[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 47 of about 47
1. Nikougoftar M, Farhadi M, Pourfathollah AA: P-glycoprotein quantitation in acute leukemia. Iran J Allergy Asthma Immunol; 2003 Jun;2(2):57-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P-glycoprotein quantitation in acute leukemia.
  • Multi drug resistance(MDR) is a major problem in the treatment ofcancer and hematological malignancies.
  • This resistance is multi factorial and is the result of decreased intra cellular drug accumulation.
  • This is partly due to the presence of a 170KD intra membranous protein termed P-glycoprotein(P-gp) that is an energy- dependent efflux pump which has increased expression on drug-resistance cells.
  • In this study we identified the presence of P-gp by staining with Fluorescent Iso Thio Cyanate (FITC) conjugated anti P-gp in acute leukemia patients and flow cytometry in addition to performing immunophenotype analysis and French, American British (FAB) classification.
  • Results revealed that one fifth of leukemic patients expressed P-gp and this phenotype was more prevalent in Acute Undifferentiated Leukemia(AUL) and Acute Myelogenous Leukemia (AML) than in Acute Lymphoblastic Leukemia(ALL).
  • There was not any association between P-gp+ phenotype and FAB and Immunophenotyping sub classification, but there was a linear relationship between CD34 and CD7 expression and P-gp+ phenotype.
  • The accumulation of P-gp molecule that was stated as Mean Fluorescence Intensity (MFI) on the blasts' membrane of AUL and AML patients showed marked increase in comparison to ALL.
  • Kepvords: Leukemia, Drug resistance, P-glycoprotein, Flowcytometry, FAB classification, Immunophenotyping, Mean Fluorescence Intensity.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17301357.001).
  • [ISSN] 1735-1502
  • [Journal-full-title] Iranian journal of allergy, asthma, and immunology
  • [ISO-abbreviation] Iran J Allergy Asthma Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  •  go-up   go-down


2. Testa U, Torelli GF, Riccioni R, Muta AO, Militi S, Annino L, Mariani G, Guarini A, Chiaretti S, Ritz J, Mandelli F, Peschle C, Foa R: Human acute stem cell leukemia with multilineage differentiation potential via cascade activation of growth factor receptors. Blood; 2002 Jun 15;99(12):4634-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human acute stem cell leukemia with multilineage differentiation potential via cascade activation of growth factor receptors.
  • The morphologic, immunophenotypic, genotypic, genomic, and functional features of an undifferentiated acute leukemia with stem cell features are reported.
  • The blasts were CD34(+), AC133(+), CD71(-), HLA-DR(-), CD38(-/dim+), CD90(+), CD117(dim+), flt3(+); did not express B, T, or myeloid-associated antigens; and showed a germline configuration of the immunoglobulin and T-cell receptor.
  • Genomic profiling documented the expression of early stem cell and myeloid-associated genes.
  • Receptors for early-acting hemopoietic growth factors (HGFs) were detected, while receptors for unilineage HGF were not expressed.
  • [MeSH-major] Leukemia / pathology. Receptors, Growth Factor / metabolism
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Cell Culture Techniques / methods. Cell Differentiation. Cell Lineage. DNA Fingerprinting. Female. Gene Expression Regulation / drug effects. Humans. Immunophenotyping. Membrane Proteins / pharmacology. Receptors, Colony-Stimulating Factor / genetics. Receptors, Colony-Stimulating Factor / metabolism

  • MedlinePlus Health Information. consumer health - 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
  • (PMID = 12036900.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Receptors, Growth Factor; 0 / flt3 ligand protein
  •  go-up   go-down


3. Konopleva M, Tabe Y, Zeng Z, Andreeff M: Therapeutic targeting of microenvironmental interactions in leukemia: mechanisms and approaches. Drug Resist Updat; 2009 Aug-Oct;12(4-5):103-13
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic targeting of microenvironmental interactions in leukemia: mechanisms and approaches.
  • Specific niches within the bone marrow microenvironment provide a sanctuary for subpopulations of leukemic cells to evade chemotherapy-induced death and allow acquisition of a drug-resistant phenotype.
  • This review focuses on molecular and cellular biology of the normal hematopoietic stem cell and the leukemia stem cell niche, and of the molecular pathways critical for microenvironment/leukemia interactions.
  • The key emerging therapeutic targets include chemokine receptors (CXCR4), adhesion molecules (VLA4 and CD44), and hypoxia-related proteins HIF-1alpha and VEGF.
  • Finally, the genetic and epigenetic abnormalities of leukemia-associated stroma will be discussed.
  • This complex interplay provides a rationale for appropriately tailored molecular therapies targeting not only leukemic cells but also their microenvironment to ensure improved outcomes in leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow / drug effects. Leukemia / drug therapy
  • [MeSH-minor] Apoptosis. Cell Communication. Hematopoiesis. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Humans. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / prevention & control


Advertisement
4. Carter BZ, Mak DH, Cortes J, Andreeff M: The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it? Semin Hematol; 2010 Oct;47(4):362-70
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it?
  • Chronic myeloid leukemia (CML) is a clonal multistep myeloproliferative disease originating from and ultimately sustained by a rare population of BCR-ABL(+) cells with multilineage stem cell properties.
  • Despite this achievement, CML is often not curable, largely due to the innate insensitivity of CML stem cells, particularly when in a quiescent state.
  • This failure of not only imatinib but also the second-generation tyrosine kinase inhibitors (TKIs) frequently leads to relapse upon drug discontinuation.
  • Thus, any curative therapy must eliminate CML stem cells.
  • A comprehensive understanding of the biological properties of CML stem cells and an elucidation of the molecular mechanisms and signaling pathways enabling these CML stem cells to self-renew, combined with insight into the regulation of apoptosis signaling and the mechanisms governing the interaction of CML stem cells with their bone marrow microenvironment, will facilitate the development of therapies for targeting these cells.
  • Here, we discuss the biological properties of CML stem cells and potential strategies to eliminate them.

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):626-33 [16428509.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1730-6 [11912147.001]
  • [Cites] Blood. 2002 May 15;99(10):3530-9 [11986204.001]
  • [Cites] Blood. 2002 May 15;99(10):3792-800 [11986238.001]
  • [Cites] J Biol Chem. 2002 Aug 9;277(32):28504-11 [12029096.001]
  • [Cites] Leukemia. 2003 Jan;17(1):155-9 [12529673.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):1033-41 [12569603.001]
  • [Cites] Apoptosis. 2003 Jun;8(3):237-49 [12766484.001]
  • [Cites] Blood. 2003 Jul 1;102(1):276-83 [12623848.001]
  • [Cites] Clin Cancer Res. 2003 Sep 15;9(11):4267-73 [14519654.001]
  • [Cites] Curr Opin Hematol. 2004 Jan;11(1):35-43 [14676625.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 1999 Sep 15;94(6):2056-64 [10477735.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):129-41 [15710326.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3303-11 [15626746.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1034-41 [15815728.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Feb;57(2):145-64 [16213151.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1555-63 [16254145.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4532-9 [16469872.001]
  • [Cites] Nat Med. 2006 Oct;12(10):1175-80 [16998483.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):375-88 [17097560.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Blood. 2007 Jan 1;109(1):58-60 [16973963.001]
  • [Cites] Leukemia. 2007 May;21(5):926-35 [17330101.001]
  • [Cites] Hematol Oncol. 2007 Jun;25(2):66-75 [17441215.001]
  • [Cites] Cell Death Differ. 2007 Sep;14(9):1667-77 [17510658.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):528-41 [18068630.001]
  • [Cites] Br J Haematol. 2008 Jan;140(2):181-90 [18028486.001]
  • [Cites] Mol Cancer Ther. 2008 Jan;7(1):48-58 [18202009.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2843-53 [18156496.001]
  • [Cites] Nat Med. 2008 May;14(5):494-5 [18463658.001]
  • [Cites] Nature. 2008 Jun 19;453(7198):1072-8 [18469801.001]
  • [Cites] Cell. 2008 Jul 11;134(1):62-73 [18614011.001]
  • [Cites] Cancer Cell. 2008 Sep 9;14(3):238-49 [18772113.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3925-9 [19237556.001]
  • [Cites] Nature. 2009 Apr 9;458(7239):776-9 [19169242.001]
  • [Cites] Nature. 2009 Apr 16;458(7240):904-8 [19212321.001]
  • [Cites] Cell Stem Cell. 2009 Jun 5;4(6):548-58 [19497283.001]
  • [Cites] Cell Stem Cell. 2009 Jun 5;4(6):559-67 [19497284.001]
  • [Cites] Mol Cancer Ther. 2009 Sep;8(9):2509-16 [19723894.001]
  • [Cites] Cell Cycle. 2009 Nov 1;8(21):3488-92 [19823023.001]
  • [Cites] Blood. 2009 Dec 10;114(25):5191-200 [19855080.001]
  • [Cites] Clin Cancer Res. 2010 Jan 1;16(1):338-47 [20048335.001]
  • [Cites] Blood. 2010 Jan 21;115(3):626-35 [19965668.001]
  • [Cites] Nature. 2010 Feb 4;463(7281):676-80 [20130650.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1862-6 [15528314.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):373-81 [16042686.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9436-44 [16230407.001]
  • [Cites] Leuk Lymphoma. 2006 Feb;47(2):207-22 [16321850.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • (PMID = 20875553.001).
  • [ISSN] 1532-8686
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA49639
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS219537; NLM/ PMC2948413
  •  go-up   go-down


5. Cui JW, Zhang XM, Wang GJ: [Progress in the studies of acute myelogenous leukemia stem cell]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2003 Oct;11(5):549-52
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Progress in the studies of acute myelogenous leukemia stem cell].
  • Acute myelogenous leukemia (AML) cells are organized in a hierarchical fashion, with only the most primitive rare population (leukemia stem cell, LSC) of AML cells capable of maintaining the leukemic clone.
  • A broad range of studies has indicated that AML results from mutations at the level of the stem cells of AML cells.
  • The changes of cellular and molecular features in these malignant stem cells determine the features of leukemic clone and give rise to different subtypes of AML.
  • LSCs share some similar characteristics with normal hematopoietic stem cells (HSC) including the ability to self-renew, and also have the potential of limited differentiation.
  • LSCs, also have some features that are not found in normal HSC.
  • Tumor-suppressor protein-death associated protein kinase and interferon regulatory factor 1 were overexpressed in LSCs, but not in normal HSC.
  • Due to a predominantly G0 cell-cycle status, LSCs may not be responsive to conventional chemotherapeutic agents, compared with leukemia blasts.
  • Although LSC population is likely to be drug-resistant, quiescent LSCs are preferentially susceptible to apoptosis induction while sparing normal HSC, with the appropriate stimulus such as proteasome inhibitor MG-132.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14575558.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 25
  •  go-up   go-down


6. Funayama K, Murai F, Shimane M, Nomura H, Asano S: Adhesion-induced drug resistance in leukemia stem cells. Pharmacology; 2010;86(2):79-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adhesion-induced drug resistance in leukemia stem cells.
  • The co-culture of TF-1 leukemia cells and MS-5 stromal cells produces a cobblestone area which partially mimics the leukemia stem cell niche.
  • The adhering leukemia cells are shown to become less sensitive to cytarabine, etoposide and daunorubicin.
  • These changes are associated with an increased proportion of the G0/G1 phase, increased upregulation of cyclin-dependent kinase inhibitors, and increased levels of Bcl-2, but not with any change in the expression of BAX or drug transporters such as ABCG2 and MDR1, compared to monocultured leukemic cells.
  • These findings suggest that adhesion alone can lead to drug resistance in leukemic stem cells by various mechanisms.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Leukemia / physiopathology. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / physiology. Stem Cell Niche / physiopathology. Stromal Cells / physiology
  • [MeSH-minor] Bone Marrow Cells / physiology. Cell Adhesion. Cell Cycle. Cell Line, Tumor. Coculture Techniques. Cyclin-Dependent Kinase Inhibitor Proteins / genetics. Cyclin-Dependent Kinase Inhibitor Proteins / metabolism. Cytarabine / pharmacology. Daunorubicin / pharmacokinetics. Daunorubicin / pharmacology. Etoposide / pharmacology. Humans. Lysosomes / metabolism. Osmolar Concentration. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Up-Regulation. Vacuolar Proton-Translocating ATPases / genetics. Vacuolar Proton-Translocating ATPases / metabolism

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • [ErratumIn] Pharmacology. 2010;86(4):202
  • (PMID = 20689339.001).
  • [ISSN] 1423-0313
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 3.6.1.- / Vacuolar Proton-Translocating ATPases; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


