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Article: Platelets and cancer: implications for antiangiogenic therapy.

Trikha, Mohit / Nakada, Marian T

2002 Volume 28, Issue 1, Page(s) 39–44

Abstract: Thromboembolism is one of the most common causes of death in cancer patients. Among the most frequent thrombotic complications in patients with cancer are disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and thrombocytosis. ... ...

Abstract	Thromboembolism is one of the most common causes of death in cancer patients. Among the most frequent thrombotic complications in patients with cancer are disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and thrombocytosis. Clearly, these complications arise as tumor cells interact with almost all components of the hemostatic system including platelets. Platelets participate in tumor progression by contributing to the metastatic cascade, protecting tumor cells from immune surveillance, regulating tumor cell invasion, and angiogenesis. Platelets contain one of the largest stores of angiogenic and mitogenic factors and the tumor vasculature is leaky, which allows platelets to come in contact with the tumor and deposit multiple angiogenic factors including vascular endothelial growth factor (VEGF) and thrombin to tumor cells, which in turn contributes to tumor progression. This article reviews the recent literature on how platelets contribute to tumor growth, angiogenesis, and metastasis.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/therapeutic use ; Blood Platelets/pathology ; Blood Platelets/physiology ; Humans ; Neoplasm Metastasis/drug therapy ; Neoplasm Metastasis/prevention & control ; Neoplasms/blood ; Neoplasms/drug therapy ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/etiology ; Thrombophilia/blood ; Thrombophilia/etiology
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2002-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-2002-20563
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Tumor necrosis factor-alpha in the pathogenesis and treatment of cancer.

Anderson, G Mark / Nakada, Marian T / DeWitte, Mark

Current opinion in pharmacology

2004 Volume 4, Issue 4, Page(s) 314–320

Abstract: The critical pathogenic role of tumor necrosis factor (TNF)alpha in inflammatory disorders such as rheumatoid arthritis and inflammatory bowel disease is well established. The role played by TNFalpha in both the treatment and pathogenesis of cancer ... ...

Abstract	The critical pathogenic role of tumor necrosis factor (TNF)alpha in inflammatory disorders such as rheumatoid arthritis and inflammatory bowel disease is well established. The role played by TNFalpha in both the treatment and pathogenesis of cancer remains less understood. Recent advances help to create a framework for understanding seemingly paradoxical effects of TNFalpha as both an anti-tumour agent and a mediator of tumour growth. High pharmacological doses of TNFalpha combined with chemotherapy can regress otherwise intractable tumours, and efforts continue to optimize delivery to avoid severe toxicities. Mounting evidence demonstrates that pathophysiological concentrations of endogenous TNFalpha act to promote tumour genesis and growth. The cellular and molecular pathways mediating these phenomena are starting to be clarified. Current data support the continued development of both TNFalpha and anti-TNFalpha therapy for clinical treatment of cancers in distinct settings.
MeSH term(s)	Animals ; Humans ; Neoplasms/etiology ; Neoplasms/therapy ; Signal Transduction ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/physiology ; Tumor Necrosis Factor-alpha/therapeutic use
Chemical Substances	Tumor Necrosis Factor-alpha
Language	English
Publishing date	2004-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2004.04.004
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5608: Show issues

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Article: Therapeutic potential of cytokine and chemokine antagonists in cancer therapy.

Yan, Li / Anderson, G Mark / DeWitte, Mark / Nakada, Marian T

European journal of cancer (Oxford, England : 1990)

2006 Volume 42, Issue 6, Page(s) 793–802

Abstract: A new paradigm is becoming widely accepted, that chronic inflammation, driven in part by chemokines and cytokines at the site of a tumour, may facilitate tumour progression instead of promoting anti-tumour immunity. Tumours and activated stromal cells ... ...

Abstract	A new paradigm is becoming widely accepted, that chronic inflammation, driven in part by chemokines and cytokines at the site of a tumour, may facilitate tumour progression instead of promoting anti-tumour immunity. Tumours and activated stromal cells secrete pro-inflammatory chemokines and cytokines that act either directly or indirectly through stimulation of the vascular endothelium to recruit leukocytes to the tumour. After activation, these tumour-associated leukocytes release angiogenic factors, mitogens, proteolytic enzymes, and chemotactic factors, recruiting more inflammatory cells and stimulating angiogenesis to sustain tumour growth and facilitate tumour metastasis. Breaking this cycle by inhibiting targets such as cytokines, chemokines and other inflammatory mediators, either alone, or more realistically, in combination with other therapies, such as anti-angiogenic or cytotoxic agents, may provide highly efficacious therapeutic regimens for the treatment of malignancies. This article reviews anti-cytokine and anti-chemokine therapies being pursued in cancer, and discusses in more detail anti-tumour necrosis factor-alpha (TNF) approaches.
MeSH term(s)	Chemokines/antagonists & inhibitors ; Cytokines/antagonists & inhibitors ; Disease Progression ; Humans ; Inflammation/physiopathology ; Neoplasms/therapy ; Risk Factors
Chemical Substances	Chemokines ; Cytokines
Language	English
Publishing date	2006-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	82061-1
ISSN	1879-0852 ; 0959-8049 ; 0277-5379 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0959-8049 ; 0277-5379 ; 0964-1947
DOI	10.1016/j.ejca.2006.01.013
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Zs.A 456: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 583: Show issues

