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1. Shu ST, Nadella MV, Dirksen WP, Fernandez SA, Thudi NK, Werbeck JL, Lairmore MD, Rosol TJ: A novel bioluminescent mouse model and effective therapy for adult T-cell leukemia/lymphoma. Cancer Res; 2007 Dec 15;67(24):11859-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel bioluminescent mouse model and effective therapy for adult T-cell leukemia/lymphoma.
  • Adult T-cell /lymphomaleukemia (ATLL) is caused by human T-cell lymphotropic virus type 1 (HTLV-1).
  • Our goal was to evaluate the effects of NF-kappaB disruption by a proteasomal inhibitor (PS-341) and osteoclastic inhibition by zoledronic acid (Zol) on the development of ATLL and HHM using a novel bioluminescent mouse model.
  • We found that PS-341 decreased cell viability, increased apoptosis, and down-regulated PTHrP expression in ATLL cells in vitro.
  • Bioluminescent imaging and tumor cell count showed a significant reduction in tumor burden in mice from all treatment groups.
  • All treatments also significantly reduced the plasma calcium concentrations.
  • Zol treatment increased trabecular bone volume and decreased osteoclast parameters.
  • Our results indicate that both PS-341 and Zol are effective treatments for ATLL and HHM, which are refractory to conventional therapy.

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  • (PMID = 18089816.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077911; United States / NCRR NIH HHS / RR / RR014324-05; United States / NCRR NIH HHS / RR / T32 RR007073-07; United States / NCRR NIH HHS / RR / RR00168; United States / NCI NIH HHS / CA / CA100730; United States / NCI NIH HHS / CA / CA100730-05; United States / NCRR NIH HHS / RR / T32 RR007073; United States / NCRR NIH HHS / RR / P51 RR000168; United States / NCRR NIH HHS / RR / RR007073; United States / NCRR NIH HHS / RR / K26 RR000168; United States / NCRR NIH HHS / RR / T32 RR007073-06; United States / NCI NIH HHS / CA / CA77911; United States / NCRR NIH HHS / RR / RR007073-06; United States / NCRR NIH HHS / RR / R01 RR014324-05; United States / NCI NIH HHS / CA / P01 CA100730-05; United States / NCRR NIH HHS / RR / RR007073-07; United States / NCI NIH HHS / CA / P01 CA100730
  • [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 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ NIHMS94364; NLM/ PMC2832603
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2. Hernandez-Ilizaliturri FJ, Reddy N, Holkova B, Ottman E, Czuczman MS: Immunomodulatory drug CC-5013 or CC-4047 and rituximab enhance antitumor activity in a severe combined immunodeficient mouse lymphoma model. Clin Cancer Res; 2005 Aug 15;11(16):5984-92
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  • [Title] Immunomodulatory drug CC-5013 or CC-4047 and rituximab enhance antitumor activity in a severe combined immunodeficient mouse lymphoma model.
  • New thalidomide derivatives CC-5013 and CC-4047 (immunomodulatory drugs, IMiD) are up to 10,000 times more potent than Thalidomide.
  • The biological effects of IMiDs are presumed to be mediated by (a) activation of some components of the innate [natural killer (NK) cells] or adoptive immune system (T cells), (b) modification of cytokine microenvironment in the tumor bed, or by (c) inhibition of angiogenesis.
  • In this article, we tested an innovative combination strategy involving rituximab and IMiDs in aggressive lymphoma cell lines and human lymphoma xenografts.
  • Treatment of non-Hodgkin's lymphoma cells with CC-5013 resulted in a 40% to 70% growth inhibition when compared with controls (P < 0.05).
  • Exposure of lymphoma cells to CC-4047 resulted in a lesser degree of growth inhibition.
  • Induction of apoptosis was shown in 10% to 26% of lymphoma cells 24 hours following exposure to either IMiD.
  • The synergistic effect between IMiDs and rituximab in our mouse model was attributed to NK cell expansion.
  • The enhancement of rituximab activity by IMiDs was abrogated by in vivo depletion of NK cells.
  • Augmenting NK cell function by CC-4047 or CC-5013 exposure may increase the antitumor effects of rituximab against B-cell lymphomas and warrants further exploration in the context of a clinical trial.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Thalidomide / therapeutic use. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / analysis. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA / biosynthesis. Drug Therapy, Combination. Female. Flow Cytometry. Humans. Immunologic Factors / pharmacology. Immunologic Factors / therapeutic use. Killer Cells, Natural / drug effects. Killer Cells, Natural / metabolism. Killer Cells, Natural / pathology. Male. Mice. Mice, SCID. Rituximab. Survival Analysis. Treatment Outcome

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  • (PMID = 16115943.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Immunologic Factors; 4F4X42SYQ6 / Rituximab; 4Z8R6ORS6L / Thalidomide; 9007-49-2 / DNA; D2UX06XLB5 / pomalidomide; F0P408N6V4 / lenalidomide
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3. Houot R, Goldstein MJ, Kohrt HE, Myklebust JH, Alizadeh AA, Lin JT, Irish JM, Torchia JA, Kolstad A, Chen L, Levy R: Therapeutic effect of CD137 immunomodulation in lymphoma and its enhancement by Treg depletion. Blood; 2009 Oct 15;114(16):3431-8
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  • [Title] Therapeutic effect of CD137 immunomodulation in lymphoma and its enhancement by Treg depletion.