10. Atallah E, Cortes J: Optimal initial therapy for patients with newly diagnosed chronic myeloid leukemia in chronic phase. Curr Opin Hematol; 2007 Mar;14(2):138-44
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimal initial therapy for patients with newly diagnosed chronic myeloid leukemia in chronic phase.
  • PURPOSE OF REVIEW: Imatinib mesylate, a tyrosine kinase inhibitor, has revolutionized the therapy of newly diagnosed patients with chronic myeloid leukemia.
  • Prior to imatinib, treatment algorithms for chronic myeloid leukemia patients recommended stem cell transplantation for patients less than 50 years old who had a donor and could undergo stem cell transplantation.
  • Other than stem cell transplantation, interferon was the only drug that could induce cytogenetic remissions in minority of patients.
  • The use of imatinib before stem cell transplant did not have an effect on mortality or morbidity posttransplant.
  • SUMMARY: Currently, imatinib is considered first line therapy in all patients with early chronic phase chronic myeloid leukemia with stem cell transplant reserved for patients who have disease resistant to imatinib therapy.
  • Our aim is to review current recommendations for initial therapy of patients with early chronic phasechronic myeloid leukemia, current areas of controversy and future directions.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / therapy
  • [MeSH-minor] Benzamides. Disease Management. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17255791.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 53
  •  go-up   go-down


11. Paolucci G, Vecchi V, Favre C, Miniero R, Madon E, Pession A, Rondelli R, De Rossi G, Lo Nigro L, Porta F, Santoro N, Indolfi P, Basso G, Conter V, Aricò M, Associazione Italiana Ematologia Oncologia Pediatrica (AIEOP): Treatment of childhood acute lymphoblastic leukemia. Long-term results of the AIEOP-ALL 87 study. Haematologica; 2001 May;86(5):478-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of childhood acute lymphoblastic leukemia. Long-term results of the AIEOP-ALL 87 study.
  • The aim of this new study was to evaluate, for all risk groups: a) the efficacy of treatment intensification achieved by adding a fourth drug (daunomycin) in the induction phase and a 3-drug reinduction phase for all risk groups;.
  • DESIGN AND METHODS: From 1987 to 1991, a total of 632 eligible and evaluable children (age 1 to < or =16 years) with non-B-cell acute lymphoblastic leukemia (ALL), were enrolled and stratified as follows: standard risk (SR, 79 patients, 12.5%) had WBC <10,000/mm3, age > or = 3 and <7 years, and FAB L1 morphology.
  • The high risk (HR, 175 patients, 27.7%) group included patients with WBC > or =50,000/mm3 or FAB L3 morphology or T immunophenotype or acute undifferentiated leukemia (AUL) or leukemia-lymphoma syndrome.
  • All patients received a 4-drug induction therapy; intermediate-dose methotrexate was given to HR patients; cranial radiotherapy was given to IR and HR patients, while SR patients received extended intrathecal methotrexate; all patients received a 3-drug reinduction phase; high dose L-asparaginase (HD-L-ASP; E.Coli, Bayer) was given to HR patients; continuation therapy with 6-mercaptopurine, i.m. methotrexate, and monthly vincristine and prednisone pulses was given to all patients.
  • These results, although obtained in a relatively large proportion of patients, in which infants were not included, indicate that the addition of high-dose L-asparaginase to a relatively non-intensive treatment may be of major benefit for HR patients and that the addition of intrathecal methotrexate during CRT, may improve the central nervous system-disease control with a marked reduction of nervous system relapses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


12. Abrams SL, Steelman LS, Shelton JG, Chappell W, Bäsecke J, Stivala F, Donia M, Nicoletti F, Libra M, Martelli AM, McCubrey JA: Enhancing therapeutic efficacy by targeting non-oncogene addicted cells with combinations of signal transduction inhibitors and chemotherapy. Cell Cycle; 2010 May;9(9):1839-46
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The effects of inhibition of the Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways and chemotherapeutic drugs on cell cycle progression and drug sensitivity were examined in cytokine-dependent FL5.12 hematopoietic cells.
  • We examined their effects, as these cells resemble normal hematopoietic precursor cells as they do not exhibit "oncogene-addicted" growth, while they do display "cytokine-addicted" proliferation as cytokine removal resulted in apoptosis in greater than 80% of the cells within 48 hrs.
  • When cytokine-dependent FL5.12 cells were cultured in the presence of IL-3, which stimulated multiple proliferation and anti-apoptotic cascades, MEK, PI3K and mTOR inhibitors transiently suppressed but did not totally inhibit cell cycle progression or induce apoptosis while chemotherapeutic drugs such as doxorubicin and paclitaxel were more effective in inducing cell cycle arrest and apoptosis.
  • Doxorubicin was more effective in inducing cell death than paclitaxel.
  • Cytokine-dependent cells which proliferate in vitro and are not "oncogene-addicted" may represent a pre-malignant stage, more refractory to treatment with targeted therapy.
  • However, these cells are sensitive to chemotherapeutic drugs.
  • It is important to develop methods to inhibit the growth of such cytokine-dependent cells as they may resemble the leukemia stem cell and other cancer initiating cells.
  • These results demonstrate the enhanced effectiveness of targeting early hematopoietic progenitor cells with combinations of chemotherapeutic drugs and signal transduction inhibitors.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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
  • [Cites] Leukemia. 2008 Jan;22(1):147-60 [17928881.001]
  • [Cites] Cell Cycle. 2008 Jan 15;7(2):216-21 [18256527.001]
  • [Cites] J Virol. 2008 Apr;82(7):3796-802 [18216097.001]
  • [Cites] Cancer Biol Ther. 2007 Nov;6(11):1684-90 [18344680.001]
  • [Cites] Leukemia. 2008 Apr;22(4):708-22 [18337766.001]
  • [Cites] Leukemia. 2008 Apr;22(4):686-707 [18337767.001]
  • [Cites] Cell Cycle. 2008 Feb 15;7(4):533-41 [18431843.001]
  • [Cites] Cell Cycle. 2008 Apr 15;7(8):965-70 [18414037.001]
  • [Cites] Cell Cycle. 2008 May 15;7(10):1360-70 [18418062.001]
  • [Cites] Cell Cycle. 2008 May 15;7(10):1371-8 [18421251.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1106-16 [18385752.001]
  • [Cites] Cell Cycle. 2008 Jun 1;7(11):1604-12 [18520179.001]
  • [Cites] Oncogene. 2008 Jul 3;27(29):4086-95 [18332865.001]
  • [Cites] Cell Cycle. 2009 May 1;8(9):1373-9 [19305144.001]
  • [Cites] Cell Cycle. 2009 May 1;8(9):1352-8 [19305151.001]
  • [Cites] Cell Cycle. 2009 May 1;8(9):1338-43 [19342894.001]
  • [Cites] Cell Cycle. 2009 May 15;8(10):1515-25 [19377304.001]
  • [Cites] Rejuvenation Res. 2008 Aug;11(4):801-8 [18729812.001]
  • [Cites] Cell Cycle. 2009 Jun 1;8(11):1711-9 [19411846.001]
  • [Cites] Cell Cycle. 2009 Jun 15;8(12):1883-7 [19448395.001]
  • [Cites] Cell Cycle. 2009 Jun 15;8(12):1888-95 [19471117.001]
  • [Cites] Cell Cycle. 2009 Jun 15;8(12):1901-4 [19471118.001]
  • [Cites] Cell Cycle. 2009 Jun 15;8(12):1896-900 [19478560.001]
  • [Cites] Cell Cycle. 2009 Jul 1;8(13):2005-13 [19550141.001]
  • [Cites] Cell Cycle. 2009 Aug 15;8(16):2509-17 [19633417.001]
  • [Cites] Cell Cycle. 2009 Sep 1;8(17):2810-8 [19657224.001]
  • [Cites] Cell Cycle. 2009 Sep 15;8(18):2975-83 [19713744.001]
  • [Cites] Cell Cycle. 2009 Sep 15;8(18):2951-63 [19713770.001]
  • [Cites] Cell Cycle. 2009 Oct 1;8(19):3208-17 [19738435.001]
  • [Cites] Cell Cycle. 2009 Oct 1;8(19):3120-4 [19755852.001]
  • [Cites] Cell Cycle. 2009 Oct 15;8(20):3303-6 [19806030.001]
  • [Cites] Adv Enzyme Regul. 2010;50(1):285-307 [19895837.001]
  • [Cites] Expert Opin Emerg Drugs. 2010 Jun;15(2):203-23 [20151845.001]
  • [Cites] Cell Cycle. 2010 May;9(9):1781-91 [20436278.001]
  • [Cites] Cell Cycle. 2010 Apr 15;9(8):1629-38 [20372086.001]
  • [Cites] Cell Cycle. 2008 Jul 1;7(13):1973-82 [18604177.001]
  • [Cites] Cell Cycle. 2008 Aug;7(15):2427-33 [18677110.001]
  • [Cites] Cell Cycle. 2008 Jun 15;7(12):1745-62 [18594202.001]
  • [Cites] Cell Cycle. 2008 Sep 1;7(17):2615-8 [18719390.001]
  • [Cites] Cell Cycle. 2008 Sep 1;7(17):2661-6 [18728388.001]
  • [Cites] Cell Cycle. 2008 Sep 15;7(18):2877-85 [18769155.001]
  • [Cites] Cell Cycle. 2008 Oct;7(19):2949-55 [18818517.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1899-908 [18650843.001]
  • [Cites] Cell Cycle. 2008 Oct;7(20):3133-6 [18927504.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2080-90 [18685611.001]
  • [Cites] Cell Cycle. 2008 Nov 1;7(21):3355-61 [18948731.001]
  • [Cites] Cell Cycle. 2008 Nov 1;7(21):3362-70 [18948750.001]
  • [Cites] Cell Cycle. 2008 Nov 1;7(21):3344-54 [18971624.001]
  • [Cites] Cell Cycle. 2008 Nov 1;7(21):3448-60 [18971636.001]
  • [Cites] Leukemia. 2009 Jan;23(1):25-42 [18800146.001]
  • [Cites] Cell Cycle. 2008 Dec 15;7(24):3798-804 [19066464.001]
  • [Cites] Cell Cycle. 2008 Dec 15;7(24):3805-9 [19098454.001]
  • [Cites] Cell Cycle. 2009 Jan 1;8(1):158-66 [19158483.001]
  • [Cites] Cell Cycle. 2009 Feb 1;8(3):403-13 [19177005.001]
  • [Cites] Nat Struct Mol Biol. 2009 Mar;16(3):294-303 [19219045.001]
  • [Cites] Cell Cycle. 2009 Apr 1;8(7):1000-2 [19270518.001]
  • [Cites] Cell Cycle. 2009 Apr 1;8(7):1026-9 [19270529.001]
  • [Cites] Cancer Res. 2009 Apr 15;69(8):3520-8 [19351820.001]
  • [Cites] Cell Cycle. 2009 May 1;8(9):1314-8 [19279406.001]
  • [Cites] Cell Growth Differ. 1996 Apr;7(4):487-500 [9052990.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1711-25 [9324293.001]
  • [Cites] Leukemia. 2006 Jun;20(6):911-28 [16642045.001]
  • [Cites] Nature. 2006 May 25;441(7092):475-82 [16598206.001]
  • [Cites] Nature. 2006 May 25;441(7092):518-22 [16633340.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1254-60 [16642049.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2358-65 [16763210.001]
  • [Cites] Cell. 2000 Feb 18;100(4):387-90 [10693755.001]
  • [Cites] Leukemia. 2000 Oct;14(10):1777-84 [11021753.001]
  • [Cites] Oncogene. 2001 Jul 19;20(32):4354-64 [11466616.001]
  • [Cites] Oncogene. 2003 Apr 24;22(16):2478-92 [12717425.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Nov;82(21):7414-8 [3933007.001]
  • [Cites] Oncogene Res. 1989;4(2):97-109 [2785667.001]
  • [Cites] Blood. 1995 Oct 15;86(8):3139-50 [7579409.001]
  • [Cites] Leukemia. 2007 Mar;21(3):427-38 [17215852.001]
  • [Cites] Leukemia. 2007 May;21(5):886-96 [17361225.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1773(8):1263-84 [17126425.001]
  • [Cites] Exp Hematol. 2007 Oct;35(10):1538-49 [17889721.001]
  • [Cites] Cell Cycle. 2007 Sep 15;6(18):2268-75 [17890906.001]
  • [Cites] J Cell Biochem. 2007 Dec 15;102(6):1389-99 [17975792.001]
  • [Cites] Leukemia. 2008 Jan;22(1):198-200 [17625605.001]
  • (PMID = 20436269.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098195; United States / NCI NIH HHS / CA / R01CA098195
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Butadienes; 0 / Chromones; 0 / Interleukin-3; 0 / Intracellular Signaling Peptides and Proteins; 0 / Morpholines; 0 / Nitriles; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; P88XT4IS4D / Paclitaxel; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC3781183
  •  go-up   go-down


