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1. Möhle R, Schittenhelm M, Failenschmid C, Bautz F, Kratz-Albers K, Serve H, Brugger W, Kanz L: Functional response of leukaemic blasts to stromal cell-derived factor-1 correlates with preferential expression of the chemokine receptor CXCR4 in acute myelomonocytic and lymphoblastic leukaemia. Br J Haematol; 2000 Sep;110(3):563-72
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  • [Title] Functional response of leukaemic blasts to stromal cell-derived factor-1 correlates with preferential expression of the chemokine receptor CXCR4 in acute myelomonocytic and lymphoblastic leukaemia.
  • We analysed SDF-1-induced intracellular calcium fluxes in leukaemic blasts from the peripheral blood of patients with newly diagnosed acute myeloid leukaemia (AML) and lymphoblastic leukaemia (B-lineage ALL), determined the effect of BM stromal cell-conditioned medium on in vitro transendothelial migration (TM) and measured expression of the SDF-1 receptor, CXCR4, by flow cytometry.
  • M3 and M4 blasts with eosinophilia (M4eo) showed intermediate activity and M6 blasts showed no functional activity.
  • Accordingly, expression of CXCR4 was low in undifferentiated (M0) AML, myeloid (M1/2) AML and erythroid (M6) AML, but high [mean fluorescence (MF) > 50] in promyelocytic (M3) AML, myelomonocytic (M4/5) AML and B-lineage ALL.
  • [MeSH-major] Chemokines, CXC / pharmacology. Leukemia, Myelomonocytic, Acute / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, CXCR4 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Calcium / metabolism. Cell Movement / drug effects. Cells, Cultured. Chemokine CXCL12. Female. Humans. Male. Middle Aged

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  • (PMID = 10997965.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Receptors, CXCR4; SY7Q814VUP / Calcium
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2. Dbaibo GS, Kfoury Y, Darwiche N, Panjarian S, Kozhaya L, Nasr R, Abdallah M, Hermine O, El-Sabban M, de Thé H, Bazarbachi A: Arsenic trioxide induces accumulation of cytotoxic levels of ceramide in acute promyelocytic leukemia and adult T-cell leukemia/lymphoma cells through de novo ceramide synthesis and inhibition of glucosylceramide synthase activity. Haematologica; 2007 Jun;92(6):753-62
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  • [Title] Arsenic trioxide induces accumulation of cytotoxic levels of ceramide in acute promyelocytic leukemia and adult T-cell leukemia/lymphoma cells through de novo ceramide synthesis and inhibition of glucosylceramide synthase activity.
  • BACKGROUND AND OBJECTIVES: Arsenic trioxide (ATO) is an effective treatment for acute promyelocytic leukemia (APL) and potentially for human T-cell leukemia virus type I (HTLV-I) associated adult T-cell leukemia/lymphoma (ATL).
  • Many cytotoxic drugs induce apoptosis through the generation and accumulation of the sphingolipid breakdown product, ceramide, a coordinator of the cellular response to stress.
  • We, therefore, investigated the contribution of ceramide to the mechanism of action of ATO in APL and ATL.
  • DESIGN AND METHODS: A human APL-derived cell line (NB4), various ATL-derived lines and an HTLV-I-negative malignant T-cell line were cultured and treated with ATO.
  • Measurements were made of ceramide, diacylglycerol, sphingomyelinase activity, sphingomyelin mass, glucosylceramide synthase activity and the de novo ceramide synthesis.
  • RESULTS: Treatment of APL and ATL-derived cells with a clinically achievable concentration of ATO induced accumulation of cytotoxic levels of ceramide.
  • The effects of ATO on ceramide levels in APL cells were more potent than those of all-trans retinoic acid (ATRA).
  • In contrast to the effect of ATRA, ATO-induced ceramide accumulation was not due to induction of acidic sphingomyelinase, but rather resulted from both de novo ceramide synthesis and inhibition of glucosylceramide synthase activity.
  • Interestingly, the effects of ATO on de novo ceramide synthesis were similar in APL and ATL-derived cells despite the defective pathway in ATL cells.
  • INTERPRETATION AND CONCLUSIONS: These results indicate that ATO-induced ceramide accumulation may represent a general mediator of the effects of ATO, which paves the way for new therapeutic interventions that target the metabolic pathway of this important sphingolipid secondary messenger.
  • [MeSH-major] Arsenicals / pharmacology. Ceramides / biosynthesis. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Oxides / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Glucosyltransferases / antagonists & inhibitors. Humans. Metabolic Networks and Pathways / drug effects