  • Despite the success of passive immunotherapy with monoclonal antibodies (mAbs), many lymphoma patients eventually relapse.
  • Immunomodulating mAbs directed against immune cell targets can be used to enhance the immune response to achieve efficient antitumor immunity.
  • Anti-CD137 agonistic mAb has demonstrated antitumor efficacy in various tumor models and has now entered clinical trials for the treatment of solid tumors.
  • Here, we investigate the therapeutic potential of anti-CD137 mAb in lymphoma.
  • We found that human primary lymphoma tumors are infiltrated with CD137+ T cells.
  • We therefore hypothesized that lymphoma would be susceptible to treatment with anti-CD137 agonistic mAb.
  • Using a mouse model, we demonstrate that anti-CD137 therapy has potent antilymphoma activity in vivo.
  • The antitumor effect of anti-CD137 therapy was mediated by both natural killer (NK) and CD8 T cells and induced long-lasting immunity.
  • Moreover, the antitumor activity of anti-CD137 mAb could be further enhanced by depletion of regulatory T cell (T(regs)).
  • These results support the evaluation of anti-CD137 therapy in clinical trials for patients with lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD137 / agonists. Immunologic Factors / pharmacology. Lymphocyte Depletion. Lymphoma / drug therapy. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 19641184.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI007290; United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233; United States / NCI NIH HHS / CA / CA33399; United States / NCI NIH HHS / CA / K99 CA143231; United States / NCI NIH HHS / CA / R37 CA033399
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD137; 0 / Immunologic Factors
  • [Other-IDs] NLM/ PMC2765679
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4. Linn YC, Hui KM: Cytokine-induced killer cells: NK-like T cells with cytotolytic specificity against leukemia. Leuk Lymphoma; 2003 Sep;44(9):1457-62
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  • [Title] Cytokine-induced killer cells: NK-like T cells with cytotolytic specificity against leukemia.
  • These cells have demonstrated higher proliferative and cytolytic activities in comparison to the reported CD3-CD56+ lymphokine activated killer (LAK) cells that are essentially activated natural killer (NK) cells.
  • CIK cells are non-MHC-restricted in target cell recognition and killing.
  • At maturity, the CIK cells exhibit potent cytotoxicity against autologous AML targets as well as allogeneic myeloid leukemia cells, regardless of the HLA types of these targets.
  • This observed cytotoxicity is not entirely due to NK cells as prior pre-absorption of the NK cells cytolytic activities does not abolish the subsequent cytotolytic activities against leukemic targets.
  • It has also been reported by others that CIK cells are cytolytic against chronic myeloid leukemia (CML) cells, both in vitro and in the SCID mouse tumor model.
  • In a mouse transplant model across MHC barrier, the CIK cells generated from the donor do not induce graft vs. host disease as observed for unfractionated donor splenocytes.
  • CIK cells also express CD94, part of the NK receptor comprising of CD94-NKG2 heterodimer.
  • The characteristic biological properties of the CIK cells would, therefore, enable them to be exploited for anti-leukemic therapy.
  • [MeSH-minor] Animals. Antigens, CD3 / analysis. Antigens, CD56 / analysis. Cells, Cultured / drug effects. Cells, Cultured / immunology. Clinical Trials, Phase I as Topic. Cytotoxicity, Immunologic. Forecasting. Humans. Immunotherapy, Adoptive. Interferon-gamma / pharmacology. Interleukin-2 / pharmacology. Lymphoma / immunology. Lymphoma / therapy. Mice. Mice, SCID. Xenograft Model Antitumor Assays

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  • (PMID = 14565644.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD56; 0 / Interleukin-2; 82115-62-6 / Interferon-gamma
  • [Number-of-references] 37
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5. Flavell DJ, Warnes SL, Noss AL, Flavell SU: Anti-CD7 antibody and immunotoxin treatment of human CD7(+)T-cell leukaemia is significantly less effective in NOD/LtSz-scid mice than in CB.17 scid mice. Br J Cancer; 2000 Dec;83(12):1755-61
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  • [Title] Anti-CD7 antibody and immunotoxin treatment of human CD7(+)T-cell leukaemia is significantly less effective in NOD/LtSz-scid mice than in CB.17 scid mice.
  • Treatment of SCID-HSB-2 mice with HB2-SAPORIN led to a significant prolongation in the time to development of signs and symptoms of disease compared with PBS sham-treated controls with 80% of animals surviving disease-free.
  • In contrast treatment with HB2-F(ab)(2)-SAPORIN was significantly less effective in SCID-HSB-2 mice with 80% of animals in this treatment group developing leukaemia over the course of the study.
  • HB2 antibody treatment of SCID-HSB-2 mice also led to a significant prolongation in time to leukaemia development compared with sham-treated controls with 37% of animals in this treatment group disease-free at termination of the study.
  • In contrast HB2 antibody treatment of NOD/SCID-HSB-2 mice had no therapeutic effect in these animals and the therapeutic effectiveness of both HB2-SAPORIN and HB2-F(ab)(2)-SAPORIN ITs was similar and significantly reduced compared to the effect observed in SCID-HSB-2 mice.
  • It was initially thought that the lack of therapeutic effect of antibody and IT in NOD-SCID-HSB-2 mice might relate to their putative lack of NK cells but flow cytometric and functional studies with NOD-SCID mouse splenocytes revealed that these animals do have some functional NK cells though fewer in number and possibly lower in functionality than those of SCID mice.