13. Marra CA, Frighetto L, Quaia CB, de Lemos ML, Warkentin DI, Marra F, Jewesson PJ: A new ciprofloxacin stepdown program in the treatment of high-risk febrile neutropenia: a clinical and economic analysis. Pharmacotherapy; 2000 Aug;20(8):931-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • SETTING: Adult leukemia and stem cell transplant unit.
  • Assessed parameters were clinical and microbiologic outcomes, adverse drug reactions (ADRs), and direct medical resource use and costs (1998 $Canadian) for the episode of febrile neutropenia.
  • Clinical success (83% P1, 81% P2), microbiologic eradication (15% P1, 24% P2), and possible ADRs (6% P1, 9% P2) did not differ.
  • Intravenous-to-intravenous dose stepdown occurred in 33% of P2 and no P1 treatment courses (p<0.001).
  • Resource use and costs were similar between phases, although a reduction was seen in the drug's mean total cost/day ($58 P1, $52 P2, p=0.04).
  • [MeSH-major] Anti-Infective Agents / economics. Anti-Infective Agents / therapeutic use. Ciprofloxacin / economics. Ciprofloxacin / therapeutic use. Fever / drug therapy. Fever / economics. Neutropenia / drug therapy. Neutropenia / economics
  • [MeSH-minor] Administration, Oral. Adult. Costs and Cost Analysis. Female. Hematopoietic Stem Cell Transplantation. Humans. Infusions, Intravenous. Leukemia / therapy. Male. Middle Aged. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Fever.
  • Hazardous Substances Data Bank. CIPROFLOXACIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10939554.001).
  • [ISSN] 0277-0008
  • [Journal-full-title] Pharmacotherapy
  • [ISO-abbreviation] Pharmacotherapy
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 5E8K9I0O4U / Ciprofloxacin
  •  go-up   go-down


14. Heuser M, Sly LM, Argiropoulos B, Kuchenbauer F, Lai C, Weng A, Leung M, Lin G, Brookes C, Fung S, Valk PJ, Delwel R, Löwenberg B, Krystal G, Humphries RK: Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal. Blood; 2009 Nov 5;114(19):3983-93
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal.
  • Although the cancer stem cell (CSC) concept implies that CSCs are rare, recent reports suggest that CSCs may be frequent in some cancers.
  • We hypothesized that the proportion of leukemia stem cells would vary as a function of the number of dysregulated pathways.
  • Leukemia-initiating cell (LIC) number and in vitro expansion potential of LICs were functionally assessed by limiting dilution analyses.
  • LIC expansion potential was 132-fold increased in the 2- compared with the 1-oncogene model, although phenotypically, both leukemias were similar.
  • Interestingly, in 201 acute myeloid leukemia (AML) patients, coexpression of MN1 and HOXA9 was restricted to patients with the poorest prognosis and was associated with highly active STAT signaling.
  • Our data demonstrate the functional heterogeneity of LICs and show that STAT signaling is critical for leukemia stem cell self-renewal in MN1- and HOXA9-expressing leukemias.
  • [MeSH-major] Leukemia, Experimental / metabolism. Leukemia, Experimental / pathology. Models, Biological. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Disease Models, Animal. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. In Vitro Techniques. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. MAP Kinase Signaling System / drug effects. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oncogene Proteins / genetics. Oncogene Proteins / metabolism. Oncogenes. Recombinant Proteins. STAT1 Transcription Factor / deficiency. STAT1 Transcription Factor / genetics. STAT1 Transcription Factor / metabolism. Signal Transduction / drug effects

  • 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
  • [CommentIn] Blood. 2009 Nov 5;114(19):3976-7 [19892722.001]
  • (PMID = 19667399.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Mn1 protein, mouse; 0 / Neoplasm Proteins; 0 / Oncogene Proteins; 0 / Recombinant Proteins; 0 / STAT1 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / Stat1 protein, mouse; 0 / Stat5b protein, mouse; 0 / homeobox protein HOXA9; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down


15. Pituch-Noworolska A: [Biological properties and sensitivity to induction therapy of differentiated cells expressing atypical immunophenotype in acute leukemia of children]. Folia Med Cracov; 2001;42(3):5-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biological properties and sensitivity to induction therapy of differentiated cells expressing atypical immunophenotype in acute leukemia of children].
  • The atypical immunophenotype (expression of determinant from the another cell lines than line of origin) of acute leukaemia blast cells are noted in a part of cases.
  • The characteristics and classification of atypical immunophenotypes are not unified and the clinical significance is not yet fully described.
  • The purpose of the study was: precise description of atypical immunophenotypes and analysis of their frequency in different types of acute leukaemia, analysis of association between expression of atypical immunophenotypes and the level of initial leukocytosis, percentage of blast cells in peripheral blood, expression of CD34, analysis of frequency of multidrug resistance molecule (MDR) expression and association between MDR and immunophenotypes of leukaemia cells, analysis of association between atypical immunophenotypes and proliferation, secretion of cytokines (IL-6, TNF) and spontaneous apoptosis of leukaemia cells, analysis of association between atypical immunophenotypes and sensitivity to induction therapy.
  • The bone marrow samples used for routine diagnosis were the basic source of leukaemia cells for the study.
  • The morphological examination and the immunophenotypes of leukaemia cells were done for classification of leukaemia.
  • The spontaneous proliferation of leukaemia cells was studied with 3H-Thymidine uptake after 3-days culture in vitro.
  • The type of proliferation (autocrine, paracrine) was defined based on comparison of shorter (3-days) and longer (6-days) culture of leukaemia cells.
  • The percentage of apoptotic leukaemia cells was analysed with flow cytometry after staining of leukaemia cells with propidium iodide in subdiploidal region of DNA profile.
  • The secretion of cytokines (IL-6 and TNF) was determined by ELISA technique in supernatants of leukaemia cells cultured for 24 hr in vitro.
  • The biological activity of TNF was determined in the bioassay using L929 mouse cells line.
  • The study included 230 children with acute leukaemia: lymphoblastic (ALL)--189 children (ALL-proB--19, common ALL--139, ALL-B--5 and ALL-T--26) and myeloid (AML)--34 children.
  • Moreover, into the study 2 cases of acute undifferentiated leukaemia (AUL) and 3--acute mixed lineage leukaemia (AMLL) and 2--biphenotypic leukaemia were included.
  • The all studies of leukaemia cells had been done before the therapy was installed.
  • Basing on the assay of immunophenotypes the following forms of atypical immunophenotypes were distinguished: immunophenotype incomplete, hyperexpression of determinants, asynchronic immunophenotype, coexpression of determinants from the other line than origin of leukaemia cells, balanced expression of determinants from two cells lines (biphenotypic leukaemia) and three cells lines (mixed lineage leukaemia).
  • The most common form of atypical immunophenotypes was coexpression of determinants from the other cell line.
  • The expression of CD34, recognised as the one of markers of poorer prognosis, was analysed regarding the leukaemia type and immunophenotype of leukaemia cells.
  • In ALL the atypical immunophenotype was associated with expression of MDR whereas in AML this association did not appear.
  • The common ALL + My leukaemia cells showed higher ability to proliferation in vitro compare with common ALL without atypical immunophenotype.
  • AML leukaemia cells with coexpression of lymphoid determinants (AML + Ly) showed lower proliferation in vitro than AML without atypical immunophenotype.
  • The autocrine type of proliferation was observed frequently in AML (35.3% of cases) than in ALL (14.2%).
  • This type of spontaneous proliferation was observed only when the leukaemia cells without changes in immunophenotype had been cultured.
  • AML leukaemia cells without changes in immunophenotype released significantly higher amount of these cytokines than AML cells with atypical immunophenotypes (AML + Ly).
  • The above observations suggested that coexpression of myeloid determinants in ALL and lymphoid determinants in AML were leading to changes of some biological properties of these cells.
  • The ALL + My leukaemia cells behaved similarly to myeloid leukaemia cells, while AML + Ly cells showed features of lymphoid leukaemia cells.
  • The common ALL and AML leukaemia cells with atypical immunophenotype showed higher percentage of apoptotic cells (16.1% and 16.9% respectively) comparing to common ALL and AML without changes in immunophenotype (9.0% and 9.2% respectively).
  • In common ALL and AML with typical immunophenotype of leukaemia cells and ALL-T the level of apoptosis was associated positively with the spontaneous proliferation, whereas this relation was negative in AML with atypical immunophenotype.
  • There were no differences of the time of cytoreduction of leukaemia cells in peripheral blood in B cell origin ALL and AML with or without changes in immunophenotype of blastic cells.
  • The results of this study suggest that coexpression of determinants from the other cell line modify the biological properties of leukaemia cells into the cells from the line of origin of these additional determinants.
  • In ALL the combined expression of MDR and atypical immunophenotype of leukaemia cells were associated with poorer response to induction therapy.
  • The clinical importance of these observations consist in characterisation of leukaemia cells potentially resistant to the induction therapy what may suggest the modification and individualization of the induction therapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Animals. Antigens, CD34 / immunology. Apoptosis. Child. Child, Preschool. Cytokines / secretion. Drug Resistance, Multiple / immunology. Humans. Immunophenotyping. Infant. Mice. Multidrug Resistance-Associated Proteins / immunology. Remission Induction

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 = 12353422.001).
  • [ISSN] 0015-5616
  • [Journal-full-title] Folia medica Cracoviensia
  • [ISO-abbreviation] Folia Med Cracov
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cytokines; 0 / Multidrug Resistance-Associated Proteins
  • [Number-of-references] 160
  •  go-up   go-down


16. Ichijo T, Chrousos GP, Kino T: Activated glucocorticoid receptor interacts with the INHAT component Set/TAF-Ibeta and releases it from a glucocorticoid-responsive gene promoter, relieving repression: implications for the pathogenesis of glucocorticoid resistance in acute undifferentiated leukemia with Set-Can translocation. Mol Cell Endocrinol; 2008 Feb 13;283(1-2):19-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activated glucocorticoid receptor interacts with the INHAT component Set/TAF-Ibeta and releases it from a glucocorticoid-responsive gene promoter, relieving repression: implications for the pathogenesis of glucocorticoid resistance in acute undifferentiated leukemia with Set-Can translocation.
  • Set/template-activating factor (TAF)-Ibeta, part of the Set-Can oncogene product found in acute undifferentiated leukemia, is a component of the inhibitor of acetyltransferases (INHAT) complex.
  • Set/TAF-Ibeta was co-precipitated with glucocorticoid response elements (GREs) of these promoters in the absence of dexamethasone, while addition of the hormone caused dissociation of Set/TAF-Ibeta from and attraction of the p160-type coactivator GRIP1 to the promoter GREs.
  • Set-Can fusion protein, on the other hand, did not interact with GR, was constitutively co-precipitated with GREs and suppressed GRIP1-induced enhancement of GR transcriptional activity and histone acetylation.
  • Thus, Set/TAF-Ibeta acts as a ligand-activated GR-responsive transcriptional repressor, while Set-Can does not retain physiologic responsiveness to ligand-bound GR, possibly contributing to the poor responsiveness of Set-Can-harboring leukemic cells to glucocorticoids.
  • [MeSH-major] Chromosomal Proteins, Non-Histone / metabolism. Glucocorticoids / pharmacology. Leukemia / pathology. Oncogene Proteins, Fusion / metabolism. Promoter Regions, Genetic / genetics. Receptors, Glucocorticoid / metabolism. Transcription Factors / metabolism. Translocation, Genetic
  • [MeSH-minor] Animals. Chromatin Immunoprecipitation. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic / drug effects. HCT116 Cells. Histone Acetyltransferases / metabolism. Histone Chaperones. Humans. Ligands. Models, Genetic. Nuclear Proteins / metabolism. Phosphoproteins / metabolism. Protein Binding / drug effects. Protein Structure, Tertiary. Rats. Repressor Proteins / metabolism. Response Elements. Transcription, Genetic / drug effects

