cites] Blood. 1994 Apr 15;83(8):2238-47 [8161789.001]

[Cites] EMBO J. 1997 Jun 16;16(12):3644-54 [9218805.001]

[Cites] Blood. 2004 May 15;103(10):3798-804 [14656882.001]

[Cites] Stem Cells. 2006 Dec;24(12):2753-65 [16931776.001]

[Cites] Cell. 2007 Jul 13;130(1):63-75 [17599403.001]

[Cites] Bone Marrow Transplant. 2003 Mar;31(5):339-45 [12634724.001]

[Cites] Cell. 2007 Jun 29;129(7):1377-88 [17604725.001]

[Cites] Methods Mol Med. 2004;91:175-82 [14573937.001]

[Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]

[Cites] N Engl J Med. 2004 Jul 15;351(3):250-9 [15254283.001]

[Cites] Cancer Cell. 2007 May;11(5):421-9 [17482132.001]

[Cites] Lancet. 2000 May 13;355(9216):1688-91 [10905245.001]

[Cites] Br J Haematol. 2005 Dec;131(5):579-87 [16351633.001]

[Cites] Science. 1999 Apr 2;284(5411):143-7 [10102814.001]

[Cites] Cell. 2007 Nov 30;131(5):861-72 [18035408.001]

[Cites] Hematol Oncol. 2006 Mar;24(1):3-6 [16270377.001]

[Cites] Nature. 2002 Apr 4;416(6880):542-5 [11932747.001]

[Cites] Am J Pathol. 2002 Aug;161(2):413-20 [12163366.001]

[Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]

[Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13950-4 [9391133.001]

[Cites] Leukemia. 1997 Nov;11(11):1978-82 [9369435.001]

[Cites] Blood. 1971 Jul;38(1):81-6 [5283675.001]

[Cites] Cell. 2004 Mar 5;116(5):639-48 [15006347.001]

[Cites] Leukemia. 2006 May;20(5):777-84 [16511515.001]

[Cites] Blood. 1978 Jun;51(6):1039-44 [274158.001]

(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

   

[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] 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

MedlinePlus Health Information. consumer health - Cardiomyopathy.

Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827857871 for PMID:19863340 [PharmGKB] .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[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.

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

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] AJNR Am J Neuroradiol. 2000 Aug;21(7):1199-206 [10954269.001]

[Cites] J Neurol. 2002 Jun;249(6):780-1 [12173578.001]

[Cites] Neurology. 1999 Apr 12;52(6):1285-8 [10214762.001]

[Cites] Epilepsia. 1998 Mar;39(3):295-9 [9578048.001]

[Cites] Stroke. 1997 May;28(5):1082-5 [9158653.001]

[Cites] Pediatr Radiol. 2005 Jul;35(7):722-7 [15756541.001]

[Cites] Pediatr Nephrol. 2001 Jul;16(7):601-3 [11465812.001]

[Cites] AJNR Am J Neuroradiol. 1998 Mar;19(3):591 [9541327.001]

[Cites] Radiology. 2001 Jun;219(3):756-65 [11376265.001]

[Cites] Arch Gynecol Obstet. 2005 Jan;271(1):79-85 [15480723.001]

[Cites] AJNR Am J Neuroradiol. 2002 Jun-Jul;23(6):1038-48 [12063238.001]

[Cites] Pediatr Neurol. 1999 Mar;20(3):241-3 [10207937.001]

[Cites] Pediatr Neurol. 2006 Mar;34(3):245-7 [16504799.001]

[Cites] Eur J Neurol. 2006 Mar;13(3):309-10 [16618354.001]

[Cites] Ann Intern Med. 1995 Oct 15;123(8):598-600 [7677301.001]

[Cites] Intern Med J. 2005 Feb;35(2):83-90 [15705136.001]

[Cites] Nephrol Dial Transplant. 1989;4(12):1065-9 [2517327.001]

[Cites] AJR Am J Roentgenol. 1992 Aug;159(2):379-83 [1632361.001]

[Cites] Pediatr Infect Dis J. 2006 Jan;25(1):85-7 [16395114.001]

[Cites] Curr Opin Pediatr. 1999 Dec;11(6):512-8 [10590909.001]

[Cites] Radiology. 1991 Aug;180(2):475-8 [2068315.001]

[Cites] Eur J Pediatr. 2004 Dec;163(12):728-30 [15322868.001]