  • We reason that the complete lack of therapeutic effect of HB2 antibody and the reduced effect of HB2-SAPORIN in NOD/SCID mice is due to the reduced cytolytic activity of NOD/SCID NK cells which is probably below a certain critical threshold value in these animals.
  • We conclude from this that immunotherapeutics like HB2-SAPORIN would be more accurately assessed for intrinsic potency in NOD/SCID mice where the effects of NK cell and possibly other non-adaptive immune mechanisms would not have a significant influence.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antigens, CD7 / immunology. Immunotoxins / administration & dosage. Leukemia-Lymphoma, Adult T-Cell / therapy. N-Glycosyl Hydrolases
  • [MeSH-minor] Animals. Antibody-Dependent Cell Cytotoxicity. Dose-Response Relationship, Drug. Female. Humans. Immunoconjugates / administration & dosage. Immunoglobulin Fab Fragments / administration & dosage. Immunophenotyping. Male. Mice. Mice, Inbred NOD. Mice, SCID. Plant Proteins / administration & dosage. Ribosome Inactivating Proteins, Type 1. Species Specificity. Specific Pathogen-Free Organisms. Spleen / cytology. Spleen / drug effects. Spleen / immunology. Survival Analysis. Survival Rate. Treatment Outcome. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2000 Cancer Research Campaign.
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  • (PMID = 11104577.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] SCOTLAND
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD7; 0 / Immunoconjugates; 0 / Immunoglobulin Fab Fragments; 0 / Immunotoxins; 0 / Plant Proteins; 0 / Ribosome Inactivating Proteins, Type 1; EC 3.2.2.- / N-Glycosyl Hydrolases; EC 3.2.2.22 / saporin
  • [Other-IDs] NLM/ PMC2363443
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6. Hamaguchi Y: [Molecular mechanisms of B lymphocyte depletion by CD20 immunotherapy]. Nihon Rinsho Meneki Gakkai Kaishi; 2009 Feb;32(1):29-34
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  • Anti-CD20 antibody immunotherapy effectively treats non-Hodgkin's lymphoma and autoimmune disease.
  • However, the cellular and molecular pathways for B cell depletion remain undefined and the in vivo effect of immunotherapy on tissue B cells and their subsets is generally unknown.
  • To identify the mechanisms for B cell depletion in vivo, a new mouse model for anti-CD20 immunotherapy was developed using a panel of twelve mouse anti-mouse CD20 monoclonal antibodies.
  • Anti-CD20 antibodies rapidly depleted the vast majority of circulating and tissue B cells in an isotype-restricted manner that was completely dependent on effector cell Fc receptor expression.
  • B cell depletion utilized FcgammaRI-, FcgammaRIII- and FcgammaRIV-dependent pathways, while B cells were not eliminated in FcR common gamma chain-deficient mice.
  • Monocytes were the dominant effector cells for B cell depletion, with no demonstrable role for T or NK cells.
  • Although most anti-CD20 antibodies activated complement in vitro, B cell depletion was completely effective in mice with genetic deficiencies in C3 complement components.
  • The considerable factors that determine the effectiveness of anti-CD20 immunotherapy are following: the expression level of CD20 on B cell surface; the dosage of anti-CD20 mAb; the association of Fcgamma receptor with the isotype of the antibies; B cell subpopulations within different tissues.
  • These findings have important clinical implications for anti-CD20 and other antibody-based therapies.
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Murine-Derived. Antibody-Dependent Cell Cytotoxicity / immunology. Autoimmune Diseases / drug therapy. Immunotherapy. Lymphoma, Non-Hodgkin / drug therapy. Mice. Receptors, IgG / immunology. Rituximab

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  • (PMID = 19252375.001).
  • [ISSN] 1349-7413
  • [Journal-full-title] Nihon Rinshō Men'eki Gakkai kaishi = Japanese journal of clinical immunology
  • [ISO-abbreviation] Nihon Rinsho Meneki Gakkai Kaishi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Receptors, IgG; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 14
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7. Flavell DJ, Boehm DA, Noss A, Warnes SL, Flavell SU: Therapy of human T-cell acute lymphoblastic leukaemia with a combination of anti-CD7 and anti-CD38-SAPORIN immunotoxins is significantly better than therapy with each individual immunotoxin. Br J Cancer; 2001 Feb;84(4):571-8
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] Therapy of human T-cell acute lymphoblastic leukaemia with a combination of anti-CD7 and anti-CD38-SAPORIN immunotoxins is significantly better than therapy with each individual immunotoxin.
  • Severe combined immunodeficient (SCID) mice injected i.v. with the human T-ALL cell line CCRF CEM (SCID-CEM mice) develop within 50 days life-threatening multi-organ growth of leukaemia cells.
  • The development of leukaemia in SCID-CEM mice treated with three 10 microg i.v. doses of the anti-CD7 immunotoxin (IT) HB2-SAPORIN or the anti-CD38 IT OKT10-SAPORIN was significantly delayed compared with PBS sham-treated animals but 90% of animals treated with either IT eventually developed disseminated leukaemia cell growth.
  • In contrast treatment of SCID-CEM mice with a combination of both ITs led not only to a significantly greater delay in time to leukaemia development but also in the numbers of animals remaining leukaemia free (60%).