  • Genetic Alliance. consumer health - Glucocorticoid Resistance.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Steroids.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):42067-77 [16249187.001]
  • [Cites] J Cell Biol. 2005 Jun 20;169(6):885-96 [15955845.001]
  • [Cites] Cell. 2001 Jan 12;104(1):119-30 [11163245.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25026-31 [11978794.001]
  • [Cites] J Immunol. 2002 Dec 1;169(11):6361-8 [12444143.001]
  • [Cites] Mol Endocrinol. 2003 Jan;17(1):67-78 [12511607.001]
  • [Cites] Curr Top Microbiol Immunol. 2003;274:237-68 [12596910.001]
  • [Cites] J Biol Chem. 2003 Aug 1;278(31):28758-64 [12759364.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Jun;85(2-5):457-67 [12943736.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(23):8528-41 [14612398.001]
  • [Cites] Mol Endocrinol. 2004 Apr;18(4):820-33 [14739255.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):23859-62 [15100215.001]
  • [Cites] Cell Death Differ. 2004 Jul;11 Suppl 1:S45-55 [15243581.001]
  • [Cites] Essays Biochem. 2004;40:137-55 [15242344.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):30850-5 [15136563.001]
  • [Cites] Cell. 1987 Apr 10;49(1):29-38 [2881624.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 May;87(10):3977-81 [2160080.001]
  • [Cites] Mol Cell Biol. 1992 Aug;12(8):3346-55 [1630450.001]
  • [Cites] Genes Chromosomes Cancer. 1992 Oct;5(3):227-34 [1384675.001]
  • [Cites] J Biol Chem. 1993 May 15;268(14):10582-7 [8486711.001]
  • [Cites] Am J Hematol. 1994 Feb;45(2):177-80 [8141124.001]
  • [Cites] N Engl J Med. 1995 May 18;332(20):1351-62 [7715646.001]
  • [Cites] Oncogene. 1995 May 4;10(9):1739-48 [7753551.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4279-83 [7753797.001]
  • [Cites] Oncogene. 1996 Oct 17;13(8):1801-8 [8895527.001]
  • [Cites] J Am Soc Nephrol. 1998 Oct;9(10):1873-80 [9773788.001]
  • [Cites] J Biol Chem. 1998 Dec 18;273(51):34511-8 [9852120.001]
  • [Cites] J Exp Med. 1999 Jan 4;189(1):51-62 [9874563.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jun 7;259(2):471-5 [10362532.001]
  • [Cites] Endocr Rev. 1999 Jun;20(3):321-44 [10368774.001]
  • [Cites] J Mol Biol. 1999 Jul 9;290(2):547-57 [10390352.001]
  • [Cites] Leuk Lymphoma. 1999 Jul;34(3-4):287-94 [10439365.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(2):797-807 [15632079.001]
  • [Cites] J Virol. 2005 Mar;79(5):2780-7 [15708996.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jun;90(6):3696-705 [15769988.001]
  • [Cites] Mol Endocrinol. 2006 Feb;20(2):335-47 [16195249.001]
  • (PMID = 18096310.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008732-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Glucocorticoids; 0 / Histone Chaperones; 0 / Ligands; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / Receptors, Glucocorticoid; 0 / Repressor Proteins; 0 / SET protein, human; 0 / SET-CAN fusion protein, human; 0 / Transcription Factors; EC 2.3.1.48 / Histone Acetyltransferases
  • [Other-IDs] NLM/ NIHMS42142; NLM/ PMC2350211
  •  go-up   go-down


17. Zheng ZJ, Hu JD, Huang SH, Wang SY, Lu LH: [Effects of SCL antisense ooligonucleotides on K562 and CEM cell lines]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2002 Oct;10(5):404-8
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of SCL antisense ooligonucleotides on K562 and CEM cell lines].
  • The stem cell leukemia (SCL) gene is a new oncogene related with leukemogenesis.
  • To explore the effects of antisense oligonucleotides of SCL on leukemic cells, SCL antisense phosphorothioate oligodeoxynucleotides (AS-PS-ODN) were used to treat K562 and CEM leukemic cell lines to observe the effects on proliferation, differentiation, apoptosis and SCL mRNA expression in the cells.
  • The results showed that incubation of K562 or CEM cells with AS-PS-ODN at different concentrations led to inhibition of cell proliferation, and the inhibitory effects varied with the incubation time.
  • The characteristics of apoptosis were observed in K562 cells treated with AS-PS-ODN, but not in CEM cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12513737.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  •  go-up   go-down


18. Williams BA, Wang XH, Keating A: Clonogenic assays measure leukemia stem cell killing not detectable by chromium release and flow cytometric cytotoxicity assays. Cytotherapy; 2010 Nov;12(7):951-60
Hazardous Substances Data Bank. DAUNORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clonogenic assays measure leukemia stem cell killing not detectable by chromium release and flow cytometric cytotoxicity assays.
  • BACKGROUND AIMS: NK-92, a permanent natural killer (NK) cell line, shows cytotoxicity against a variety of tumors and has been tested in a phase I trial.
  • We tested the toxicity of NK-92 and chemotherapy drugs against the stem cell capacity of the acute leukemia cell line, KG1.
  • METHODS: KG1 was assessed for stem cell frequency by serial dilution, single-cell sorting and colony growth in methylcellulose.
  • RESULTS: The culture-initiating cell frequency of whole KG1 was between 1 in 100 to 1000 by serial dilution and single-cell sorting.
  • The cumulative flow cytotoxicity assay was more sensitive than the chromium-release assay in detecting target cell killing.
  • At a 10:1 ratio NK-92 eliminated the clonogenic capacity of KG1, which was not predicted by the chromium-release assay.
  • CONCLUSIONS: Clonogenic assays provide a more sensitive means of assessing the effect of a cytotoxic agent against putative cancer stem cells within cell lines, provided that they grow well in liquid culture medium or methylcellulose.
  • [MeSH-major] Flow Cytometry. Killer Cells, Natural / metabolism. Leukemia / immunology. Neoplastic Stem Cells / metabolism. Tumor Stem Cell Assay
  • [MeSH-minor] Antigens, CD34 / biosynthesis. Antigens, CD38 / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Culture Techniques. Cell Line, Tumor. Cell Separation. Chromium Isotopes / metabolism. Cytarabine / pharmacology. Cytarabine / therapeutic use. Cytotoxicity Tests, Immunologic / methods. Cytotoxicity, Immunologic. Daunorubicin / pharmacology. Daunorubicin / therapeutic use. Humans. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20230219.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Chromium Isotopes; 04079A1RDZ / Cytarabine; EC 3.2.2.5 / Antigens, CD38; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


19. Göthert JR, Gustin SE, Hall MA, Green AR, Göttgens B, Izon DJ, Begley CG: In vivo fate-tracing studies using the Scl stem cell enhancer: embryonic hematopoietic stem cells significantly contribute to adult hematopoiesis. Blood; 2005 Apr 1;105(7):2724-32
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo fate-tracing studies using the Scl stem cell enhancer: embryonic hematopoietic stem cells significantly contribute to adult hematopoiesis.
  • Evidence for the lineage relationship between embryonic and adult hematopoietic stem cells (HSCs) in the mouse is primarily indirect.
  • In order to study this relationship in a direct manner, we expressed the tamoxifen-inducible Cre-ER(T) recombinase under the control of the stem cell leukemia (Scl) stem-cell enhancer in transgenic mice (HSC-SCL-Cre-ER(T)).
  • Flow cytometric and transplantation studies revealed tamoxifen-dependent recombination occurring in more than 90% of adult long-term HSCs, whereas the targeted proportion within mature progenitor populations was significantly lower.
  • In order to investigate whether the de novo HSC generation is completed during embryogenesis, HSC-SCL-Cre-ER(T)-marked fetal liver cells were transplanted into adult recipients.
  • Strikingly, the proportion of marked cells within the transplanted and the in vivo-remaining HSC compartment was not different, implying that no further HSC generation occurred during late fetal and neonatal stages of development.
  • [MeSH-major] Enhancer Elements, Genetic. Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Integrases / genetics
  • [MeSH-minor] Age Factors. Animals. Antineoplastic Agents, Hormonal / pharmacology. Biomarkers. Cell Lineage. Gene Expression / drug effects. Hematopoietic Stem Cell Transplantation. Lac Operon. Mice. Mice, Inbred C57BL. Mice, Transgenic. Recombination, Genetic. Tamoxifen / pharmacology. Transgenes / physiology

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • 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
  • (PMID = 15598809.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers; 094ZI81Y45 / Tamoxifen; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  •  go-up   go-down


20. Linker C: Thrombopoietin in the treatment of acute myeloid leukemia and in stem-cell transplantation. Semin Hematol; 2000 Apr;37(2 Suppl 4):35-40
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thrombopoietin in the treatment of acute myeloid leukemia and in stem-cell transplantation.
  • Recent studies indicate that thrombopoietin (TPO) may be highly effective in mobilizing autologous peripheral blood stem cells (PBSCs) for transplantation in patients undergoing intensive chemotherapy.
  • However, the effect of TPO in patients with hematologic malignancies undergoing induction or postremission chemotherapy or in the stem-cell transplantation setting has not been demonstrated.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Thrombopoietin / therapeutic use
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / adverse effects. Clinical Trials as Topic. Hematopoietic Stem Cell Mobilization. Humans. Polyethylene Glycols / therapeutic use. Recombinant Proteins / therapeutic use. Thrombocytopenia / chemically induced. Thrombocytopenia / drug therapy

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10831287.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 0 / polyethylene glycol-recombinant human megakaryocyte growth and development factor; 30IQX730WE / Polyethylene Glycols; 9014-42-0 / Thrombopoietin
  • [Number-of-references] 20
  •  go-up   go-down


21. Xavier L, Cunha M, Gonçalves C, Teixeira Mdos A, Coutinho J, Ribeiro AC, Lima M: Hematological remission and long term hematological control of acute myeloblastic leukemia induced and maintained by granulocyte-colony stimulating factor (G-CSF) therapy. Leuk Lymphoma; 2003 Dec;44(12):2137-42
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematological remission and long term hematological control of acute myeloblastic leukemia induced and maintained by granulocyte-colony stimulating factor (G-CSF) therapy.
  • We describe a case of a patient with CD34+, TdT+, CD13-, CD33-, MPO- undifferentiated acute leukemia who refused chemotherapy and who achieved complete hematological remission 14 months after the diagnosis, during a short course of granulocyte-colony stimulating factor (G-CSF) for neutropenia and life threatening infection.
  • Finally, the patient developed progressive neutropenia, anemia, thrombocytopenia and acute leukemia in spite of G-CSF therapy, dying 64 months after initial diagnosis (50 months after starting G-CSF therapy) with overt G-CSF resistant acute myeloblastic leukemia (AML), after failure of conventional induction chemotherapy.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14959860.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 1.11.1.7 / Peroxidase; EC 2.7.7.31 / DNA Nucleotidylexotransferase; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down


22. Unger C, Kärner E, Treschow A, Stellan B, Felldin U, Concha H, Wendel M, Hovatta O, Aints A, Ahrlund-Richter L, Dilber MS: Lentiviral-mediated HoxB4 expression in human embryonic stem cells initiates early hematopoiesis in a dose-dependent manner but does not promote myeloid differentiation. Stem Cells; 2008 Oct;26(10):2455-66

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lentiviral-mediated HoxB4 expression in human embryonic stem cells initiates early hematopoiesis in a dose-dependent manner but does not promote myeloid differentiation.
  • The variation of HoxB4 expression levels might be a key regulatory mechanism in the differentiation of human embryonic stem cell (hESC)-derived hematopoietic stem cells (HSCs).
  • High levels of HoxB4 expression correlated to an improved yield of cells expressing CD34, CD38, the stem cell leukemia gene, and vascular epithelium-cadherin.
  • However, no improvement in myeloid cell maturation was observed, as determined by colony formation assays.
  • In contrast, hESCs with low HoxB4 levels did not show any elevated hematopoietic development.
  • These data suggest that HoxB4-induced effects on hESC-derived HSCs are concentration-dependent during in vitro development and reduce proliferation of other cell types in vitro and in vivo.
  • The application of the transcription factor HoxB4 during early hematopoiesis from hESCs might provide new means for regenerative medicine, allowing efficient differentiation and engraftment of genetically modified hESC clones.
  • [MeSH-major] Cell Differentiation. Embryonic Stem Cells / cytology. Embryonic Stem Cells / metabolism. Hematopoiesis / genetics. Homeodomain Proteins / genetics. Lentivirus / genetics. Myeloid Cells / cytology. Transcription Factors / genetics
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Proliferation. Colony-Forming Units Assay. Gene Expression Regulation, Developmental. Genetic Vectors / genetics. Green Fluorescent Proteins / metabolism. HeLa Cells. Humans. Male. Mice. Mice, SCID. Octamer Transcription Factor-3 / metabolism. Teratoma / pathology. Transduction, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18617691.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / Transcription Factors; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
  •  go-up   go-down