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  • (PMID = 17550847.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Ceramides; 0 / Oxides; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase; S7V92P67HO / arsenic trioxide
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3. Puga BL, Cabrera ME, Undurraga MS, Etcheverry R, Vacarezza R, Ducach G, Toledo H: [Acute myeloid leukemia in the adult. Results of the National Antineoplastic Drug Protocol at the Hospital del Salvador, 1990-1998]. Rev Med Chil; 2000 Nov;128(11):1191-8
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  • [Title] [Acute myeloid leukemia in the adult. Results of the National Antineoplastic Drug Protocol at the Hospital del Salvador, 1990-1998].
  • [Transliterated title] Leucemia mieloide aguda del adulto. Resultados del Protocolo Nacional de Drogas Antineoplásica. Hospital del Salvador 1990-1998.
  • BACKGROUND: The incidence of acute myeloid leukemia is 3 cases per 100,000 inhabitants/year and its five years event free survival is 15 to 20%.
  • Since the incorporation of trans retinoic acid, event free survival of M3 acute myeloid leukemia is 80%.
  • AIM: To report the results of acute myeloid leukemia treatment at the Hospital del Salvador, between 1990 and 1998.
  • RESULTS: Sixteen percent of patients had M3 acute myeloid leukemia.
  • DR and CD34 were negative in seven of nine patients with M3 acute myeloid leukemia.
  • In M3 acute myeloid leukemia, the figure is 50%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Chemotherapy, Adjuvant. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease-Free Survival. Female. Humans. Idarubicin / therapeutic use. Immunophenotyping. Male. Middle Aged. Mitoxantrone / therapeutic use. Prognosis. Retrospective Studies. Treatment Outcome

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  • (PMID = 11347505.001).
  • [ISSN] 0034-9887
  • [Journal-full-title] Revista médica de Chile
  • [ISO-abbreviation] Rev Med Chil
  • [Language] spa
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Chile
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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4. Lehmann S, Bengtzen S, Broberg U, Paul C: Effects of retinoids on cell toxicity and apoptosis in leukemic blast cells from patients with non-M3 AML. Leuk Res; 2000 Jan;24(1):19-25
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  • [Title] Effects of retinoids on cell toxicity and apoptosis in leukemic blast cells from patients with non-M3 AML.
  • All-trans retinoic acid (ATRA) induces complete remission in acute promyelocytic leukemia (APL or M3).
  • In this study we measured the effect of retinoids alone and in combination with daunorubicin (DNR) on cell growth and apoptosis in blast cells from patients with non-M3 AML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Hematopoietic Stem Cells / drug effects. Leukemia, Myeloid / pathology. Neoplastic Stem Cells / drug effects. Tretinoin / pharmacology
  • [MeSH-minor] Acute Disease. Adenosine Triphosphate / analysis. Adult. Aged. Aged, 80 and over. Antibiotics, Antineoplastic / pharmacology. Antigens, CD34 / analysis. Daunorubicin / pharmacology. Drug Synergism. Female. Humans. Male. Middle Aged. Tumor Cells, Cultured / drug effects