  • The native HB2 and OKT10 antibodies (both murine IgG1antibodies) exerted significant, though relatively weak therapeutic effects, probably mediated through an antibody-dependent cellular cytotoxicity (ADCC) mechanism.
  • Moreover, there was no in vivo additivity of therapeutic effect when both antibodies were used in combination.
  • Apparent, however, was that the combination of HB2-SAPORIN IT with OKT10 antibody led to an intermediate therapeutic effect that was significantly greater than that obtained when either was used alone but significantly less than that obtained when the two IT combination was utilized.
  • This result suggests that the therapeutic effect of IT + antibody treatment results from an additivity between antibody-mediated delivery of saporin combined with a SCID mouse NK cell-mediated ADCC attack on the target cell directed through target cell bound antibody Fc engagement with FcgammaRIII on the NK cell surface.
  • The combination of both ITs however gave the best therapeutic outcome in SCID-CEM mice probably as the result of (i) delivery of greater amounts of saporin to target CEM cells positive for both CD7 and CD38, (ii) delivery of an effective dose of saporin to CEM cells downregulated or negative for one of the target antigens and (iii) through ADCC mechanisms that interact additively with IT action.
  • We have previously proposed that combination IT therapy would be one means of overcoming the problem of heterogeneity of antigen expression within a global tumour cell population and these additional findings support this and provide a further strengthening of the rationale for employing cocktails of ITs for the treatment of human malignancies.
  • [MeSH-major] Antibodies, Neoplasm / pharmacology. Antigens, CD. Antigens, CD7 / immunology. Antigens, Differentiation / immunology. Antineoplastic Agents, Phytogenic / pharmacology. Carrier Proteins. Immunotoxins / pharmacology. Leukemia-Lymphoma, Adult T-Cell / immunology. Lipoproteins, HDL. N-Glycosyl Hydrolases. NAD+ Nucleosidase / immunology. Plant Proteins / pharmacology. RNA-Binding Proteins
  • [MeSH-minor] ADP-ribosyl Cyclase. Animals. Antibody Formation. Antigens, CD38. Disease Models, Animal. Drug Therapy, Combination. Female. Flow Cytometry. Immunoglobulin G / immunology. Male. Membrane Glycoproteins. Mice. Mice, SCID. Receptors, Lipoprotein. Ribosome Inactivating Proteins, Type 1

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  • [Copyright] Copyright 2001 Cancer Research Campaign.
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  • (PMID = 11207056.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, CD7; 0 / Antigens, Differentiation; 0 / Antineoplastic Agents, Phytogenic; 0 / Carrier Proteins; 0 / Immunoglobulin G; 0 / Immunotoxins; 0 / Lipoproteins, HDL; 0 / Membrane Glycoproteins; 0 / Plant Proteins; 0 / RNA-Binding Proteins; 0 / Receptors, Lipoprotein; 0 / Ribosome Inactivating Proteins, Type 1; 0 / high density lipoprotein receptors; 147605-06-9 / high density lipoprotein binding protein; EC 3.2.2.- / N-Glycosyl Hydrolases; EC 3.2.2.22 / saporin; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / Cd38 protein, mouse; EC 3.2.2.5 / NAD+ Nucleosidase
  • [Other-IDs] NLM/ PMC2363766
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8. Akamatsu S, Arai N, Hanaya T, Arai S, Tanimoto T, Fujii M, Kohno K, Micallef MJ, Ikeda M, Kurimoto M: Antitumor activity of interleukin-18 against the murine T-cell leukemia/lymphoma EL-4 in syngeneic mice. J Immunother; 2002 Mar-Apr;25 Suppl 1:S28-34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Antitumor activity of interleukin-18 against the murine T-cell leukemia/lymphoma EL-4 in syngeneic mice.
  • Interleukin (IL)-18 induces interferon (IFN)-gamma production by T cells and natural killer (NK) cells, and augments NK cell activity in mouse spleen cell cultures.
  • In this study, the antitumor effects of IL-18 against murine T-cell leukemia (EL-4) were evaluated.
  • When 4 x 10(6) EL-4 cells were transplanted intravenously, the antitumor effects of IL-18 were not pronounced, and only a slight prolongation of the mean survival times was observed.
  • However, when mice were transplanted intravenously with 5 x 10(5) EL-4 cells, the extent of experimental visceral dissemination of EL-4 was markedly reduced in mice treated subcutaneously with IL-18, resulting in an increase in survival time with some mice even cured.
  • Although IL-18 was highly effective at inhibiting the development of EL-4 lymphoma dissemination in C57BL/6 mice, it could not inhibit the development of dissemination in mutant C57BL/6 beige (bg/bg) mice lacking NK cell activity.
  • These results suggest that antitumor efficacy of IL-18 is mediated primarily by NK cells, but that T cells are also required for the complete antitumor efficacy of IL-18.
  • [MeSH-major] Interferon-gamma / drug effects. Interleukin-18 / pharmacology. Leukemia, T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Animals. Cytokines / drug effects. Cytokines / metabolism. Disease Models, Animal. Female. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm Transplantation. Reference Values. Sensitivity and Specificity. Treatment Outcome

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  • (PMID = 12048348.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-18; 82115-62-6 / Interferon-gamma
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9. Ohsugi T, Horie R, Kumasaka T, Ishida A, Ishida T, Yamaguchi K, Watanabe T, Umezawa K, Urano T: In vivo antitumor activity of the NF-kappaB inhibitor dehydroxymethylepoxyquinomicin in a mouse model of adult T-cell leukemia. Carcinogenesis; 2005 Aug;26(8):1382-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo antitumor activity of the NF-kappaB inhibitor dehydroxymethylepoxyquinomicin in a mouse model of adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I).