23. Göthert JR, Gustin SE, van Eekelen JA, Schmidt U, Hall MA, Jane SM, Green AR, Göttgens B, Izon DJ, Begley CG: Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium. Blood; 2004 Sep 15;104(6):1769-77
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium.
  • Tumor growth is dependent in part on "neoangiogenesis."
  • We generated Cretransgenic mice (endothelial-SCL-Cre-ER(T)) using the tamoxifen-inducible Cre-ER(T) recombinase driven by the 5' endothelial enhancer of the stem cell leukemia (SCL) locus.
  • Subsequently, BM from endothelial-SCL-Cre-ER(T);R26R mice was transplanted into irradiated recipients.
  • Thus, this genetic model strongly suggests that BM cells do not contribute to tumor endothelium and demonstrates the lineage relation between pre-existing endothelium and newly generated tumor endothelial cells.
  • [MeSH-major] Bone Marrow Cells / cytology. Cell Lineage. Endothelial Cells / metabolism. Endothelial Cells / pathology. Endothelium / metabolism. Endothelium / pathology. Neoplasms / genetics. Neoplasms / pathology
  • [MeSH-minor] Aging / physiology. Alleles. Animals. Cell Differentiation. Embryo, Mammalian / metabolism. Embryo, Mammalian / pathology. Flow Cytometry. Genes, Reporter / genetics. Mice. Mice, Transgenic. Neovascularization, Pathologic. Recombination, Genetic / drug effects. Tamoxifen / pharmacology

  • Hazardous Substances Data Bank. TAMOXIFEN .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15187022.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen
  •  go-up   go-down


24. Jordan CT: The potential of targeting malignant stem cells as a treatment for leukemia. Future Oncol; 2005 Apr;1(2):205-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The potential of targeting malignant stem cells as a treatment for leukemia.
  • Malignant stem cells have recently been described as the source of several types of human cancer.
  • These unique cell types are typically rare and possess properties that are distinct from most other tumor cells.
  • In leukemia, the natural properties of cancer stem cells indicate that current chemotherapy drugs will not be effective.
  • Consequently, new strategies are required that specifically and preferentially target the cancer stem cell population, whilst sparing normal stem cells.
  • This perspective article summarizes recent findings in the leukemia stem cell field and discusses new directions for therapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Leukemia / drug therapy. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Animals. Forecasting. Humans

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16555992.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 22
  •  go-up   go-down


25. Brandts CH, Berdel WE, Serve H: Oncogenic signaling in acute myeloid leukemia. Curr Drug Targets; 2007 Feb;8(2):237-46
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncogenic signaling in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a malignant disease of the bone marrow.
  • It is increasingly recognized that AML represents a hierarchical disease, originating from a leukemia stem cell population.
  • Our current understanding of the biology of AML has fueled the development of promising anti-leukemic agents, which may improve the treatment of the disease in the future.
  • [MeSH-major] Leukemia, Myeloid / genetics. Oncogenes. Signal Transduction
  • [MeSH-minor] Acute Disease. Animals. Cell Differentiation. Cell Proliferation. Humans. Models, Animal

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17305501.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 135
  •  go-up   go-down


26. Graf M, Hecht K, Reif S, Pelka-Fleischer R, Pfister K, Schmetzer H: Expression and prognostic value of hemopoietic cytokine receptors in acute myeloid leukemia (AML): implications for future therapeutical strategies. Eur J Haematol; 2004 Feb;72(2):89-106
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and prognostic value of hemopoietic cytokine receptors in acute myeloid leukemia (AML): implications for future therapeutical strategies.
  • OBJECTIVES: Hemopoietic cytokines regulate hemopoietic cell functions via specific cell surface receptors.
  • There is evidence to suggest, that those receptors (R) could play a role in leukemia with respect to cell differentiations and its regulation, prognosis, and pathobiology.
  • METHODS: We have studied the expression of CKR on mononuclear bone marrow (BM) cells of 89 patients with acute myeloid leukemia (AML) at first diagnosis, three patients at relapse or with persisting AML and eight healthy probands by fluorescence-activated cell sorting (FACS) analysis using directly fluorescein-conjugated antibodies: CD114 (hG-CSF-R), CD116 (hGM-CSF-R), CD117 (hSCF-R), CD123 (hIL-3-R), CD130 (gp130subunit), CD135 (hFL-R).
  • Monocytic subtypes (FAB-type M4/M5) showed significantly more GM-CSF-R(+) (P = 0.001) and FL-R(+) (P = 0.001) and significantly less stem cell factor-R (SCF-R(+)) (P = 0.02) cases.
  • Highest proportions of G-CSF-R(+) blasts were observed in FAB-type M3.
  • In undifferentiated leukemias (FAB-type M1, M2) high amounts of SCF-R(+), IL-3-R(+), and FL-R(+) blasts could be detected.
  • FL-R was the only CKR, which was positive in FAB-type M0 (n = 2).
  • Separating our patient cohorts in cytogenetic risk groups we could detect a significant higher proportion of G-CSF-R(+) blasts in the cytogenetic good risk group than in the bad risk group (P = 0.027), but G-CSF-R-expression did not correlate with remission-rate or relapse-free survival probability of the patients.
  • Patients with more than 32.5% IL-3-R(+) cells also showed a tendency to a lower relapse-free survival probability (P = 0.26), whereas patients with more than 33% GM-CSF-R(+) (P = 0.06) and patients with more than 52% G-CSF-R(+) (P = 0.175) blasts tended to have a higher relapse-free survival probability.
  • With respect to the individual CKR status the benefit of cytokines as priming agents, as agents to treat neutropenia or to influence the metabolism of chemotherapy can be discussed under new points of view.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Receptors, Cytokine / blood


27. Wang Z, Iwasaki M, Ficara F, Lin C, Matheny C, Wong SH, Smith KS, Cleary ML: GSK-3 promotes conditional association of CREB and its coactivators with MEIS1 to facilitate HOX-mediated transcription and oncogenesis. Cancer Cell; 2010 Jun 15;17(6):597-608
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Acute leukemias induced by MLL chimeric oncoproteins are among the subset of cancers distinguished by a paradoxical dependence on GSK-3 kinase activity for sustained proliferation.
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation.
  • This mechanism also applies to hematopoietic cells transformed by other HOX genes, including CDX2, which is highly expressed in a majority of acute myeloid leukemias, thus providing a molecular approach based on GSK-3 inhibitory strategies to target HOX-associated transcription in a broad spectrum of leukemias.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • PhosphoSitePlus. gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [Cites] Oncogene. 2000 Feb 3;19(5):608-16 [10698505.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2762-74 [17942707.001]
  • [Cites] Curr Cancer Drug Targets. 2007 Jun;7(4):317-24 [17979626.001]
  • [Cites] Blood. 2008 Jan 1;111(1):309-19 [17855634.001]
  • [Cites] Int J Hematol. 2008 Jan;87(1):10-8 [18224408.001]
  • [Cites] Leukemia. 2008 Mar;22(3):665-7 [17805329.001]
  • [Cites] Neuropsychopharmacology. 2008 Sep;33(10):2407-15 [18046304.001]
  • [Cites] Cancer Res. 2008 Oct 1;68(19):8156-63 [18829575.001]
  • [Cites] Leuk Lymphoma. 2008 Oct;49(10):1945-53 [18728964.001]
  • [Cites] Nature. 2008 Oct 30;455(7217):1205-9 [18806775.001]
  • [Cites] J Biol Chem. 2008 Dec 5;283(49):33902-10 [18801732.001]
  • [Cites] Cancer Lett. 2009 Jan 18;273(2):194-200 [18606491.001]
  • [Cites] Clin Cancer Res. 2009 Feb 1;15(3):887-97 [19188159.001]
  • [Cites] Cell Stem Cell. 2009 Feb 6;4(2):129-40 [19200802.001]
  • [Cites] Biosci Rep. 2009 Apr;29(2):77-87 [18717645.001]
  • [Cites] Blood. 2009 Apr 23;113(17):4049-51 [19218548.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6061-8 [19289854.001]
  • [Cites] J Biol Chem. 2009 Jul 10;284(28):18904-12 [19473990.001]
  • [Cites] PLoS One. 2009;4(10):e7443 [19823589.001]
  • [Cites] Brain Res Brain Res Rev. 2000 Aug;33(1):1-12 [10967351.001]
  • [Cites] FEBS J. 2007 Jul;274(13):3224-32 [17565603.001]
  • [Cites] Oncogene. 2000 Oct 26;19(45):5134-41 [11064450.001]
  • [Cites] Bioorg Med Chem Lett. 2001 Mar 12;11(5):635-9 [11266159.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Endocrinology. 2002 Feb;143(2):674-82 [11796524.001]
  • [Cites] J Med Chem. 2002 Mar 14;45(6):1292-9 [11881998.001]
  • [Cites] Gene. 2002 Jun 26;293(1-2):169-79 [12137955.001]
  • [Cites] Stem Cells. 2002;20(5):364-79 [12351808.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):777-85 [12360280.001]
  • [Cites] Mol Cell Biol. 2002 Nov;22(21):7678-87 [12370314.001]
  • [Cites] J Cell Sci. 2003 Apr 1;116(Pt 7):1175-86 [12615961.001]
  • [Cites] Mol Cell. 2003 Aug;12(2):413-23 [14536081.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):45937-45 [12928438.001]
  • [Cites] Cancer Biol Ther. 2003 Sep-Oct;2(5):518-23 [14614318.001]
  • [Cites] Nat Rev Cancer. 2004 Mar;4(3):177-83 [14993899.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3192-9 [15070702.001]
  • [Cites] Nat Rev Drug Discov. 2004 Jun;3(6):479-87 [15173837.001]
  • [Cites] Virology. 1982 Jan 15;116(1):221-35 [6278709.001]
  • [Cites] J Biol Chem. 1994 Dec 23;269(51):32187-93 [7798217.001]
  • [Cites] Oncogene. 1997 Jun 19;14(24):2917-26 [9205098.001]
  • [Cites] EMBO J. 1997 Jul 16;16(14):4226-37 [9250666.001]
  • [Cites] J Biol Chem. 1997 Dec 5;272(49):31016-21 [9388250.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):764-76 [9858599.001]
  • [Cites] Mol Cell Biol. 1999 Jul;19(7):5134-42 [10373562.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10119-27 [15654074.001]
  • [Cites] Nat Immunol. 2005 Aug;6(8):777-84 [16007092.001]
  • [Cites] Trends Neurosci. 2005 Aug;28(8):436-45 [15982754.001]
  • [Cites] Cell. 2005 Oct 21;123(2):207-18 [16239140.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] EMBO J. 2006 Apr 5;25(7):1469-80 [16525506.001]
  • [Cites] Blood. 2006 Jul 1;108(1):297-304 [16507773.001]
  • [Cites] J Virol. 2006 Jul;80(14):7052-9 [16809310.001]
  • [Cites] J Biol Chem. 2006 Sep 29;281(39):29245-55 [16835220.001]
  • [Cites] Oncogene. 2007 Jan 4;26(1):1-10 [16799638.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):209-17 [17210701.001]
  • [Cites] J Clin Invest. 2007 Apr;117(4):1037-48 [17347684.001]
  • [CommentIn] Nat Rev Cancer. 2010 Aug;10(8):529 [20677349.001]
  • [CommentIn] Cancer Cell. 2010 Jun 15;17(6):529-31 [20541696.001]
  • (PMID = 20541704.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE21842
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009151; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / T32 CA009151-37; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / T32 CA09151; United States / NCI NIH HHS / CA / CA009151-37; United States / NCI NIH HHS / CA / CA116606; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [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 / CRTC1 protein, human; 0 / CRTC2 protein, human; 0 / Cdx4 protein, mouse; 0 / Cyclic AMP Response Element-Binding Protein; 0 / DNA-Binding Proteins; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / Hoxb4 protein, mouse; 0 / Indoles; 0 / Maleimides; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Pbx1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / SB 216763; 0 / Transcription Factors; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 0 / pbx1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ NIHMS203816; NLM/ PMC2919232
  •  go-up   go-down