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Book: Cancer and inflammation

Morgan, Douglas W / Forssmann, Ulf J / Nakada, Marian T

(Progress in inflammation research)

2004

Author's details	Douglas W. Morgan, Ulf J. Forssmann, Marian T. Nakada, editors
Series title	Progress in inflammation research
MeSH term(s)	Neoplasms/etiology ; Neoplasms/immunology ; Neoplasms/pathology ; Inflammation/immunology ; Inflammation/pathology
Language	English
Size	ix, 201 p. :, ill. ;, 24 cm.
Publisher	Birkhäuser
Publishing place	Basel ; Boston
Document type	Book
ISBN	9783764365929 ; 3764365927
Database	Catalogue of the US National Library of Medicine (NLM)

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Article: Monoclonal antibodies as therapeutics in oncology.

Trikha, Mohit / Yan, Li / Nakada, Marian T

Current opinion in biotechnology

2002 Volume 13, Issue 6, Page(s) 609–614

Abstract: The specificity of antibodies has been harnessed to target cancer cells and the first therapeutic antibodies for use in oncology are now finding application in the clinic. Studies are currently under way to develop new and improved antibodies. Recent ... ...

Abstract	The specificity of antibodies has been harnessed to target cancer cells and the first therapeutic antibodies for use in oncology are now finding application in the clinic. Studies are currently under way to develop new and improved antibodies. Recent developments have been made in the identification of novel targets, including the use of genomic and proteomic technologies. Several methods are also being developed to enhance antibody efficacy.
MeSH term(s)	Animals ; Antibodies, Monoclonal/classification ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/therapeutic use ; Antigens, Neoplasm/immunology ; Clinical Trials, Phase III as Topic ; Combined Modality Therapy/methods ; Drug Approval ; Humans ; Immunotherapy/methods ; Mice ; Neoplasms/immunology ; Neoplasms/therapy ; Quality Control ; Radioimmunotherapy/methods
Chemical Substances	Antibodies, Monoclonal ; Antigens, Neoplasm
Language	English
Publishing date	2002-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1052045-4
ISSN	1879-0429 ; 0958-1669
ISSN (online)	1879-0429
ISSN	0958-1669
DOI	10.1016/s0958-1669(02)00348-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 3071: Show issues

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Article: Platelets and Cancer: Implications for Antiangiogenic Therapy

Trikha, Mohit / Nakada, Marian T.

Seminars in Thrombosis and Hemostasis

2002 Volume 28, Issue 01, Page(s) 39–44

Abstract	Thromboembolism is one of the most common causes of death in cancer patients. Among the most frequent thrombotic complications in patients with cancer are disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and thrombocytosis. Clearly, these complications arise as tumor cells interact with almost all components of the hemostatic system including platelets. Platelets participate in tumor progression by contributing to the metastatic cascade, protecting tumor cells from immune surveillance, regulating tumor cell invasion, and angiogenesis. Platelets contain one of the largest stores of angiogenic and mitogenic factors and the tumor vasculature is leaky, which allows platelets to come in contact with the tumor and deposit multiple angiogenic factors including vascular endothelial growth factor (VEGF) and thrombin to tumor cells, which in turn contributes to tumor progression. This article reviews the recent literature on how platelets contribute to tumor growth, angiogenesis, and metastasis.
Keywords	Platelets ; cancer ; metastasis ; angiogenesis ; integrins
Language	English
Publishing date	2002-01-01
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-2002-20563
Database	Thieme publisher's database

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Zs.A 1259: Show issues

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Article: Tumor-stroma interaction: positive feedback regulation of extracellular matrix metalloproteinase inducer (EMMPRIN) expression and matrix metalloproteinase-dependent generation of soluble EMMPRIN.

Tang, Yi / Kesavan, Prabakaran / Nakada, Marian T / Yan, Li

Molecular cancer research : MCR

2004 Volume 2, Issue 2, Page(s) 73–80

Abstract: Matrix metalloproteinases (MMPs) are metal-dependent endopeptidases that play pivotal roles in tumor disease progression. In many solid tumors, MMPs are indeed produced by tumor stromal cells, rather than by tumor cells. This expression pattern is, at ... ...