[Cites] Pediatr Neurol. 2001 May;24(5):361-4 [11516610.001]

[Cites] Pediatr Blood Cancer. 2007 Aug;49(2):198-203 [16123992.001]

[Cites] AJNR Am J Neuroradiol. 1995 Jun-Jul;16(6):1344-6 [7677037.001]

[Cites] AJNR Am J Neuroradiol. 2008 Mar;29(3):447-55 [18079186.001]

[Cites] Radiology. 2000 Nov;217(2):371-6 [11058630.001]

[Cites] Pediatr Nephrol. 2003 Nov;18(11):1161-6 [14505162.001]

[Cites] Pediatr Nephrol. 1993 Apr;7(2):194-5 [8476718.001]

[Cites] Neurology. 2001 Feb 13;56(3):388-91 [11171907.001]

[Cites] Neurology. 1998 Nov;51(5):1369-76 [9818862.001]

[Cites] J Comput Assist Tomogr. 2007 Jan-Feb;31(1):148-56 [17259848.001]

[Cites] N Engl J Med. 1996 Feb 22;334(8):494-500 [8559202.001]

[Cites] Clin Neurol Neurosurg. 1997 Aug;99(3):222-6 [9350407.001]

[Cites] AJNR Am J Neuroradiol. 1997 Jan;18(1):101-6 [9010526.001]

[Cites] Postgrad Med J. 2001 Jan;77(903):24-8 [11123390.001]

[Cites] Blood. 2003 Jan 15;101(2):415-9 [12393443.001]

[Cites] Neurology. 1997 Oct;49(4):1174-5 [9339716.001]

[Cites] BMJ. 1989 Nov 18;299(6710):1258-9 [2513901.001]

(PMID = 19809787.001).

[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

   

[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] 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.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11464-9 [10500199.001]

[Cites] Immunity. 1999 Jan;10(1):117-25 [10023776.001]

[Cites] J Immunol. 2005 Jan 1;174(1):367-75 [15611260.001]

[Cites] Blood. 2005 May 1;105(9):3434-41 [15650057.001]

[Cites] J Exp Med. 2005 Jun 6;201(11):1837-52 [15939795.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13266-71 [16141323.001]

[Cites] Blood. 2005 Nov 15;106(10):3559-66 [16046533.001]

[Cites] Oncogene. 2006 Feb 16;25(7):1118-24 [16205638.001]

[Cites] Oncogene. 2006 Aug 24;25(37):5180-6 [16636677.001]

[Cites] Blood. 2006 Oct 15;108(8):2703-11 [16794253.001]

[Cites] J Exp Med. 2006 Dec 25;203(13):2829-40 [17130299.001]

[Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]

[Cites] Immunity. 2007 Mar;26(3):335-44 [17363301.001]

[Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]

[Cites] J Exp Med. 2007 May 14;204(5):1157-66 [17485517.001]

[Cites] J Immunol. 2007 Aug 15;179(4):2055-9 [17675462.001]

[Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]

[Cites] Nat Immunol. 2008 Jun;9(6):623-31 [18488031.001]

[Cites] Blood. 2009 Feb 12;113(7):1483-92 [19047679.001]

[Cites] J Exp Med. 2009 Aug 3;206(8):1739-53 [19620627.001]

[Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]

[Cites] Science. 1999 Dec 3;286(5446):1954-7 [10583958.001]

[Cites] Immunity. 1999 Nov;11(5):547-54 [10591180.001]

[Cites] Nat Genet. 2000 Jan;24(1):57-60 [10615128.001]

[Cites] J Exp Med. 2000 Jan 3;191(1):23-32 [10620602.001]

[Cites] Blood. 2000 Jul 1;96(1):9-23 [10891425.001]

[Cites] Immunol Rev. 2000 Jun;175:104-11 [10933595.001]

[Cites] Immunity. 2000 Aug;13(2):243-53 [10981967.001]

[Cites] Immunol Rev. 2000 Dec;178:75-90 [11213809.001]

[Cites] Annu Rev Immunol. 2001;19:595-621 [11244048.001]

[Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]

[Cites] J Immunol. 2002 Jun 15;168(12):6286-93 [12055243.001]

[Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]

[Cites] J Clin Invest. 2002 Oct;110(7):1029-35 [12370281.001]

[Cites] Mol Cell. 2002 Nov;10(5):1057-69 [12453414.001]