28. Buzzai M, Licht JD: New molecular concepts and targets in acute myeloid leukemia. Curr Opin Hematol; 2008 Mar;15(2):82-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New molecular concepts and targets in acute myeloid leukemia.
  • PURPOSE OF REVIEW: Most patients with acute myeloid leukemia treated with chemotherapy relapse.
  • It is increasingly recognized that the cause of chemoresistance and relapse resides within the leukemia stem cell population.
  • Successful eradication of leukemia stem cells would require a comprehensive profile of both the acquired molecular lesions and intrinsic features of leukemia stem cells.
  • This review describes recent work identifying molecular markers that may lead to development of novel therapeutics, ultimately aiming to eradicate leukemia stem cells in acute myeloid leukemia.
  • RECENT FINDINGS: In recent years, novel specific cell surface antigens have allowed identification of leukemia stem cells and permitted their distinction from normal hematopoietic stem cells.
  • Novel concepts of leukemia stem cells and niche interaction have elucidated the mechanisms that control leukemia stem cell survival and chemoresistance.
  • Recent detection of genetic aberrations affecting regulators of HOX gene expression and chromatin modifying enzymes, such as CDX2 and hDOT1L, respectively, elucidates new key players in stem cell self-renewal and leukemic transformation.
  • SUMMARY: The discovery of novel markers and survival pathways for leukemia stem cells has increased our potential to specifically target and eliminate the leukemic stem cell compartment, which is likely to improve clinical outcomes in acute myeloid leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem Cells / drug effects. Leukemia, Myeloid, Acute
  • [MeSH-minor] Genes, Homeobox / genetics. Humans. Immunoconjugates / therapeutic use. Natural Cytotoxicity Triggering Receptor 2. Neoplasm, Residual. Receptors, Immunologic / drug effects. Receptors, Interleukin-3 / drug effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18300752.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoconjugates; 0 / NCR2 protein, human; 0 / Natural Cytotoxicity Triggering Receptor 2; 0 / Receptors, Immunologic; 0 / Receptors, Interleukin-3
  • [Number-of-references] 51
  •  go-up   go-down


29. McCubrey JA, Steelman LS, Abrams SL, Bertrand FE, Ludwig DE, Bäsecke J, Libra M, Stivala F, Milella M, Tafuri A, Lunghi P, Bonati A, Martelli AM: Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy. Leukemia; 2008 Apr;22(4):708-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy.
  • The Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways are frequently activated in leukemia and other hematopoietic disorders by upstream mutations in cytokine receptors, aberrant chromosomal translocations as well as other genetic mechanisms.
  • Effective targeting of these pathways may result in suppression of cell growth and death of leukemic cells.
  • Furthermore it may be possible to combine various chemotherapeutic and antibody-based therapies with low molecular weight, cell membrane-permeable inhibitors which target the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to ultimately suppress the survival pathways, induce apoptosis and inhibit leukemic growth.
  • In this review, we summarize how suppression of these pathways may inhibit key survival networks important in leukemogenesis and leukemia therapy as well as the treatment of other hematopoietic disorders.
  • Targeting of these and additional cascades may also improve the therapy of chronic myelogenous leukemia, which are resistant to BCR-ABL inhibitors.
  • Furthermore, we discuss how targeting of the leukemia microenvironment and the leukemia stem cell are emerging fields and challenges in targeted therapies.
  • [MeSH-major] Apoptosis / drug effects. Drug Delivery Systems. Leukemia / drug therapy. Signal Transduction / drug effects


30. Zhou J, Zhang H, Gu P, Bai J, Margolick JB, Zhang Y: NF-kappaB pathway inhibitors preferentially inhibit breast cancer stem-like cells. Breast Cancer Res Treat; 2008 Oct;111(3):419-27
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-kappaB pathway inhibitors preferentially inhibit breast cancer stem-like cells.
  • Accumulating evidence indicates that breast cancer is caused by cancer stem cells and cure of breast cancer requires eradication of breast cancer stem cells.
  • Previous studies with leukemia stem cells have shown that NF-kappaB pathway is important for leukemia stem cell survival.
  • In this study, by using MCF7 sphere cells as model of breast cancer stem-like cells, we evaluated the effect of NF-kappaB pathway specific inhibitors on human breast cancer MCF7 sphere cells.
  • Three inhibitors including parthenolide (PTL), pyrrolidinedithiocarbamate (PDTC) and its analog diethyldithiocarbamate (DETC) were found to preferentially inhibit MCF7 sphere cell proliferation.
  • These compounds also showed preferential inhibition in term of proliferation and colony formation on MCF7 side population (SP) cells, a small fraction of MCF7 cells known to enrich in breast cancer stem-like cells.
  • This study suggests that breast cancer stem-like cells could be selectively inhibited by targeting signaling pathways important for breast cancer stem-like cells.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Oct 15;98(8):2301-7 [11588023.001]
  • [Cites] J Natl Cancer Inst. 2001 Jun 6;93(11):824-42 [11390532.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Genes Dev. 2003 May 15;17(10):1253-70 [12756227.001]
  • [Cites] Br J Pharmacol. 2003 Jul;139(5):1041-9 [12839879.001]
  • [Cites] Brain Res Bull. 2001 Jun;55(3):375-86 [11489345.001]
  • [Cites] Chem Biol. 2001 Aug;8(8):759-66 [11514225.001]
  • [Cites] Nat Med. 2001 Sep;7(9):1028-34 [11533706.001]
  • [Cites] J Biol Chem. 1998 Mar 13;273(11):6373-9 [9497367.001]
  • [Cites] Arch Biochem Biophys. 1998 Apr 1;352(1):59-70 [9521814.001]
  • [Cites] Lancet. 1998 May 16;351(9114):1451-67 [9605801.001]
  • [Cites] Lancet. 1998 Sep 19;352(9132):930-42 [9752815.001]
  • [Cites] Carcinogenesis. 1998 Sep;19(9):1583-9 [9771928.001]
  • [Cites] Clin Cancer Res. 1997 Jul;3(7):1149-56 [9815794.001]
  • [Cites] J Biol Chem. 1999 Sep 17;274(38):27307-14 [10480951.001]
  • [Cites] Br J Cancer. 1999 Oct;81(3):440-8 [10507768.001]
  • [Cites] Curr Opin Cell Biol. 2004 Dec;16(6):708-12 [15530785.001]
  • [Cites] Carcinogenesis. 2005 Apr;26(4):703-11 [15459022.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):275-84 [15803154.001]
  • [Cites] Cell Cycle. 2005 Feb;4(2):203-5 [15655356.001]
  • [Cites] J Leukoc Biol. 2005 Jun;77(6):975-83 [15784689.001]
  • [Cites] Mol Cancer Ther. 2005 Jun;4(6):1004-12 [15956258.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5506-11 [15994920.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6207-19 [16024622.001]
  • [Cites] J Clin Pharmacol. 2005 Aug;45(8):872-7 [16027397.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):373-81 [16042686.001]
  • [Cites] Expert Opin Biol Ther. 2005 Sep;5(9):1147-52 [16120045.001]
  • [Cites] Stem Cells. 2005 Sep;23(8):1059-65 [16002779.001]
  • [Cites] JAMA. 2005 Sep 21;294(11):1359-66 [16174694.001]
  • [Cites] Biochem Soc Trans. 2005 Dec;33(Pt 6):1531-3 [16246162.001]
  • [Cites] Curr Opin Genet Dev. 2006 Feb;16(1):60-4 [16377171.001]
  • [Cites] Breast Cancer Res. 2005;7(6):R1097-110 [16457690.001]
  • [Cites] Nat Med. 2006 Mar;12(3):296-300 [16520777.001]
  • [Cites] Nature. 2006 May 25;441(7092):475-82 [16598206.001]
  • [Cites] N Engl J Med. 2006 Sep 21;355(12):1253-61 [16990388.001]
  • [Cites] J Natl Cancer Inst. 2006 Dec 20;98(24):1777-85 [17179479.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Apoptosis. 2003 Oct;8(5):539-45 [14601560.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):781-6 [14711994.001]
  • [Cites] Cancer Control. 2004 Mar-Apr;11(2):97-104 [15024346.001]
  • [Cites] J Natl Cancer Inst. 2004 Apr 21;96(8):583-5 [15100335.001]
  • [Cites] Curr Opin Genet Dev. 2004 Feb;14(1):43-7 [15108804.001]
  • [Cites] J Exp Med. 1992 May 1;175(5):1181-94 [1314883.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] J Biol Chem. 1995 Oct 20;270(42):24995-5000 [7559628.001]
  • [Cites] J Exp Med. 1996 Apr 1;183(4):1797-806 [8666936.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] FEBS Lett. 1997 Aug 18;413(2):354-8 [9280312.001]
  • [Cites] Nat Med. 1997 Dec;3(12):1337-45 [9396603.001]
  • [Cites] J Biol Chem. 1998 Jan 16;273(3):1288-97 [9430659.001]
  • [Cites] J Immunol. 1999 Nov 15;163(10):5617-23 [10553091.001]
  • [Cites] Lancet. 2000 May 20;355(9217):1822 [10832853.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4403-11 [10969785.001]
  • [Cites] Gastroenterology. 2000 Nov;119(5):1209-18 [11054378.001]
  • [Cites] Nucleic Acids Res. 2001 Feb 15;29(4):E21 [11160941.001]
  • [Cites] J Biol Chem. 2001 Oct 26;276(43):39713-20 [11500489.001]
  • (PMID = 17965935.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI042855-03; United States / NIAID NIH HHS / AI / R01 AI044063; United States / NIAID NIH HHS / AI / AI44063
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Pyrrolidines; 0 / Sesquiterpenes; 0 / Thiocarbamates; 25769-03-3 / pyrrolidine dithiocarbamic acid; 2RDB26I5ZB / parthenolide; 99Z2744345 / Ditiocarb; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS365443; NLM/ PMC3320112
  •  go-up   go-down


31. Schmid C, Weisser M, Ledderose G, Stötzer O, Schleuning M, Kolb HJ: [Dose-reduced conditioning before allogeneic stem cell transplantation: principles, clinical protocols and preliminary results]. Dtsch Med Wochenschr; 2002 Oct 18;127(42):2186-92
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Dose-reduced conditioning before allogeneic stem cell transplantation: principles, clinical protocols and preliminary results].
  • BACKGROUND AND OBJECTIVE: In the treatment of leukemia by stem cell transplantation, the immunological effects of allogeneic T-lymphocytes presumably play a greater part than high-dosage total-body irradiation (TBI) and chemotherapy.
  • Using this immunological effect, attempts are currently being made to reduce the dosage of pre-treatment that is toxic to stem cell, such as TBI, thereby making transplantation available for a larger group of patients at high risk for transplantation.
  • PATIENTS AND METHODS: Elderly patients with chronic myeloid leukemia (CML) have an increased transplantation risk.
  • Patients with advanced and refractory myeloid leukemia were treated with chemotherapy and dose-reduced TBI (FLAMSA protocol; n = 54).
  • RESULTS: All three protocols of TBI gave results that were not worse than those of previous studies.
  • Relapse ocurred not more frequently in patients with CML.
  • Autologous-allogeneic tandem transplantation was well tolerated and led to a good response in all patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Multiple Myeloma / therapy. Stem Cell Transplantation. Transplantation Conditioning / methods. Whole-Body Irradiation / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Radiotherapy Dosage. Survival Rate. Treatment Outcome


32. Chan WI, Huntly BJ: Leukemia stem cells in acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):326-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia stem cells in acute myeloid leukemia.
  • At the apex of these hierarchies sit so-called cancer stem cells or cancer-initiating cells, which are wholly responsible for the continued growth and propagation of the tumor.
  • The first such cancer stem cells were described in acute myeloid leukemia (AML).
  • Following treatment, the majority of tumors, including leukemias, initially respond.
  • A likely explanation for this is that leukemia stem cells are relatively insensitive to current therapies and that tumor bulk reduction reflects the death of leukemic blasts that lack tumor initiation potential.
  • This review will focus on what is known of the molecular and cellular biology of the leukemia stem cell and the leukemia stem cell niche in AML and then will identify molecular pathways critical for leukemia stem cells.
  • Finally, we will identify current and prospective therapeutic targets to facilitate eradication of leukemia stem cells.
  • It is hoped that, in defining the biology of cancer stem cells and how they differ from their adult tissue stem cell counterpart, we should identify therapeutic targets to improve treatment outcomes in leukemia and other malignant diseases.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Apoptosis. Cell Differentiation. Cell Lineage. Drug Delivery Systems. Humans. Signal Transduction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18692683.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/187
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 64
  •  go-up   go-down