Abstract	Matrix metalloproteinases (MMPs) are metal-dependent endopeptidases that play pivotal roles in tumor disease progression. In many solid tumors, MMPs are indeed produced by tumor stromal cells, rather than by tumor cells. This expression pattern is, at least in part, regulated by tumor-stroma interaction via tumor cell-associated extracellular matrix metalloproteinase inducer (EMMPRIN). In vitro, recombinant EMMPRIN dose-dependently stimulated MMP-1 production by primary human fibroblast cells. Interestingly, in addition to stimulating MMP expression, EMMPRIN also induced its own gene expression. To further explore this potential positive feedback regulatory mechanism, we generated human breast cancer cells expressing different levels of EMMPRIN. Coculture of EMMPRIN-positive tumor cells with fibroblast cells resulted in a concomitant stimulation of MMP-2, MMP-9, and EMMPRIN production. This induction was EMMPRIN dependent, was further enhanced by overexpression, and was reduced by antisense suppression of EMMPRIN expression in tumor cells. Increased expression of membrane-associated EMMPRIN was accompanied by an MMP-dependent generation of a soluble form of EMMPRIN representing a proteolytic cleavage product lacking the carboxyl terminus. On the basis of these findings, we propose a model in which tumor cell-associated EMMPRIN stimulates MMPs, as well as EMMPRIN expression in tumor stroma. Increased MMP activity in tumor local environment results in proteolytic cleavage of membrane-associated EMMPRIN, releasing soluble EMMPRIN. Soluble EMMPRIN in turn acts in a paracrine fashion on stroma cells that are both adjacent and distant to tumor sites to further stimulate the production of MMPs and additional EMMPRIN, which consequently contributes to tumor angiogenesis, tumor growth, and metastasis.
MeSH term(s)	Antigens, CD/biosynthesis ; Antigens, CD/genetics ; Antigens, CD/metabolism ; Antigens, CD/pharmacology ; Antigens, Neoplasm/biosynthesis ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/metabolism ; Antigens, Neoplasm/pharmacology ; Basigin ; Breast Neoplasms/enzymology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/secretion ; Cell Line, Tumor ; Cells, Cultured ; Coculture Techniques ; Feedback, Physiological ; Fibroblasts ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Matrix Metalloproteinase 1/biosynthesis ; Matrix Metalloproteinase 1/genetics ; Matrix Metalloproteinase 1/metabolism ; Matrix Metalloproteinases/biosynthesis ; Matrix Metalloproteinases/genetics ; Matrix Metalloproteinases/metabolism ; Recombinant Proteins/pharmacology ; Solubility ; Stromal Cells/cytology ; Stromal Cells/metabolism ; Transfection
Chemical Substances	Antigens, CD ; Antigens, Neoplasm ; BSG protein, human ; Recombinant Proteins ; Basigin (136894-56-9) ; Matrix Metalloproteinases (EC 3.4.24.-) ; Matrix Metalloproteinase 1 (EC 3.4.24.7)
Language	English
Publishing date	2004-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5744: Show issues

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Article: c7E3 Fab inhibits human tumor angiogenesis in a SCID mouse human skin xenograft model.

Nakada, Marian T / Cao, Gaoyuan / Sassoli, Patricia M / DeLisser, Horace M

Angiogenesis

2006 Volume 9, Issue 4, Page(s) 171–176

Abstract: The alphavbeta3 integrin plays an important role in tumor growth and angiogenesis. Inhibition of this receptor by intact bivalent antibodies has been shown to inhibit angiogenesis and tumor growth. In this study we tested the chimeric Fab of 7E3 (c7E3 ... ...

Abstract	The alphavbeta3 integrin plays an important role in tumor growth and angiogenesis. Inhibition of this receptor by intact bivalent antibodies has been shown to inhibit angiogenesis and tumor growth. In this study we tested the chimeric Fab of 7E3 (c7E3 Fab), an antibody reactive with human platelet GPIIb/IIIa and alphavbeta3 to determine if it would inhibit in vivo angiogenesis and tumor growth in a SCID mouse/human skin tumor growth and angiogenesis model. c7E3 Fab inhibited human tumor angiogenesis and tumor growth. These data suggest monovalent antibody fragments devoid of antibody effector function can have efficacy in preclinical models of angiogenesis.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Animals ; Antibodies, Monoclonal/pharmacology ; Cell Line, Tumor ; Humans ; Immunoglobulin Fab Fragments/pharmacology ; Mice ; Mice, SCID ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/prevention & control ; Skin Transplantation ; Transplantation, Heterologous
Chemical Substances	Angiogenesis Inhibitors ; Antibodies, Monoclonal ; Immunoglobulin Fab Fragments ; abciximab (X85G7936GV)
Language	English
Publishing date	2006
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1484717-6
ISSN	0969-6970
ISSN	0969-6970
DOI	10.1007/s10456-006-9053-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5094: Show issues

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Article: The β3 Integrin Antagonist m7E3 Reduces Matrix Metalloproteinase Activity and Smooth Muscle Cell Migration

Bendeck, Michelle P. / Nakada, Marian T.