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  • (PMID = 10634641.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin; 8L70Q75FXE / Adenosine Triphosphate; ZS7284E0ZP / Daunorubicin
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5. Zhang XH, Hu Y, Bao L, Jiang Q, Yang LH, Lu XJ, Hong M, Xia LH, Guo T, Shen GX, Zhu HH, Zhao T, Song SJ: Arsenic trioxide downregulates the expression of annexin II in bone marrow cells from patients with acute myelogenous leukemia. Chin Med J (Engl); 2009 Sep 5;122(17):1969-73
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  • [Title] Arsenic trioxide downregulates the expression of annexin II in bone marrow cells from patients with acute myelogenous leukemia.
  • BACKGROUND: Most patients with acute myelogenous leukemia (AML) suffer from disordered hemostasis.
  • We have previously shown that annexin II (Ann II), a high-affinity co-receptor for plasminogen/tissue plasminogen activator, plays a central role in primary hyperfibrinolysis in patients with acute promyelocytic leukemia (APL).
  • RESULTS: Before As2O3 treatment, Ann II mRNA expression (real-time PCR) was the highest in M3 cells (P < 0.05), higher in M5 cells than that in M1, M2, M4, and M6 cells (P < 0.001), and positively correlated with Ann II protein expression (flow cytometry) (r = 0.752, P < 0.01).
  • Exposure for up to 120 hours to As2O3 (1 micromol/L) had no significant effect on Ann II protein in M1 and M2 leukemic cells, but decreased Ann II protein expression twofold within 48 hours of exposure in M3 cells (P < 0.05) and twofold within 96 hours in M5 cells (P < 0.05).
  • The rate of plasmin generation was higher in APL, M5, and M4 cells than in M1, M2, and M6 cells.
  • Furthermore, As2O3 affects more than one form of AML (APL, M4 and M5), suggesting its potential role in their management.
  • [MeSH-major] Annexin A2 / metabolism. Arsenicals / pharmacology. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Down-Regulation / drug effects. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Adult. Cell Survival / drug effects. Cells, Cultured. Female. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19781379.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Annexin A2; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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6. Lehmann S, Paul C, Törmä H: Retinoid receptor expression and its correlation to retinoid sensitivity in non-M3 acute myeloid leukemia blast cells. Clin Cancer Res; 2001 Feb;7(2):367-73
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  • [Title] Retinoid receptor expression and its correlation to retinoid sensitivity in non-M3 acute myeloid leukemia blast cells.
  • All-trans-retinoic acid (ATRA) has significantly improved the treatment results in acute promyelocytic leukemia (M3).
  • In non-M3 acute myeloid leukemia (AML), the effects are less clear, and there is a pronounced heterogeneity in the sensitivity to the growth-inhibitory effects of retinoids in leukemic cells from different non-M3 AML patients.
  • In this study, we determined the expression of RAR alpha, RAR beta, RAR gamma, and RXR alpha by real-time PCR in four cell lines and in blast cells from patients with non-M3 AML before and after ATRA incubation.
  • We conclude that RAR alpha, RAR beta, RAR gamma, and RXR alpha are expressed in non-M3 AML blast cells and that ATRA-induced expression of RAR beta may be a marker for retinoid sensitivity.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Receptors, Retinoic Acid / genetics. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD14 / metabolism. Cell Division / drug effects. Cell Transformation, Neoplastic / drug effects. DNA Primers / chemistry. Dose-Response Relationship, Drug. Female. Gene Expression. Humans. Male. Middle Aged. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. Transcription, Genetic / drug effects

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  • (PMID = 11234892.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 5688UTC01R / Tretinoin
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7. Sato Y, Izumi T, Kanamori H, Davis EM, Miura Y, Larson RA, Le Beau MM, Ozawa K, Rowley JD: t(1;3)(p36;p21) is a recurring therapy-related translocation. Genes Chromosomes Cancer; 2002 Jun;34(2):186-92
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  • Chromosome bands 1p36 and 3p21 are known to be recurring breakpoints in therapy-related (t-) leukemia.
  • We identified a recurring translocation, t(1;3)(p36;p21), in eight patients with various hematologic malignancies: three patients with ALL, one with chronic myelogenous leukemia (CML) in accelerated phase (AP), two with MDS, and two with AML(M3).
  • Five of the eight patients had a history of chemotherapy, including alkylating agents in three, before the translocation was detected.
  • The results of the present study suggest that t(1;3)(p36;p21) in hematologic diseases is associated with prior exposure to mutagens, including alkylating agents.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 3 / genetics. Translocation, Genetic / drug effects. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Child. Chromosome Breakage / genetics. Chromosome Mapping / methods. Female. Humans. In Situ Hybridization, Fluorescence / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / chemically induced. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Promyelocytic, Acute / chemically induced. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Recurrence

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 11979552.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA42557
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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8. Tri NK, Xinh PT, Nagao H, Izumi T, Ozawa K, Toyoda A, Hattori M, Sakaki Y, Tokunaga K, Sato Y: Identification of the breakpoints at 1p36.2 and 3p21.3 in an AML(M3) patient who had t(1;3)(p36.2;p21.3) at the third relapse. Genes Chromosomes Cancer; 2002 Dec;35(4):365-7
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  • [Title] Identification of the breakpoints at 1p36.2 and 3p21.3 in an AML(M3) patient who had t(1;3)(p36.2;p21.3) at the third relapse.
  • Recently, we reported that a recurrent translocation, t(1;3)(p36;p21) is closely associated with prior chemotherapy including alkylating agents, assessing eight patients with various hematologic malignancies (Genes, Chromosomes and Cancer 34:186-192), 2002).
  • In this report, we identified the 1p36 and 3p21 breakpoints of an AML (M3) patient who is included in the previous patient series.
  • The patient showed t(1;3)(p36;p21) together with t(15;17) at the third relapse.
  • The patients with t(1;3)(p36;p21) should be subclassified according to the precise breakpoints or the genes involved.
  • [MeSH-major] Chromosome Breakage / genetics. Chromosome Mapping / methods. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Recurrence, Local / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Genetic Markers / genetics. Humans. Male

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12378531.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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