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Archive | 1991

Eicosanoids and Other Bioactive Lipids in Cancer and Radiation Injury

Kenneth V. Honn; Lawrence J. Marnett; Santosh Nigam; Thomas L. Walden

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Archive | 1990

Role of 12-Lipoxygenase Metabolites and Integrin Glycoprotein Receptors in Metastasis

Kenneth V. Honn; Irma M. Grossi; Clement A. Diglio; John D. Taylor

The metastatic cascade is a multi-factorial process, the successful completion of which requires distinct but coordinated responses by tumor cells both to their own internal stimuli and to external stimuli presented by the host (for comprehensive reviews see Weiss et al, 1988 and 1989). During the hematogenous phase of the metastatic process tumor cells undergo a variety of cell-cell interactions, some of which are deleterious (i.e. interaction with effectors of the cellular immune system) and some of which favor tumor cell survival (i.e. interaction with platelets and attachment to endothelial cells). Tumor cell arrest in the microvasculature is a critical event in hematogenous metastasis as tumor cells which do not arrest, or arrest but do not form stable adhesions to endothelium, are released into circulation where they are rapidly destroyed (Weiss et al, 1989). Therefore, failure to arrest and adhere may be viewed as a critical barrier to successful tumor cell metastasis. This implies that the factors (i.e. receptors, platelets, eicosanoids, hemodynamic factors, etc.) regulating initial tumor cell arrest and adhesion are of critical importance to the development or the prevention of a successful metastatic lesion (Weiss et al, 1989). Eicosanoids produced by tumor cells, platelets and endothelial cells may be critical determinants during the hematogenous phase of the metastatic cascade (Honn et al., 1981a, b, 1983).


Archive | 1986

Chemical Mechanisms of Modulation of Tumor Growth and Metastasis by Prostaglandins

Lawrence J. Marnett; Kenneth V. Honn

Prostaglandins are powerful local hormones that are biosynthesized from unsaturated fatty acids, in particular arachidonic acid. Their actions appear to be mediated by receptors and in some cases via stimulation of adenylate cyclase (1–4). Numerous reports indicate that they can modulate tumor initiation, promotion and progression (5,6). This chapter discusses mechanisms by which prostaglandins inhibit tumor cell proliferation and mechanisms by which pharmacological agents inhibit metastasis by modulating prostaglandin biosynthesis.


Advances in Heterocyclic Chemistry | 1992

CYCLIC HYDROXAMIC ACIDS

Kenneth V. Honn; Carl R. Johnson; Yung-fa Chen; Katsu-ichi Shimoji; Lawrence J. Marnett


Archive | 1993

Aryl aliphatic acids

Carl R. Johnson; Gilles Gorins; Kenneth V. Honn; Lawrence J. Marnett


Archive | 1985

PROSTAGLANDINS, LEUKOTRIENES, AND CANCER

Kenneth V. Honn; Lawrence J. Marnett


Archive | 1986

4-(nitrone aryl) dihydropyridines

Carl R. Johnson; John D. Taylor; Kenneth V. Honn; Soan Cheng


Archive | 2013

12-lipoxygenase Eicosanoid regulation of angiogenesis: role of endothelial arachidonate

Daotai Nie; Keqin Tang; Clement A. Diglio; Kenneth V. Honn


Archive | 1986

Verfahren und zusammensetzungen zur behandlung von tumoren mit gehalt an einer calcium-channel-blocker-verbindung aus der klasse der dihydropyridine und an einer platin-koordinationsverbindung. Methods and compositions for the treatment of tumors with content on a calcium-channel-blocker-compound from the class of dihydropyridines and a platinum coordination compound.

Kenneth V. Honn; John D. Taylor; James M. Onoda


Archive | 1986

Verfahren und zusammensetzungen zur behandlung von tumoren mit gehalt an einer calcium-channel-blocker-verbindung aus der klasse der dihydropyridine und an einer platin-koordinationsverbindung.

Kenneth V. Honn; John D. Taylor; James M. Onoda

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Daotai Nie

Southern Illinois University School of Medicine

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Keqin Tang

Wayne State University

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