33. Shouldice E, Fernandez C, McCully B, Schmidt M, Fraser R, Cook C: Voriconazole treatment of presumptive disseminated Aspergillus infection in a child with acute leukemia. J Pediatr Hematol Oncol; 2003 Sep;25(9):732-4
Hazardous Substances Data Bank. AMPHOTERICIN B .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Voriconazole treatment of presumptive disseminated Aspergillus infection in a child with acute leukemia.
  • The authors describe a pediatric patient receiving chemotherapy for acute undifferentiated leukemia who developed presumptive Aspergillus species infection disseminated to lung, liver, spleen, and bone.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Leukemia / complications. Pyrimidines / therapeutic use. Triazoles / therapeutic use
  • [MeSH-minor] Acute Disease. Adolescent. Amphotericin B / administration & dosage. Amphotericin B / therapeutic use. Combined Modality Therapy. Debridement. Drug Therapy, Combination. Female. Hepatitis / drug therapy. Hepatitis / microbiology. Humans. Lung Diseases, Fungal / drug therapy. Opportunistic Infections / drug therapy. Osteomyelitis / drug therapy. Osteomyelitis / microbiology. Osteomyelitis / surgery. Remission Induction. Sacroiliac Joint / microbiology. Sacroiliac Joint / surgery. Splenic Diseases / drug therapy. Splenic Diseases / microbiology. Voriconazole

  • MedlinePlus Health Information. consumer health - Aspergillosis.
  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12972810.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; JFU09I87TR / Voriconazole
  •  go-up   go-down


34. Attar EC, De Angelo DJ, Supko JG, D'Amato F, Zahrieh D, Sirulnik A, Wadleigh M, Ballen KK, McAfee S, Miller KB, Levine J, Galinsky I, Trehu EG, Schenkein D, Neuberg D, Stone RM, Amrein PC: Phase I and pharmacokinetic study of bortezomib in combination with idarubicin and cytarabine in patients with acute myelogenous leukemia. Clin Cancer Res; 2008 Mar 1;14(5):1446-54
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacokinetic study of bortezomib in combination with idarubicin and cytarabine in patients with acute myelogenous leukemia.
  • PURPOSE: Proteasome inhibition results in cytotoxicity to the leukemia stem cell in vitro.
  • We conducted this phase I study to determine if the proteasome inhibitor bortezomib could be safely added to induction chemotherapy in patients with acute myelogenous leukemia (AML).
  • Pharmacokinetic studies revealed that the total body clearance of bortezomib decreased significantly (P < 0.01, N = 26) between the first (mean +/- SD, 41.9 +/- 17.1 L/h/m(2)) and third (18.4 +/- 7.0 L/h/m(2)) doses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor. Boronic Acids / administration & dosage. Bortezomib. Cohort Studies. Cytarabine / administration & dosage. Female. Gene Expression Profiling. Humans. Idarubicin / administration & dosage. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Oligonucleotide Array Sequence Analysis. Pyrazines / administration & dosage. Tissue Distribution. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18316568.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / Pyrazines; 04079A1RDZ / Cytarabine; 69G8BD63PP / Bortezomib; ZRP63D75JW / Idarubicin
  •  go-up   go-down


35. van Gosliga D, Schepers H, Rizo A, van der Kolk D, Vellenga E, Schuringa JJ: Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells. Exp Hematol; 2007 Oct;35(10):1538-49
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells.
  • OBJECTIVE: With the emergence of the concept of the leukemia stem cell, assays to study them remain pivotal in understanding (leukemic) stem cell biology.
  • METHODS: We have cultured acute myeloid leukemia CD34(+) cells on bone marrow stroma.
  • RESULTS: A strong expansion was observed in about 75% of the acute myeloid leukemia cases (n = 30) and long-term cultures could be maintained for up to 24 weeks on MS5 bone marrow stromal cells.
  • Self-renewal within these L-CAs was determined by sequential passaging of these L-CAs onto new MS5 stromal layers, which resulted in the generation of second, third, and fourth L-CAs, which were able to sustain long-term expansion and generated high numbers of immature undifferentiated suspension cells.
  • CONCLUSION: We present a novel long-term leukemic stem/progenitor assay in which new drugs can be tested and in which genes can be overexpressed or downmodulated using a lentiviral approach in order to obtain more insight into the process of leukemic transformation and self-renewal.
  • [MeSH-major] Bone Marrow Cells / pathology. Cell Line, Tumor / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Tumor Stem Cell Assay
  • [MeSH-minor] Antigens, CD34. Gene Expression Regulation, Leukemic. Homeodomain Proteins / biosynthesis. Humans. Neoplasm Proteins / biosynthesis. Nuclear Proteins / biosynthesis. Polycomb Repressive Complex 1. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis. Stromal Cells / metabolism. Stromal Cells / pathology. Time Factors

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17889721.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
  •  go-up   go-down


36. Escobar MA, Hoelz DJ, Sandoval JA, Hickey RJ, Grosfeld JL, Malkas LH: Profiling of nuclear extract proteins from human neuroblastoma cell lines: the search for fingerprints. J Pediatr Surg; 2005 Feb;40(2):349-58
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Profiling of nuclear extract proteins from human neuroblastoma cell lines: the search for fingerprints.
  • PURPOSE: Neuroblastoma (NB) commonly presents with advanced disease at diagnosis and is associated with poor survival.
  • METHODS: Three different human NB cell lines SK-N-AS, SK-N-DZ, and SK-N-FI were subjected to series of biochemical fractionation steps to extract nuclear proteins.
  • These proteins were analyzed for differential expression by 2-dimensional polyacrylamide gel electrophoresis.
  • RESULTS: Multiple proteins were identified in these human NB cell lines including SET (a ubiquitous nuclear protein), stathmin (a cytosolic signal transduction protein), and grp94 (a heat shock protein).
  • SET is a putative oncogene associated with the chromosomal translocation (6;9) leading to acute undifferentiated leukemia.
  • The first protein has not been previously associated with NB.
  • CONCLUSIONS: The identification of these 3 previously unrecognized cancer-related potential biomarkers in human NB cell lines may prove useful in developing diagnostic tests.
  • The proteomic methodology of 2-dimensional polyacrylamide gel electrophoresis/mass spectrometry also provides an improved opportunity to understand the natural history of NB and develop novel chemotherapeutic agents for this prevalent childhood malignancy with a dismal outcome.
  • [MeSH-major] Biomarkers, Tumor / analysis. Neuroblastoma / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Chromatography, Liquid. Chromosomal Proteins, Non-Histone / analysis. DNA Fingerprinting. Electrophoresis, Gel, Two-Dimensional. Gene Expression Profiling. HSP70 Heat-Shock Proteins / analysis. Histone Chaperones. Humans. Mass Spectrometry / methods. Membrane Proteins / analysis. Proteomics / methods. Stathmin / analysis. Transcription Factors / analysis

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • 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 = 15750928.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA57350; United States / NCI NIH HHS / CA / CA83199
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromosomal Proteins, Non-Histone; 0 / HSP70 Heat-Shock Proteins; 0 / Histone Chaperones; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / SET protein, human; 0 / Stathmin; 0 / Transcription Factors; 0 / glucose-regulated proteins
  •  go-up   go-down


37. Miller DR: A tribute to Sidney Farber-- the father of modern chemotherapy. Br J Haematol; 2006 Jul;134(1):20-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • He recognised that folic acid stimulated leukaemic cell growth and enhanced disease progression.
  • His landmark study, published in 1948, demonstrated that a number of folic acid antagonists, including 4-aminopteroyl-glutamic acid (aminopterin) produced temporary remissions in children with acute undifferentiated leukaemia.
  • These observations lead to the development and use of other chemotherapeutic agents, either singly or, more effectively, in combination for treating childhood and adult malignancies.
  • [MeSH-major] Hematology / history
  • [MeSH-minor] History, 20th Century. Humans. Leukemia / drug therapy. United States

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16803563.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Biography; Historical Article; Journal Article
  • [Publication-country] England
  • [Personal-name-as-subject] Farber S
  •  go-up   go-down


38. Oh SH, Park TS, Cho SY, Kim MJ, Huh J, Kim B, Song SA, Lee JY, Jun KR, Shin JH, Kim HR, Lee JN: Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature. Cancer Genet Cytogenet; 2010 Oct 1;202(1):43-6
Hazardous Substances Data Bank. DAUNORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature.
  • Translocation (10;17)(p13-15;q12-21) in acute leukemia is rarely reported in the literature.
  • Here, we present both a novel t(10;17) case study and a review of relevant literature on t(10;17) in acute leukemia (10 cases).
  • In summary, we came to the following preliminary conclusions: t(10;17) is associated with poorly differentiated acute leukemia subtype [90%; eight cases of acute myeloid leukemia (AML M0, M1) and one case of acute undifferentiated leukemia], phagocytic activity by blasts occurs (30%), and the survival time was short in three of the seven t(10;17) cases for whom follow-up data were available (median, 8 months).
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 17. Leukemia / drug therapy. Leukemia / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804920.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 1.11.1.7 / Peroxidase; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


39. Wang J, Zhao HP, Lin G, Xie CQ, Nie DS, Wang QR, Lu GX: In vitro hematopoietic differentiation of human embryonic stem cells induced by co-culture with human bone marrow stromal cells and low dose cytokines. Cell Biol Int; 2005 Aug;29(8):654-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro hematopoietic differentiation of human embryonic stem cells induced by co-culture with human bone marrow stromal cells and low dose cytokines.
  • Human embryonic stem (hES) cells randomly differentiate into multiple cell types during embryoid body (EB) development and limited studies have focused on directed hematopoietic differentiation.
  • Here, we report that the treatment of hES cells during EBs development with a combination of low dose hematopoietic cytokines, including stem cell factor (SCF), Flt-3 ligand, vascular endothelial growth factor (VEGF) and human bone marrow stromal cells (hBMSCs), generated cell clusters that contained 8.81% KDR-positive hemangioblasts, 9.94% CD34-positive hematopoietic stem cells and 25.7% CD45-positive mature hematopoietic cells, and expressed hematopoietic genes such as KDR, stem cell leukemia (scl) and runt-related transcription factor 1 (Runx1).
  • [MeSH-major] Bone Marrow Cells / physiology. Cell Differentiation / drug effects. Cytokines / pharmacology. Embryo, Mammalian / cytology. Hematopoietic Stem Cells / cytology. Stem Cells / cytology. Stromal Cells / physiology
  • [MeSH-minor] Antigens, CD / metabolism. Basic Helix-Loop-Helix Transcription Factors. Biomarkers / metabolism. Cell Lineage. Coculture Techniques. Colony-Forming Units Assay. Core Binding Factor Alpha 2 Subunit. DNA-Binding Proteins / metabolism. Dose-Response Relationship, Drug. Fetus. Flow Cytometry. Humans. Proto-Oncogene Proteins / metabolism. Stem Cell Factor / metabolism. Transcription Factors / metabolism. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15950498.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Stem Cell Factor; 0 / Transcription Factors; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 135471-20-4 / TAL1 protein, human
  •  go-up   go-down


40. Grigg A, Kannan K, Schwarer AP, Spencer A, Szer J: Chemotherapy and granulocyte colony stimulating factor-mobilized blood cell infusion followed by interferon-alpha for relapsed malignancy after allogeneic bone marrow transplantation. Intern Med J; 2001 Jan-Feb;31(1):15-22
MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy and granulocyte colony stimulating factor-mobilized blood cell infusion followed by interferon-alpha for relapsed malignancy after allogeneic bone marrow transplantation.
  • This property may also be used to enhance a graft-versus-leukaemia effect (GVL) after donor leucocyte infusion (DLI), a mode of therapy increasingly offered to patients relapsing after allo BMT.
  • AIM: The aims of the present study were to examine the efficacy and toxicity of IFN therapy administered after granulocyte colony-stimulating factor (G-CSF)-stimulated blood cells given as DLI in patients with acute myeloid leukaemia (AML), chronic myeloid leukaemia (CML), acute lymphoblastic leukaemia (ALL), acute undifferentiated leukaemia (AUL) and multiple myeloma relapsing after allo BMT.
  • METHODS: Between October 1996 and September 1999, 27 patients (16 AML, four ALL, three CML, three multiple myeloma, one AUL) who relapsed after allo BMT were treated with chemotherapy followed by DLI, collected after G-CSF stimulation in all but two cases.
  • RESULTS: Eighteen patients received IFN following DLI, 14 of whom developed significant GVHD (grade II-IV acute or extensive chronic); thereafter, GVHD resolved with cessation of IFN alone in four patients, but 10 required systemic immunosuppression.
  • [MeSH-minor] Acute Disease. Adult. Female. Graft vs Host Disease / etiology. Graft vs Leukemia Effect / drug effects. Humans. Leukemia / drug therapy. Leukemia / therapy. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / therapy. Male. Middle Aged. Multiple Myeloma / etiology. Remission Induction. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11478351.001).
  • [ISSN] 1444-0903
  • [Journal-full-title] Internal medicine journal
  • [ISO-abbreviation] Intern Med J
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Interferon-alpha; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