[Cites] Nat Immunol. 2003 Jan;4(1):38-43 [12436112.001]

[Cites] Nature. 2003 May 22;423(6938):452-6 [12761551.001]

[Cites] J Exp Med. 2004 Mar 1;199(5):673-85 [14993251.001]

[Cites] Nature. 1985 Jun 27-Jul 3;315(6022):758-61 [2989703.001]

[Cites] Cell. 1993 Sep 10;74(5):833-43 [8104101.001]

[Cites] Cell. 1994 Apr 8;77(1):133-43 [8156589.001]

[Cites] Immunity. 1996 Dec;5(6):537-49 [8986714.001]

[Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]

[Cites] J Exp Med. 1998 Jan 5;187(1):71-7 [9419212.001]

[Cites] Immunity. 1998 Jul;9(1):93-103 [9697839.001]

[Cites] Immunity. 1998 Oct;9(4):543-53 [9806640.001]

[Cites] J Clin Invest. 1999 Oct;104(8):1115-21 [10525050.001]

(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

   

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

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

[Title] Treatment of 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

Genetic Alliance. consumer health - Lymphoblastic lymphoma.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Stem Cells.

COS Scholar Universe. author profiles.

Jackson Laboratory JAX®Mice Database. culture/stock collections - B6.129S1-Etv6<tm1(RUNX1)Haho>/J (subscription/membership/fee required).

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

SciCrunch. Marmoset Gene list: Data: Gene Annotation .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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.

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

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

COS Scholar Universe. author profiles.

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

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

[Cites] Am J Clin Nutr. 2004 Dec;80(6):1521-5 [15585763.001]

[Cites] Eur J Endocrinol. 2005 Jul;153(1):81-9 [15994749.001]

[Cites] Circulation. 2006 Apr 18;113(15):1888-904 [16618833.001]

[Cites] Diabet Med. 2006 May;23(5):469-80 [16681555.001]

[Cites] Bone Marrow Transplant. 2006 Jun;37(12):1109-17 [16699534.001]

[Cites] Cancer. 2006 Sep 15;107(6):1303-12 [16894525.001]

[Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4401-7 [16954158.001]

[Cites] Blood. 2007 Feb 15;109(4):1765-72 [17047152.001]

[Cites] Cardiovasc Res. 2007 Apr 1;74(1):11-8 [17140553.001]

[Cites] J Pediatr Hematol Oncol. 2007 Aug;29(8):529-34 [17762493.001]

[Cites] J Clin Endocrinol Metab. 2007 Oct;92(10):3816-21 [17652222.001]

[Cites] Blood. 2007 Nov 1;110(9):3463-71 [17664354.001]

[Cites] Cancer. 2007 Nov 15;110(10):2313-20 [17896787.001]

[Cites] J Pediatr. 2008 Feb;152(2):160-4 [18206681.001]

[Cites] J Pediatr. 2008 Feb;152(2):177-84 [18206686.001]

[Cites] J Pediatr. 2008 Feb;152(2):185-90 [18206687.001]

[Cites] Diabetes Metab. 2008 Feb;34(1):2-11 [18093861.001]

[Cites] Hematol Oncol Clin North Am. 2008 Apr;22(2):319-42, viii [18395153.001]

[Cites] Bone Marrow Transplant. 2008 May;41(9):797-804 [18195686.001]

[Cites] Best Pract Res Clin Haematol. 2008 Jun;21(2):129-38 [18503981.001]

[Cites] Br J Haematol. 2008 Jul;142(1):11-26 [18430191.001]

[Cites] Clin Endocrinol (Oxf). 2008 Nov;69(5):819-27 [18429947.001]

[Cites] J Pediatr Hematol Oncol. 2008 Nov;30(11):815-22 [18989158.001]

[Cites] J Clin Oncol. 2008 Dec 1;26(34):5537-43 [18809605.001]

[Cites] Bone Marrow Transplant. 2009 Jan;43(1):49-54 [18724397.001]

[Cites] J Clin Oncol. 2009 Aug 1;27(22):3698-704 [19564534.001]

[Cites] PLoS Genet. 2009 Dec;5(12):e1000768 [20011104.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):170-81 [20056636.001]

[Cites] Biol Blood Marrow Transplant. 2010 Apr;16(4):515-24 [19961945.001]

[Cites] Lancet. 2000 Sep 16;356(9234):993-7 [11041401.001]