  • To examine the effect of a novel NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on ATL in vivo, we developed an improved severe combined immunodeficiency (SCID) mouse model for ATL.
  • Five-week-old SCID mice in which natural killer (NK) cell activity had been eliminated were inoculated intraperitoneally with the HTLV-I-infected cell lines, TL-Om1, MT-1, MT-2 and HUT-102.
  • In contrast, inoculation of mice with MT-2 and HUT-102 cells elicited high mortality, 100% frequency of gross tumor formation and tumor cell infiltration of various organs, all of which were reduced by coadministration of DHMEQ during the inoculation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Benzamides / pharmacology. Cyclohexanones / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. NF-kappa B / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Base Sequence. Binding Sites. Cell Division / drug effects. Cell Line, Tumor. Consensus Sequence. Disease Models, Animal. Human T-lymphotropic virus 1 / drug effects. Human T-lymphotropic virus 1 / physiology. Humans. Mice. Transplantation, Heterologous

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  • (PMID = 15831528.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Cyclohexanones; 0 / NF-kappa B; 0 / dehydroxymethylepoxyquinomicin
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10. Loong SL, Hwang JS, Lim ST, Yap SP, Tao M, Chong TW, Tan LH, Huynh H: An Epstein-Barr virus positive natural killer lymphoma xenograft derived for drug testing. Leuk Lymphoma; 2008 Jun;49(6):1161-7
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  • [Title] An Epstein-Barr virus positive natural killer lymphoma xenograft derived for drug testing.
  • Natural killer (NK) lymphomas occurring more frequently in the Far East and South America respond poorly to anthracycline-based regimens.
  • Here we report an in vivo NK lymphoma xenograft (NK-S1) derived from the testicular metastasis of a patient with an extranodal NK lymphoma (nasal type).
  • The NK-S1 xenograft, established in severe combined immune deficient (SCID) mice retained the same imunophenotypic features as the original tumor.
  • NK-S1 disseminated intra-abdominally to the testis, intestine and liver.
  • Although doxorubicin, rapamycin, bevacizumab, rapamycin-doxorubicin, and bevacizumab-doxorubicin had no effects on the growth of subcutaneous NK-S1 xenografts, intraperitoneal (IP) delivery of cyclophosphamide caused complete tumor regression; this tumor regression was associated with apoptosis, upregulation of activated caspase-3, and cleaved Poly(ADP-ribose) polymerase (PARP).
  • In an IP model of NK lymphoma, cyclophosphamide also prolonged the survival of mice and potently inhibited tumor dissemination and ascites formation.
  • Our data suggest that the NK-S1 xenograft is a useful tool for screening preclinical drugs, and cyclophosphamide may be a useful drug for the treatment of this disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Epstein-Barr Virus Infections / drug therapy. Herpesvirus 4, Human / isolation & purification. Killer Cells, Natural / drug effects. Lymphoma, T-Cell, Peripheral / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Apoptosis / drug effects. Bevacizumab. Blotting, Western. Caspase 3 / metabolism. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Enzyme Activation / drug effects. Humans. Injections, Intraperitoneal. Male. Mice. Mice, SCID. Middle Aged. Neoplasm Transplantation. Poly(ADP-ribose) Polymerases / metabolism. Sirolimus / administration & dosage. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 18452087.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; W36ZG6FT64 / Sirolimus
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11. Kanwar JR, Berg RW, Yang Y, Kanwar RK, Ching LM, Sun X, Krissansen GW: Requirements for ICAM-1 immunogene therapy of lymphoma. Cancer Gene Ther; 2003 Jun;10(6):468-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Requirements for ICAM-1 immunogene therapy of lymphoma.
  • Intercellular cell adhesion molecule-1 (ICAM-1) is a cell-surface glycoprotein capable of eliciting bidirectional signals that activate signalling pathways in leukocytes, endothelial, and smooth muscle cells.
  • To begin to address this question, we constructed four different therapeutic expression vectors encoding full-length ICAM-1, and forms in which the N-terminal ligand-binding domains and cytoplasmic tail had been deleted.
  • Mouse EL-4 tumors (0.5 cm in diameter), which actively suppress the immune response, were significantly inhibited in their growth following injection of expression plasmids encoding either full-length xenogenic (human) ICAM-1, or a functional cytoplasmic domain-deficient form that retains ligand-binding activity.
  • Efficacy of ICAM-1-mediated antitumor immunity was significantly augmented by administration of the antivascular drug 5,6-dimethylxanthenone-4-acetic acid (DMXAA), which suppressed blood supply to the tumor, leading to enhanced leukocyte infiltration, and complete tumor eradication in a gene dosage and CD8(+) T cell and NK cell-dependent fashion.
  • Generation of potent cytotoxic T cell (CTL)-mediated antitumor immunity was reflected by ICAM-1-facilitated apoptosis of tumor cells in situ.