41. Hashmi KU, Khan B, Ahmed P, Raza S, Hussain I, Mahmood A, Iqbal H, Malik HS, Anwar M: FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study. J Pak Med Assoc; 2005 Jun;55(6):234-8
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study.
  • OBJECTIVE: To evaluate the efficacy and toxicity profile of the combination of fludarabine, high dose cytarabine, idarubicin, and granulocyte colony stimulating factor in refractory relapsed cases of acute leukaemia, a study is being conducted at Armed Forces Bone Marrow Transplant Centre (AFBMTC) Rawalpindi since January 2003.
  • METHODS: Twelve Patients with refractory/relapsed (Ref/Rel) acute leukaemia (AL) were treated with fludarabine 30 mg/m2 and cytosine arabinoside (AraC) Arac 2 g/m2 for 5 days, idarubicin 10 mg/m2 for 3 days, and granulocyte colony stimulating factor G-CSF 5 micro g/kg from day 0 till neutrophil recovery (ANC > 1.0 x 10(9)/1).
  • RESULTS: Patients included were refractory acute lymphoblastic leukaemia (ALL) (n=2), relapsed ALL (n = 3), refractory acute myeloid leukaemia (AML) (n = 3), secondary AML (n=2) relapsed AML (n = 1) and acute undifferentiated leukaemia (AUL) (n = 1).
  • Out of 8 patients who achieved CR, 4 underwent allogeneic bone marrow transfusion (BMT), 1 is being evaluated for the same, 1 received idorubicin, AraC and etopuside (ICE) and high dose AraC, 1 did not receive further chemotherapy and 1 relapsed two months after remission.
  • CONCLUSION: In our experience, FLAG-IDA is well tolerated and effective regimen in relapsed/refractory acute leukaemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Child. Cytarabine / therapeutic use. Female. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / therapeutic use. Male. Middle Aged. Recurrence

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16045091.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
  •  go-up   go-down


42. Funke I, Wiesneth M, Platow S, Kubanek B: Palliative cytoreduction in refractory acute leukemia: a retrospective study of 57 adult patients. Ann Hematol; 2000 Mar;79(3):132-7
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Palliative cytoreduction in refractory acute leukemia: a retrospective study of 57 adult patients.
  • The efficiency and toxicity of treatment regimens for nonintensive cytoreduction in 57 outpatients with refractory acute leukemia (mean age 56 years, 51 AML, six ALL/AUL) were retrospectively studied.
  • The median leukocyte count was higher for M (73 x 10(9)/l) than for the other treatment regimens (T: 27 x 10(9)/l, T+ C: 37 x 10(9)/l, MP: 24 x 10(9)/l, MP + MTX: 30 x 10(9)/l, E: 31 x 10(9)/l).
  • E led to stomatitis (WHO 1,2) in 4/5 and M to nausea/vomiting (WHO 1,2) in 5/22 and to stomatitis (WHO 2) in 4/22 cases.
  • Palliative cytoreductive therapy does not reduce the quality of life and can prevent complications of significant leukocytosis in refractory acute leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy. Palliative Care
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. 6-Mercaptopurine / adverse effects. Acute Disease. Administration, Oral. Adult. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Cytarabine / toxicity. Diarrhea / chemically induced. Female. Humans. Injections, Intravenous. Injections, Subcutaneous. Leukocyte Count / drug effects. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Middle Aged. Nausea / chemically induced. Retrospective Studies. Stomatitis / chemically induced. Thioguanine / administration & dosage. Thioguanine / toxicity

  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Palliative Care.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10803935.001).
  • [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] 04079A1RDZ / Cytarabine; E7WED276I5 / 6-Mercaptopurine; FTK8U1GZNX / Thioguanine; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


43. Afkir S, Nguelefack TB, Aziz M, Zoheir J, Cuisinaud G, Bnouham M, Mekhfi H, Legssyer A, Lahlou S, Ziyyat A: Arbutus unedo prevents cardiovascular and morphological alterations in L-NAME-induced hypertensive rats Part I: cardiovascular and renal hemodynamic effects of Arbutus unedo in L-NAME-induced hypertensive rats. J Ethnopharmacol; 2008 Mar 5;116(2):288-95
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of the present study was to investigate whether chronic treatment with Arbutus unedo leaf (AuL) or root (AuR) aqueous extracts can prevent these alterations.
  • Six groups of rats were used: control group received tap water; N(G)-nitro-l-arginine methyl-ester (L-NAME) group treated with L-NAME at 40 mg/kg/day; AuL and AuR groups received simultaneously L-NAME (40 mg/kg/day) and Au leaves or roots extract at the same concentration 250 mg/kg/day; l-arginine and enalapril groups received simultaneously L-NAME (40 mg/kg/day) and l-arginine at 50mg/kg/day or enalapril at 15 mg/kg/day.
  • Treatment of rats during 4 weeks with L-NAME caused an increase of the systolic blood pressure (SBP) accompanied by a ventricular hypertrophy, an impairment of endothelium-dependent vasorelaxation, an increase of the cardiac baroreflex sensitivity and a decrease of water, sodium and potassium excretion.
  • The co-administration of AuL or AuR extracts with L-NAME reduces the development of increased SBP, ameliorates the vascular reactivity as well as the baroreflex sensitivity and normalizes the renal function.
  • AuR reduces the ventricular hypertrophy but AuL do not.
  • [MeSH-major] Ericaceae / chemistry. Hemodynamics / drug effects. Hypertension / prevention & control. NG-Nitroarginine Methyl Ester / administration & dosage. Plant Extracts / pharmacology
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Body Weight / drug effects. In Vitro Techniques. Organ Size / drug effects. Rats. Rats, Wistar

  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18191352.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Plant Extracts; V55S2QJN2X / NG-Nitroarginine Methyl Ester
  •  go-up   go-down


44. Rodríguez-Rodríguez CE, Marco-Urrea E, Caminal G: Degradation of naproxen and carbamazepine in spiked sludge by slurry and solid-phase Trametes versicolor systems. Bioresour Technol; 2010 Apr;101(7):2259-66
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Detectable laccase activity levels were found in the 10 and 25%-cultures (up to 1308 and 2588 AUL(-1), respectively) while it was negligible in the 38%-culture.
  • Results showed that T. versicolor may be an interesting bioremediation agent for elimination of emerging pollutants in sewage sludge.

  • Hazardous Substances Data Bank. NAPROXEN .
  • Hazardous Substances Data Bank. CARBAMAZEPINE .
  • Hazardous Substances Data Bank. GLUCOSE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031398.001).
  • [ISSN] 1873-2976
  • [Journal-full-title] Bioresource technology
  • [ISO-abbreviation] Bioresour. Technol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Sewage; 33CM23913M / Carbamazepine; 57Y76R9ATQ / Naproxen; EC 1.10.3.2 / Laccase; IY9XDZ35W2 / Glucose
  •  go-up   go-down


45. Rossi S, Canal F, Licci S, Zanatta L, Laurino L, Gottardi M, Gherlinzoni F, Dei Tos AP: Cytogenetic evidence of metastatic myxoid liposarcoma and therapy-related myelodysplastic syndrome in a bone marrow biopsy. Hum Pathol; 2009 Jul;40(7):1040-4
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We describe an exceptional case of metastatic myxoid liposarcoma of the spine associated with therapy-related refractory anemia with excess of blasts in a 37-year-old woman who underwent multi-agent chemotherapy for a myxoid liposarcoma of the left thigh.
  • Microscopic examination of the bone marrow biopsy revealed dysplastic features, with abnormal localization of immature precursors and micromegakaryocytes, and islands of undifferentiated oval small/medium-size cells, suggestive of acute myeloid leukemia arising in the setting of a myelodysplastic syndrome.
  • Immunohistochemistry was not discriminant.
  • Cytogenetic analyses of bone marrow aspirate disclosed the presence of 2 different rearrangements, subsequently confirmed by fluorescent in situ hybridization and was crucial in making the correct diagnosis.
  • [MeSH-minor] Adult. Anemia, Refractory / pathology. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Cells / pathology. Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Female. Humans. Leukemia, Myeloid, Acute / pathology. Soft Tissue Neoplasms / pathology. Thigh / pathology


46. Eiter LC, Hall NW, Day CS, Saluta G, Kucera GL, Bierbach U: Gold(I) analogues of a platinum-acridine antitumor agent are only moderately cytotoxic but show potent activity against Mycobacterium tuberculosis. J Med Chem; 2009 Nov 12;52(21):6519-22
Hazardous Substances Data Bank. GOLD, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gold(I) analogues of a platinum-acridine antitumor agent are only moderately cytotoxic but show potent activity against Mycobacterium tuberculosis.
  • Cationic gold(I) complexes containing 1-[2-(acridin-9-ylamino)ethyl]-1,3-dimethylthiourea (1), [AuL(1)](n+) (where L is Cl(-), Br(-), SCN(-), PEt(3), PPh(3), or 1), derived from a class of analogous platinum(II) antitumor agents, have been synthesized.
  • Unlike platinum, gold does not form permanent adducts with DNA, and its complexes are 2 orders of magnitude less cytotoxic in non-small-cell lung cancer cells than the most active platinum-based agent.

  • Genetic Alliance. consumer health - Tuberculosis.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. UREA .
  • Hazardous Substances Data Bank. THIOUREA .
  • Hazardous Substances Data Bank. PLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Med Chem. 2001 Dec 6;44(25):4492-6 [11728195.001]
  • [Cites] J Med Chem. 2008 Dec 11;51(23):7574-80 [19012390.001]
  • [Cites] J Hist Med Allied Sci. 2004 Jan;59(1):50-89 [15011812.001]
  • [Cites] J Biol Inorg Chem. 2004 Jun;9(4):453-61 [15067524.001]
  • [Cites] J Inorg Biochem. 1984 May;21(1):21-9 [6547163.001]
  • [Cites] Biochem Pharmacol. 1986 May 1;35(9):1427-33 [3707609.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 Oct;56(4):337-43 [15895232.001]
  • [Cites] J Med Chem. 2006 Jun 1;49(11):3204-14 [16722638.001]
  • [Cites] J Med Chem. 2006 Jun 29;49(13):3933-7 [16789749.001]
  • [Cites] Dalton Trans. 2006 Aug 14;(30):3708-15 [16865184.001]
  • [Cites] J Med Chem. 2007 May 3;50(9):2259-63 [17408248.001]
  • [Cites] Nat Rev Cancer. 2007 Aug;7(8):573-84 [17625587.001]
  • [Cites] J Inorg Biochem. 2008 Mar;102(3):555-63 [18164406.001]
  • [Cites] J Am Chem Soc. 2008 Sep 24;130(38):12570-1 [18729360.001]
  • [Cites] Science. 2008 Sep 19;321(5896):1644-5 [18801989.001]
  • [Cites] J Med Chem. 2009 Feb 12;52(3):763-70 [19123857.001]
  • [Cites] Biochem Pharmacol. 2002 Jul 15;64(2):191-200 [12123739.001]
  • (PMID = 19803526.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101880-06; United States / NCI NIH HHS / CA / R01 CA101880; United States / NCI NIH HHS / CA / CA101880; United States / NCI NIH HHS / CA / R01 CA101880-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(2-(acridin-9-ylamino)ethyl)-1,3-dimethylthiourea; 0 / Acridines; 0 / Antineoplastic Agents; 0 / Antitubercular Agents; 0 / Chelating Agents; 0 / Coordination Complexes; 0 / DNA Adducts; 0 / DNA, Bacterial; 0 / Ligands; 0 / Organogold Compounds; 49DFR088MY / Platinum; 7440-57-5 / Gold; 8W8T17847W / Urea; GYV9AM2QAG / Thiourea
  • [Other-IDs] NLM/ NIHMS150910; NLM/ PMC3176588
  •  go-up   go-down


47. Estrov Z: The leukemia stem cell. Cancer Treat Res; 2010;145:1-17
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The leukemia stem cell.
  • [MeSH-major] Leukemia / pathology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Differentiation. Cell Transformation, Neoplastic. Clone Cells / cytology. Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / cytology. Humans. Leukemia, Myeloid, Acute / pathology. Mice. Mice, Inbred NOD. Mice, SCID. Mice, Transgenic. Models, Biological. Recurrence. Transcription Factors / physiology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20306242.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors
  • [Number-of-references] 125
  •  go-up   go-down






Advertisement