[Cites] JAMA. 2001 May 16;285(19):2486-97 [11368702.001]

[Cites] J Nutr. 2001 Aug;131(8):2184-91 [11481415.001]

[Cites] Arch Intern Med. 2003 Feb 24;163(4):427-36 [12588201.001]

[Cites] Arch Pediatr Adolesc Med. 2003 Aug;157(8):821-7 [12912790.001]

[Cites] J Pediatr Hematol Oncol. 2004 Feb;26(2):81-90 [14767193.001]

[Cites] Pediatrics. 2004 Aug;114(2 Suppl 4th Report):555-76 [15286277.001]

[Cites] J Clin Oncol. 2004 Sep 1;22(17):3558-62 [15337805.001]

[Cites] J Pediatr. 2004 Oct;145(4):439-44 [15480363.001]

[Cites] Diabetologia. 1985 Jul;28(7):412-9 [3899825.001]

[Cites] Can J Public Health. 1986 Sep-Oct;77(5):359-62 [3791117.001]

[Cites] Am J Epidemiol. 1996 Jun 15;143(12):1219-28 [8651220.001]

[Cites] J Clin Endocrinol Metab. 1996 Aug;81(8):3051-5 [8768873.001]

[Cites] N Engl J Med. 1998 Jun 4;338(23):1650-6 [9614255.001]

[Cites] Transplantation. 2004 Nov 15;78(9):1376-83 [15548978.001]

(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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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.

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.

MedlinePlus Health Information. consumer health - Folic Acid.

Hazardous Substances Data Bank. LEUCOVORIN .

Hazardous Substances Data Bank. METHOTREXATE .

Hazardous Substances Data Bank. FOLIC ACID .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Hazardous Substances Data Bank. RITUXIMAB .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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] 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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Retinoblastoma.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Oncogene. 2000 Jan 27;19(4):562-70 [10698526.001]

[Cites] Cell. 2000 Mar 31;101(1):79-89 [10778858.001]

[Cites] Cancer Res. 2000 Aug 15;60(16):4320-3 [10969768.001]

[Cites] Biochem Biophys Res Commun. 2000 Sep 7;275(3):877-84 [10973815.001]

[Cites] J Biol Chem. 2003 May 23;278(21):19358-66 [12646568.001]

[Cites] Cell. 2003 Aug 22;114(4):431-43 [12941272.001]

[Cites] Nat Genet. 2003 Sep;35(1):25-31 [12923533.001]

[Cites] EMBO J. 2003 Sep 15;22(18):4794-803 [12970191.001]

[Cites] Curr Biol. 2003 Oct 14;13(20):1775-85 [14561402.001]

[Cites] Lancet Oncol. 2004 Jan;5(1):27-36 [14700606.001]

[Cites] Biochem Biophys Res Commun. 2004 May 7;317(3):779-86 [15081408.001]

[Cites] Cell. 2004 Apr 16;117(2):239-51 [15084261.001]

[Cites] Cell. 2004 Aug 20;118(4):477-91 [15315760.001]

[Cites] Cell. 2004 Aug 20;118(4):493-504 [15315761.001]

[Cites] Science. 1989 Nov 3;246(4930):603-8 [2683075.001]

[Cites] Cell. 1991 May 3;65(3):381-93 [2018973.001]

[Cites] Cell. 1991 Oct 18;67(2):293-302 [1655277.001]

[Cites] Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):6914-8 [8346196.001]

[Cites] Mol Cell Biol. 1993 Oct;13(10):6501-8 [8413249.001]

[Cites] Mol Cell Biol. 1994 Mar;14(3):2066-76 [8114738.001]

[Cites] Leukemia. 1994 Jun;8(6):940-5 [8207988.001]

[Cites] Cell. 1994 Jul 15;78(1):161-72 [8033208.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3215-20 [8622916.001]

[Cites] Cell. 2005 Dec 16;123(6):1093-106 [16360038.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14317-22 [11114185.001]

[Cites] Leukemia. 2001 Jan;15(1):1-9 [11243375.001]

[Cites] Mol Cell Biol. 2001 Jul;21(14):4773-84 [11416152.001]

[Cites] Nature. 2001 Sep 6;413(6851):83-6 [11544530.001]

[Cites] EMBO Rep. 2001 Sep;2(9):794-9 [11520855.001]