  • [MeSH-major] Genetic Therapy / methods. Immunotherapy / methods. Intercellular Adhesion Molecule-1 / genetics. Lymphoma / therapy
  • [MeSH-minor] Animals. CD8-Positive T-Lymphocytes / metabolism. COS Cells. Cell Adhesion. Cytoplasm / metabolism. DNA, Complementary / metabolism. Flow Cytometry. Gene Transfer Techniques. Genetic Vectors. Humans. Killer Cells, Natural / metabolism. Leukocytes / metabolism. Mice. Mutation. Neoplasms / blood supply. Plasmids / metabolism. Protein Structure, Tertiary. Signal Transduction. Time Factors. Transfection. Transgenes. Xanthones / chemistry

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  • (PMID = 12768192.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Xanthones; 0829J8133H / vadimezan; 126547-89-5 / Intercellular Adhesion Molecule-1
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12. Sakurai T, Misawa E, Yamada M, Hayasawa H, Motoyoshi K: Effects of macrophage-colony-stimulating factor on cyclophosphamide-injected mouse NK1.1+ cell activity. Cancer Immunol Immunother; 2000 May;49(2):94-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of macrophage-colony-stimulating factor on cyclophosphamide-injected mouse NK1.1+ cell activity.
  • We injected cyclophosphamide into mice and examined their natural killer (NK) activity both in vitro and in vivo.
  • Cyclophosphamide injection temporarily abrogated the lung clearance activity of Yac-1 lymphoma cells, which is considered to be an index of NK activity in vivo.
  • To clarify whether the administration of rhM-CSF activated NK cells, we purified NK1.1+ cells from mice treated with cyclophosphamide and/or rhM-CSF and examined their functions (cytotoxicity, proliferation, and interferon gamma production) in vitro.
  • These results suggested that the temporary abrogation of NK activity in vivo caused by cyclophosphamide injection was due to a decrease in the number and not to suppression of the functions of NK1.1+ cells.
  • However, treatment with rhM-CSF recovered the anti-metastatic activity in the lungs of cyclophosphamide-injected mice.
  • These results show that administration of rhM-CSF restores NK activity suppressed by cyclophosphamide injection in vivo.
  • [MeSH-major] Antigens / analysis. Cyclophosphamide / pharmacology. Killer Cells, Natural / drug effects. Macrophage Colony-Stimulating Factor / pharmacology. Proteins / analysis
  • [MeSH-minor] Animals. Antigens, Ly. Antigens, Surface. Hematopoiesis / drug effects. Interferon-gamma / biosynthesis. Lectins, C-Type. Lung Neoplasms / secondary. Male. Melanoma, Experimental / drug therapy. Melanoma, Experimental / secondary. Mice. Mice, Inbred C57BL. NK Cell Lectin-Like Receptor Subfamily B. Recombinant Proteins / pharmacology

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  • (PMID = 10823419.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, Ly; 0 / Antigens, Surface; 0 / KLRB1 protein, human; 0 / Klrb1c protein, mouse; 0 / Lectins, C-Type; 0 / NK Cell Lectin-Like Receptor Subfamily B; 0 / Proteins; 0 / Recombinant Proteins; 81627-83-0 / Macrophage Colony-Stimulating Factor; 82115-62-6 / Interferon-gamma; 8N3DW7272P / Cyclophosphamide
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13. Melo PS, Justo GZ, Durán N, Haun M: Natural killer cell activity and anti-tumour effects of dehydrocrotonin and its synthetic derivatives. Eur J Pharmacol; 2004 Mar 8;487(1-3):47-54
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  • [Title] Natural killer cell activity and anti-tumour effects of dehydrocrotonin and its synthetic derivatives.
  • Treatment of Ehrlich ascites tumour-bearing mice with 20 mg/kg dehydrocrotonin for 4 days significantly increased survival, whereas administration of dehydrocrotonin derivatives was ineffective in affording protection.
  • Investigation of the effects of dehydrocrotonin treatment on total natural killer (NK) cell activity of tumour-bearing mice as a possible mechanism of dehydrocrotonin action in vivo revealed that this sesquiterpene lactone significantly improved NK cytotoxicity against YAC-1, a Moloney virus-induced mouse T-cell lymphoma of A/SN origin.
  • As expected, tumour growth in non-treated mice markedly suppressed NK cell cytolysis.
  • No effects on NK functional activity were observed in normal mice receiving dehydrocrotonin.
  • [MeSH-major] Antineoplastic Agents, Phytogenic. Diterpenes, Clerodane / pharmacology. Killer Cells, Natural / drug effects
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / drug therapy. Cell Survival / drug effects. Croton / chemistry. Immune System / drug effects. Male. Mice. Mice, Inbred BALB C. Phosphoric Monoester Hydrolases / metabolism. Spleen / cytology. Spleen / immunology. T-Lymphocytes, Regulatory / drug effects. T-Lymphocytes, Regulatory / immunology. Tetrazolium Salts. Thiazoles

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  • (PMID = 15033375.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Diterpenes, Clerodane; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / dehydrocrotonin; 298-93-1 / thiazolyl blue; EC 3.1.3.- / Phosphoric Monoester Hydrolases
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14. Tsirigotis P, Economopoulos T: Monoclonal antibodies in the treatment of lymphoid malignancies. J Steroid Biochem Mol Biol; 2008 Feb;108(3-5):267-71
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  • [Title] Monoclonal antibodies in the treatment of lymphoid malignancies.