Journal of Vascular Research

2001 Volume 38, Issue 6, Page(s) 590–599

Abstract: Treatment with c7E3 (abciximab, ReoPro) has been associated with a reduction in coronary events and the need for revascularization. Some of these beneficial effects may be due to blockade of the αvβ3 integrin receptor on smooth muscle cells (SMCs), ... ...

Institution	Departments of Laboratory Medicine and Pathobiology and Medicine, University of Toronto, Ont., Canada and Centocor Inc., Malvern, Pa., USA
Abstract	Treatment with c7E3 (abciximab, ReoPro) has been associated with a reduction in coronary events and the need for revascularization. Some of these beneficial effects may be due to blockade of the αvβ3 integrin receptor on smooth muscle cells (SMCs), however very little is known about the mechanisms involved. The current studies were designed to test the hypothesis that β3 integrin antagonists inhibit the arterial response to injury by reducing matrix metalloproteinase (MMP) activity in the vessel wall. Male Sprague-Dawley rats were treated with daily intraperitoneal injections of the monoclonal antibody m7E3 at a dose of 6 mg/kg/day. MMP-9 activity was reduced by 73%, and MMP-2 activity by 75%, in the injured carotids of the m7E3-treated rats compared to saline-treated controls. By contrast, tissue inhibitor metalloproteinase (TIMP) activity was not changed. SMC migration assayed at 4 days after injury was reduced from 56.7 ± 14 cells/mm2 intimal surface area in controls to 17.5 ± 5 cells/mm2 in m7E3-treated rats (p = 0.02). Medial cell replication measured at 4 days and intimal cell replication measured at 7 days were not affected. Intimal cross-sectional area, measured 14 days after injury was reduced by 28% after m7E3 treatment (p = 0.05). Intimal smooth muscle cell number and the ratio of intima/media cross-section area were also reduced. By contrast, intimal SMC density was not affected by m7E3 treatment, indicating no effect on matrix accumulation. We conclude that treatment with m7E3 reduced SMC migration following vascular injury, possibly via an inhibitory effect on MMP activity, and this resulted in a decrease in intimal size at 14 days after injury.
Keywords	Smooth muscle cell ; m7E3 ; αvβ3 integrin ; Arterial injury ; Matrix metalloproteinase
Language	English
Publishing date	2001-12-07
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Research Paper
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000051095
Database	Karger publisher's database

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Zs.A 513: Show issues

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Article: Pharmacological Properties of Abciximab

Mascelli, Mary Ann / Nakada, Marian T.

Hämostaseologie

1999 Volume 19, Issue 03, Page(s) 101–107

Abstract: Abciximab is the first of a new class of therapeutic agents that specifically block the function of the platelet cell adhesion receptor, glycoprotein (GP) IIb/IIIa and the subsequent platelet aggregation that contributes to thrombosis. Abciximab displays ...

Abstract	Abciximab is the first of a new class of therapeutic agents that specifically block the function of the platelet cell adhesion receptor, glycoprotein (GP) IIb/IIIa and the subsequent platelet aggregation that contributes to thrombosis. Abciximab displays high avidity for the GPIIb/IIIa receptor, which results in a prolonged platelet-bound half-life, and a sustained duration of platelet inhibition resulting from the redistribution and equilibration of abciximab molecules among circulating platelets at gradually diminishing levels of GPIIb/IIIa receptor occupancy. In contrast to its extended platelet bound life-span, unbound abciximab is cleared rapidly (half-life <10 min) after an intravenous bolus dose. Nevertheless, a subsequent continuous infusion that maintains relatively low concentrations of free abciximab (50 to 100 ng/ml) sustains the pharmacologic GPIIb/IIIa receptor blockade throughout the duration of treatment. In addition, abciximab also interacts with other potentially important biological targets. The agent binds with equal affinity to the other β 3 containing integrin, the vitronectin (α v β 3 ) receptor, and more weakly to the leukocyte Mac-1 receptor. The high avidity and multi-receptor specificity of abciximab are consistent both short- and long-term therapeutic benefits in patients with acute coronary syndromes.
Keywords	Abciximab ; glycoprotein IIb/IIIa
Language	English
Publishing date	1999-07-01
Publisher	Schattauer GmbH
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	801512-0
ISSN	2567-5761 ; 0720-9355
ISSN (online)	2567-5761
ISSN	0720-9355
DOI	10.1055/s-0038-1660390
Database	Thieme publisher's database

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