[Cites] J Biochem Mol Biol. 2003 Jan 31;36(1):60-5 [12542976.001]

[Cites] J Biol Chem. 1996 Apr 5;271(14):8313-20 [8626527.001]

[Cites] Mol Cell Biol. 1996 Dec;16(12):7173-81 [8943373.001]

[Cites] EMBO J. 1996 Dec 16;15(24):7060-9 [9003781.001]

[Cites] Oncogene. 1997 Jan 16;14(2):249-54 [9010227.001]

[Cites] Br J Haematol. 1997 Feb;96(2):366-8 [9029026.001]

[Cites] Mol Biol Cell. 1997 Feb;8(2):287-301 [9190208.001]

[Cites] J Biol Chem. 1997 May 9;272(19):12738-46 [9139732.001]

[Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]

[Cites] Mol Cell Biol. 1997 Oct;17(10):5771-83 [9315635.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10699-704 [9380698.001]

[Cites] Oncogene. 1997 Dec 4;15(23):2855-66 [9419977.001]

[Cites] Mol Cell Biol. 1998 Feb;18(2):753-61 [9447971.001]

[Cites] Carcinogenesis. 1998 May;19(5):765-9 [9635861.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10493-8 [9724731.001]

[Cites] J Biol Chem. 1999 Apr 2;274(14):9463-71 [10092628.001]

[Cites] Pediatr Res. 1999 May;45(5 Pt 1):692-6 [10231867.001]

[Cites] Cell. 1999 Sep 17;98(6):859-69 [10499802.001]

[Cites] Mol Cell. 2004 Dec 3;16(5):831-7 [15574337.001]

[Cites] J Biochem. 2005 Mar;137(3):381-6 [15809340.001]

[Cites] Cancer Cell. 2005 Jun;7(6):591-8 [15950907.001]

[Cites] Stem Cells. 2005 Aug;23(7):1002-11 [15941859.001]

[Cites] Nat Cell Biol. 2005 Aug;7(8):831-6 [16007079.001]

[Cites] Blood. 2005 Aug 15;106(4):1400-6 [15878982.001]

[Cites] Leukemia. 2005 Oct;19(10):1783-7 [16107892.001]

(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

   

[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] Correlation of telomerase activity to apoptosis and survival in adult acute lymphoblastic leukemia: an Egyptian single-center study.

The goal of this study was to investigate the levels and relationship of telomerase activity to apoptosis and its impact on the survival of Egyptian adult acute lymphoblastic leukemia patients.

Telomerase activity was quantified by polymerase chain reaction (PCR) and detected by enzyme-linked immunosorbent assay (ELISA), while apoptosis was measured at the single-cell level by fluorescence in situ detection using flow cytometry in 15 control subjects and 40 acute lymphoblastic leukemia (ALL) patients at presentation.

This makes the measurement of telomerase activity in ALL patients a potential tool to predict disease with unfavorable outcome and a candidate tumor marker.

[MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Telomerase / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Disease-Free Survival. Egypt. Enzyme Activation / genetics. Female. Follow-Up Studies. Humans. Male. Middle Aged. Polymerase Chain Reaction. Predictive Value of Tests. Survival Rate. Time Factors

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18175116.001).

[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 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 2.7.7.49 / Telomerase

   

[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] Apoptosis induction by Maackia amurensis agglutinin in childhood acute lymphoblastic leukemic cells.

Malignant transformation is known to be associated with changes in cell surface carbohydrate-architecture, which can be detected by lectins.

In the present study, Maackia amurensis agglutinin (MAA), specific for NeuNAcalpha(2-->3)Gal/GalNAc showed strong binding with lymphoblasts of children having acute lymphoblastic leukemia (ALL) as compared to cells from children with non-hematological disorders ("Controls").

[MeSH-major] Apoptosis / drug effects. Phytohemagglutinins / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

[MeSH-minor] Blotting, Western. Cell Line. Child. Child, Preschool. Enzyme-Linked Immunosorbent Assay. Female. Flow Cytometry. Glycoproteins / metabolism. Humans. Lymphocytes / metabolism. Male. Neuraminidase / chemistry

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17889364.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Glycoproteins; 0 / Phytohemagglutinins; 0 / leukoagglutinins, plants; EC 3.2.1.- / sialidase L; EC 3.2.1.18 / Neuraminidase

   

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

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

[Title] Impact of age, leukocyte count and day 21-bone marrow response to chemotherapy on the long-term outcome of children with philadelphia chromosome-positive acute lymphoblastic leukemia in the pre-imatinib era: results of the FRALLE 93 study.