  • Rituximab (Rit) was the first monoclonal antibody approved for therapeutic use in cancer patients.
  • Rit is a chimeric mouse/human monoclonal antibody, consisting of the human IgG1 and k constant Fc region, and a mouse variable Fab region specific against the B-cell antigen CD20.
  • Effector cytotoxic cells such as natural killer cells (NK) are activated after binding to the Fc portion of the anti-CD20 molecule.
  • Activated NK cells kill the coated lymphoma cells with the use of granzyme-perforin system.
  • The relative contribution of these mechanisms in vivo and in different lymphoma subtypes is not well known and remains to be further evaluated.
  • Among the different histological groups, follicular lymphoma (FL) has been proven to be the most sensitive to Rit when used as a single agent, with overall response rates of 80% and 50% in untreated and previously treated patients, respectively.
  • Moreover, Rit in combination with chemotherapy is superior to chemotherapy alone in terms of response rate and event-free survival, while early data indicate a significant prolongation in overall survival as well.
  • Similarly, the addition of Rit to standard chemotherapy improves the disease-free and overall survival of patients with diffuse large B-cell lymphoma.
  • However, we need to understand better the mechanisms of its action as well as the mechanisms of resistance to Rit, in order to design more effective treatment modalities.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma / drug therapy
  • [MeSH-minor] Antibodies, Bispecific / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / immunology. Antigens, CD20 / metabolism. Humans. Lymphoma, Follicular / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Rituximab

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  • (PMID = 17935974.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 30
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15. Ríhová B, Jelínková M, Strohalm J, Subr V, Plocová D, Hovorka O, Novák M, Plundrová D, Germano Y, Ulbrich K: Polymeric drugs based on conjugates of synthetic and natural macromolecules. II. Anti-cancer activity of antibody or (Fab')(2)-targeted conjugates and combined therapy with immunomodulators. J Control Release; 2000 Feb 14;64(1-3):241-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymeric drugs based on conjugates of synthetic and natural macromolecules. II. Anti-cancer activity of antibody or (Fab')(2)-targeted conjugates and combined therapy with immunomodulators.
  • We provide data on in vivo targeting of the Thy 1.2 (CDw90) cell surface receptor expressed on neoplastic T cells, mouse EL4 T cell lymphoma.
  • The targeting antibody and the anticancer drug, doxorubicin (DOX) were conjugated to a water-soluble copolymer based on N-(2-hydroxypropyl)methacrylamide (HPMA) acting as a carrier responsible for controlled intracellular release of the conjugated drug.
  • The in vivo therapeutic efficacy of HPMA copolymer-bound DOX targeted with anti-EL4 antibody, polyclonal anti-thymocyte globulin (ATG), monoclonal anti-Thy 1.2 antibody or its F(ab')(2) fragment was compared with the efficacy of DOX conjugated to HPMA copolymer containing nonspecific IgG or bovine serum albumin (BSA).
  • Patients with advanced cancer are often immunocompromised due to dysfunction of their immune system induced by cancer and cytotoxic drugs.
  • A significant decrease of unwanted side-effects of targeted drugs against a number of vital organs was already documented.
  • In this study we have compared immunotoxic effects of free DOX with those of its antibody-targeted form on NK cells and cytolytic T lymphocytes (CTLs) isolated from C57BL/10 mice bearing EL4 T cell lymphoma.
  • In the same model we have tested the combination therapy with immunomodulators (beta-glucan or AM-2) injected together with targeted daunomycin.
  • We have observed a significant protective effect of targeted DOX against NK cells and CTLs.
  • Moreover, the data revealed that combination therapy considerably enhances antitumor efficacy of the targeted anticancer drug.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Antibodies / administration & dosage. Antineoplastic Agents / therapeutic use. Doxorubicin. Immunoglobulin Fab Fragments / administration & dosage. Lymphoma / pathology
  • [MeSH-minor] Animals. Cattle. Delayed-Action Preparations / pharmacokinetics. Drug Carriers / chemistry. Drug Synergism. Drug Therapy, Combination. Immunoglobulin G / immunology. In Vitro Techniques. Killer Cells, Natural / immunology. Male. Methacrylates / chemistry. Mice. Mice, Inbred C57BL. Polymers / therapeutic use. Random Allocation. Serum Albumin / immunology. Solubility. T-Lymphocytes / immunology. Time Factors. Tumor Cells, Cultured

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  • (PMID = 10640661.001).
  • [ISSN] 0168-3659
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibodies; 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; 0 / Drug Carriers; 0 / Immunoglobulin Fab Fragments; 0 / Immunoglobulin G; 0 / Methacrylates; 0 / Polymers; 0 / Serum Albumin; 27813-02-1 / hydroxypropyl methacrylate; 80168379AG / Doxorubicin
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16. Ríhová B, Strohalm J, Kubácková K, Jelínková M, Hovorka O, Kovár M, Plocová D, Sírová M, St'astný M, Rozprimová L, Ulbrich K: Acquired and specific immunological mechanisms co-responsible for efficacy of polymer-bound drugs. J Control Release; 2002 Jan 17;78(1-3):97-114
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired and specific immunological mechanisms co-responsible for efficacy of polymer-bound drugs.
  • We present data providing new evidence that poly[N-(2-hydroxypropyl)methacrylamide] (PHPMA)-bound drugs, unlike free drugs, have both cytostatic and immunomobilizing activity (CIA).