BACKGROUND: We explored the heterogeneity of philadelphia chromosome-positive acute lymphoblastic leukemia (Ph1-ALL) in a study of the effect of early features on prognosis in children.

Overall five-year disease-free survival (DFS) was 42 +/- 9.7%.

The combination of available tools such as minimal residual disease assessment with determination of these simple factors could be useful for refining indications for BMT in the current era of tyrosine-kinase inhibitor-based therapy.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols. Bone Marrow / drug effects. Leukocyte Count. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage

[MeSH-minor] Acute Disease. Adolescent. Age Factors. Anthracyclines. Asparaginase. Benzamides. Bone Marrow Transplantation. Child. Child, Preschool. Cortisone. Female. Humans. Imatinib Mesylate. Infant. Male. Prednisone / administration & dosage. Recurrence. Treatment Outcome. Vincristine. Young Adult

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Hazardous Substances Data Bank. IMATINIB MESYLATE .

Hazardous Substances Data Bank. PREDNISONE .

Hazardous Substances Data Bank. VINCRISTINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Leukemia. 2005 Apr;19(4):628-35 [15744351.001]

[Cites] Br J Haematol. 2005 Apr;129(1):35-44 [15801953.001]

[Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]

[Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]

[Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]

[Cites] Blood. 2007 Feb 15;109(4):1408-13 [17062730.001]

[Cites] J Clin Oncol. 2007 Apr 10;25(11):1341-9 [17312329.001]

[Cites] Blood. 2007 Apr 1;109(7):2791-3 [17119111.001]

[Cites] Haematologica. 2007 Dec;92(12):1723-4 [18056006.001]

[Cites] Bone Marrow Transplant. 2008 Mar;41(5):447-53 [17968326.001]

[Cites] Leukemia. 2000 Dec;14(12):2205-22 [11187912.001]

[Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]

[Cites] J Clin Oncol. 2008 Mar 20;26(9):1496-503 [18349402.001]

[Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]

[Cites] Leukemia. 2003 Sep;17(9):1700-6 [12970767.001]

[Cites] Bone Marrow Transplant. 2004 Jan;33(1):39-45 [14566329.001]

[Cites] Blood. 2004 Feb 1;103(3):1043-9 [14525776.001]

[Cites] Blood. 1994 Nov 1;84(9):3122-33 [7949185.001]

[Cites] Blood. 1995 Aug 15;86(4):1292-5 [7632935.001]

[Cites] Leukemia. 1997 Sep;11(9):1493-6 [9305603.001]

[Cites] Clin Cancer Res. 2005 Oct 15;11(20):7209-19 [16243790.001]

(PMID = 19144139.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Anthracyclines; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 5J49Q6B70F / Vincristine; 8A1O1M485B / Imatinib Mesylate; EC 3.5.1.1 / Asparaginase; V27W9254FZ / Cortisone; VB0R961HZT / Prednisone; FRALLE 93 protocol

[Other-IDs] NLM/ PMC2629767

[Investigator] Pautard B; Bauduer JF; Abgrall JF; Berthou C; Paillard C; Kanold J; Couillault G; Damay M; de Lumley L; Michel G; Thuret I; Chambost H; Bordigoni P; Sommel D; Leblanc T; Schaison G; Tabone MD; Donadieu J; Landman-Parker J; Auvrignon A; Thomas C; Fisher A; Dommergues JP; Bader-Meunier B; Bernaudin F; Lemerle S; Choulot J; Doireau V; Edan C; Bergeron C; Schneider P; Lamagnere JP; Berger C; Cornu G; Vermylen C

   

[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] Infant acute leukemia and maternal exposures during pregnancy.

Infant acute leukemia (IAL) has a unique profile characterized by the high incidence of translocations involving the MLL gene located at the 11q23 region.

[MeSH-major] Leukemia, Myeloid / etiology. Maternal Exposure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Prenatal Exposure Delayed Effects

[MeSH-minor] Acute Disease. Brazil / epidemiology. Case-Control Studies. Female. Histone-Lysine N-Methyltransferase. Hospitals. Humans. Infant. Infant, Newborn. Male. Maternal-Fetal Exchange. Myeloid-Lymphoid Leukemia Protein / genetics. Pregnancy. Translocation, Genetic

Genetic Alliance. consumer health - Pregnancy.