  • Immediately after injection, due to the high level of the drug, the main activity of the polymeric conjugate is cytotoxic and cytostatic.
  • Later on, long-term circulating PHPMA-bound drug, at concentrations lower than its minimal inhibitory levels, mobilizes the defense mechanisms of the host.
  • Cytotoxic and cytostatic effects of drug-PHPMA were repeatedly confirmed.
  • The following data support the concept of the immunomobilizing activity of the N-(2-hydroxypropyl)methacrylamide (HPMA) conjugates: (a) pre-treatment with free drugs (doxorubicin, cyclosporin A) accelerates the appearance of EL4 mouse T-cell lymphoma while a similar pre-treatment with doxorubicin-PHPMA induces limited but definitive mobilization of the host's defense mechanisms;.
  • (b) mice cured of EL4 mouse T-cell lymphoma, BCL1 mouse B-cell leukemia and 38C13 mouse B-cell lymphoma by injection of doxorubicin-PHPMA conjugate targeted with monoclonal antibodies (anti-Thy 1.2 for EL4, anti-B1 for BCL1 and anti-CD71 for 38C13) and re-transplanted with a lethal dose of the same cancer cells survive without any treatment considerably longer than control mice;.
  • (c) increased NK activity and anti-cancer antibody was detected only in animals treated with doxorubicin-PHPMA conjugate; and (d) considerably increased NK and LAK activity was seen in a human patient treated for generalized breast carcinoma with doxorubicin-PHPMA-IgG.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems. Methacrylates / administration & dosage
  • [MeSH-minor] Animals. Antibody-Dependent Cell Cytotoxicity. Breast Neoplasms / drug therapy. Doxorubicin / administration & dosage. Hemangiosarcoma / drug therapy. Hemangiosarcoma / immunology. Killer Cells, Natural / immunology. Mice. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / immunology. Tumor Cells, Cultured

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  • (PMID = 11772452.001).
  • [ISSN] 0168-3659
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Methacrylates; 27813-02-1 / hydroxypropyl methacrylate; 80168379AG / Doxorubicin
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17. da Silva SL, Figueiredo PM, Yano T: Chemotherapeutic potential of the volatile oils from Zanthoxylum rhoifolium Lam leaves. Eur J Pharmacol; 2007 Dec 8;576(1-3):180-8
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  • Treatment of Ehrlich ascites tumor-bearing mice with 20 mg/kg of the volatile oil and beta-caryophyllene for 4 days has significantly increased survival, whereas administration of alpha-humulene, alpha-pinene and beta-pinene were ineffective in affording protection.
  • Investigation of the effects of the volatile oil (and terpenes) treatment on total natural killer cells (NK cell) activity from tumor-bearing mice as a possible mechanism of these compounds in vivo revealed that volatile oil and beta-caryophyllene significantly improved NK cell cytotoxicity against YAC-1, a Moloney virus-induced mouse T-cell lymphoma of A/SN origin and Ehrlich ascites cells.
  • As expected, tumor growth in non-treated mice markedly suppressed NK cell cytolysis while the volatile oil and beta-caryophyllene reversed this effect when mice were treated with 20-mg/kg dosages of these compounds for 4 days.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Oils, Volatile / therapeutic use. Zanthoxylum / chemistry
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Male. Mice. Mice, Inbred BALB C. Plant Leaves / chemistry. Rats. Rats, Sprague-Dawley. Terpenes / blood. Terpenes / pharmacology. Terpenes / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 17716654.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oils, Volatile; 0 / Terpenes
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18. Schaffrath B, Mengs U, Schwarz T, Hilgers RD, Beuth J, Möckel B, Lentzen H, Gerstmayer B: Anticancer activity of rViscumin (recombinant mistletoe lectin) in tumor colonization models with immunocompetent mice. Anticancer Res; 2001 Nov-Dec;21(6A):3981-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The antitumoral and immunostimulating properties of rViscumin (recombinant mistletoe lectin) were investigated in two mouse tumor models.
  • Another set was carried out to analyze the effect of rViscumin treatment on the number of tumor colonies in infiltrated lungs (RAW-117P) or liver (L-1) and the activation of immune cell subsets, respectively.
  • An overall prolonged survival time after treatment with rViscumin and a reduction in the number of tumor colonies after administration of certain rViscumin doses was observed.
  • Immunophenotyping of the peripheral leukocytes of treated mice revealed increased numbers of T-lymphocytes, pan-NK cells and activated monocytes.
  • The results indicate that rViscumin has antineoplastic properties and might therefore be a promising candidate in cancer therapy.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Antineoplastic Agents / pharmacology. Plant Preparations. Plant Proteins. Sarcoma, Experimental / drug therapy. Toxins, Biological / pharmacology
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Immunocompetence. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / immunology. Liver Neoplasms, Experimental / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / immunology. Lung Neoplasms / secondary. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / immunology. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Recombinant Proteins / pharmacology. Ribosome Inactivating Proteins, Type 2. Tumor Cells, Cultured

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  • (PMID = 11911280.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents; 0 / Plant Preparations; 0 / Plant Proteins; 0 / Recombinant Proteins; 0 / Ribosome Inactivating Proteins, Type 2; 0 / Toxins, Biological; 0 / ribosome inactivating protein, Viscum
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