MedlinePlus Health Information. consumer health - Reproductive Hazards.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2331 [17164352.001]

(PMID = 17164354.001).

[ISSN] 1055-9965

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

   

[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] Bone marrow recurrence after initial intensive treatment for childhood acute lymphoblastic leukemia.

BACKGROUND: The authors studied the clinical outcome of 106 children with acute lymphoblastic leukemia (ALL) who developed a bone marrow recurrence as the first adverse event after contemporary intensified therapy.

On multivariate analysis, time to first disease recurrence and blast cell lineage were found to be independent predictors of a second EFS (P = 0.008 and P = 0.028, respectively).

The 5-year EFS estimate in patients with an initial disease remission of >/= 36 months was 42.6% +/- 7.8% but was only 12.5% +/- 3.9% among children with a short duration of disease remission (< 36 months).

These estimates were 28.7% +/- 4.9% and 5.0% +/- 3.4%, respectively, for B blast and T blast cell lineages.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / epidemiology. Bone Marrow / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

[MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Cohort Studies. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Humans. Incidence. Male. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / pathology. Probability. Prognosis. Proportional Hazards Models. Remission Induction. Retrospective Studies. Risk Assessment. Severity of Illness Index. Sex Distribution. Survival Rate

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2004 American Cancer Society.

(PMID = 15599932.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[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

   

[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] Emerging therapy for the treatment of acute lymphoblastic leukemia.

IMPORTANCE OF THE FIELD: Over the last few decades, advances in acute lymphoblastic leukemia (ALL) therapy have led to long-term survival rates of > 80% in children; however, comparable rates have yet to be achieved in adults, and a large majority of patients relapse from their disease.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drugs, Investigational / therapeutic use. Neoplasm, Residual / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Adult. Aged. Child. Disease-Free Survival. Humans. Salvage Therapy / methods. Stem Cell Transplantation

Genetic Alliance. consumer health - Acute Lymphoblastic 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 = 20055690.001).

[ISSN] 1744-7623

[Journal-full-title] Expert opinion on emerging drugs

[ISO-abbreviation] Expert Opin Emerg Drugs

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Drugs, Investigational

[Number-of-references] 68

   

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

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

[Title] Prognostic impact of age in children and adolescents with acute lymphoblastic leukemia: data from the trials ALL-BFM 86, 90, and 95.

Large progress has been made in the treatment of acute lymphoblastic leukemia (ALL) of childhood and adolescence over the past 30 years.

The proportion of T-ALL as compared to precursor B-cell ALL (pB-ALL) was lower in younger children, due to an incidence peak of pB-ALL in toddlers and at pre-school age compared to a constant incidence of T-ALL.

Within the T-ALL group, no correlation of age with sex, initial white blood cell count, CNS disease, or early treatment response was found.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

[MeSH-minor] 6-Mercaptopurine / adverse effects. 6-Mercaptopurine / therapeutic use. Adolescent. Age Factors. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / adverse effects. Asparaginase / therapeutic use. Child. Child, Preschool. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Cytarabine / adverse effects. Cytarabine / therapeutic use. Daunorubicin / adverse effects. Daunorubicin / therapeutic use. Disease-Free Survival. Female. Humans. Infant. Male. Methotrexate / adverse effects. Methotrexate / therapeutic use. Multicenter Studies as Topic. Prednisolone / adverse effects. Prednisolone / therapeutic use. Prednisone / adverse effects. Prednisone / therapeutic use. Prognosis. Randomized Controlled Trials as Topic. Survival Analysis. Vincristine / adverse effects. Vincristine / therapeutic use

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. DAUNORUBICIN .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

Hazardous Substances Data Bank. PREDNISOLONE .

Hazardous Substances Data Bank. MERCAPTOPURINE .

Hazardous Substances Data Bank. PREDNISONE .

Hazardous Substances Data Bank. VINCRISTINE .

Hazardous Substances Data Bank. METHOTREXATE .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16307416.001).

[ISSN] 0300-8630

[Journal-full-title] Klinische Pädiatrie

[ISO-abbreviation] Klin Padiatr

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; AIEOP acute lymphoblastic leukemia protocol; ALL-BFM-95 protocol; BFM-86 protocol