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  • 1
    Electronic Resource
    Electronic Resource
    Temporal effects of ACTH, indomethacin and 7-oxa-13-prostynoic acid upon glucocorticoid production by the human adrenal (1977)
    Springer
    Cellular and molecular life sciences 33 (1977), S. 545-546 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Indomethacin or 7-oxa-13-prostynoic acid does not alter basal adrenal cortisol output. Preincubation in either, depresses subsequent ACTH-stimulated cortisol output below ACTH alone and controls. Either inhibitor following ACTH preincubation blunts normal ACTH-stimulated cortisol production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01922264
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  • 2
    Electronic Resource
    Electronic Resource
    Calcium channel blocker treatment of tumor cells induces alterations in the cytoskeleton, mobility of the integrin αIIbβ3 and tumor-cell-induced platelet aggregation (1992)
    Springer
    Journal of cancer research and clinical oncology 118 (1992), S. 425-434 
    Details
    ISSN: 1432-1335
    Keywords: Walker 256 carcinosarcoma ; αIIbβ3 ; Platelet aggregation ; Cytoskeleton ; Diltiazem ; Verapamil ; Nifedipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Calcium channel blockers of the phenylalkylamine (i.e. verapamil), benzothiazepine (i.e. diltiazem) and dihydropyridine (i.e. nifedipine) classes were evaluated for effects on the tumor cell/platelet interactions using Walker 256 carcinosarcoma cells (W256 cells). When W256 cells were pretreated for 15 min with channel blockers at concentrations of 50–200 μM, macroscopic tumor-cell-induced platelet aggregation was inhibited (order of potency; nifedipine〉diltiazem≫verapamil). However, ultrastructural analysis revealed limited, focal platelet aggregates associated with tumor cell plasma membranes of verapamil- and diltiazem-treated cells. There was no evidence of platelet activation or platelet association with the tumor cell membrane in cells pretreated with nifedipine. Walker 256 cells possess the integrin αIIbβ3. Tumor cell αIIbβ3 was shown to mediate tumor cell/platelet interactions in vitro [Chopra et al. (1988) Cancer Res. 48:3787]. Patching and capping of surface αIIbβ3 were inhibited by nifedipine〉diltiazem≫verapamil. The degree of inhibition of αIIbβ3 receptor mobility parallels the inhibition of tumor-cell-induced platelet aggregation. W256 cells are characterized by a well-developed microfilament and intermediate filament network and by the absence of a distinct microtubular network. Calcium channel blockers had no effect on the low polymerization level of tubulin. However, they induced rearrangement of microfilament stress fibers. Intermediate filaments were also rearranged but to varying degrees. The order of effectiveness for alteration of intermediate filament organization was nifedipine〉diltiazem while verapamil was ineffective. We propose that the previously reported inhibition of tumor cell/platelet interaction and tumor cell metastasis by calcium channel blockers [Honn et al. (1984) Clin Exp Metastasis 1:61] is due not only to the effects of the Ca2+ channel blockers on platelets, but also to their effect on the tumor cell cytoskeleton resulting in an inhibition of the mobility and function of the αIIbβ3 receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01629425
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  • 3
    Electronic Resource
    Electronic Resource
    Is there a role for the tumor cell integrin αIIbβ3 and cytoskeleton in tumor cell-platelet interaction? (1992)
    Springer
    Clinical & experimental metastasis 10 (1992), S. 125-137 
    Details
    ISSN: 1573-7276
    Keywords: B16a melanoma ; cytoskeleton ; intermediate filaments ; microfilaments ; αIIbβ3 integrin ; tumor cell-induced platelet aggregation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: In vitro tumor cell-platelet interaction was examined using B16 amelanotic (B16a) melanoma cells. These tumor cells express the αIIbβ3-type cytoadhesin. Aggregation studies demonstrated that tumor cell surface αIIbβ3 mediates the recognition of platelets since pretreatment of tumor cells with antibody against αIIbβ3 prevents platelet-tumor cell interaction as well as platelet activation measured by aggregometry, platelet eicosanoid metabolism and ultrastructural analysis. In B16a cells, disruption of the microfilaments and intermediate filaments inhibits mobility of αIIbβ3 on the cell surface. Microtubules do not play a role in receptor mobility, because B16a cells do not possess well-defined microtubules in interphase and colchicine does not affect receptor mobility. Disruption of microfilaments or intermediate filaments results in an inhibition of tumor cell-platelet interaction as evidenced by aggregometry studies and ultrastructural analysis. We suggest that platelet interaction with tumor cells begins with αIIbβ3-mediated receptor recognition followed by not only platelet activation but also microfilament- and vimentin intermediate filament-dependent tumor cell activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00114589
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  • 4
    Electronic Resource
    Electronic Resource
    Hemostasis and malignancy: an overview (1992)
    Springer
    Cancer and metastasis reviews 11 (1992), S. 223-226 
    Details
    ISSN: 1573-7233
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01307178
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  • 5
    Electronic Resource
    Electronic Resource
    Platelets and cancer metastasis: A causal relationship? (1992)
    Springer
    Cancer and metastasis reviews 11 (1992), S. 325-351 
    Details
    ISSN: 1573-7233
    Keywords: platelet ; metastasis ; TCIPA ; adhesion ; αIIbβ3 ; 12(S)-HETE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cancer metastasis is a highly coordinated and dynamic multistep process in which cancer cells undergo extensive interactions with various host cells before they establish a secondary metastatic colony. Ample morphological studies have documented the close association of circulating tumor cells with host platelets. Several lines of evidence provide strong support for the concept that tumor cell-platelet interactions (i.e., TCIPA) significantly contribute to hematogenous metastasis. Clinically, cancer patients with advanced diseases are characterized by a variety of thromboembolic disorders including thrombocytosis. Pharmacologically, various anti-platelet agents/anticoagulants have demonstrated potent inhibitory effects on tumor cell-platelet interactions as well as spontaneous or experimental metastasis. Experimentally, interference with many of the intermediate steps of tumor cell-platelet interactions has resulted in diminished platelet aggregation induced by tumor cells and blocked cancer metastasis. Platelet interaction with tumor cells is a sequential process which involves two general types of mediators, i.e., membrane-bound molecules (adhesion molecules) and soluble release products. αIIbβ3 integrin receptors present on both platelets as well as on tumor cells and 12(S)-HETE, a 12-lipoxygenase metabolite of arachidonic acid, are prototypical examples of each category. Mechanistically, platelets may contribute to metastasis by: (1) stabilizing tumor cell arrest in the vasculature, (2) stimulating tumor cell proliferation, (3) promoting tumor cells extravasation by potentiating tumor cell-induced endothelial cell retraction, and (4) enhancing tumor cell interaction with the extracellular matrix.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01307186
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  • 6
    Electronic Resource
    Electronic Resource
    Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix (1992)
    Springer
    Cancer and metastasis reviews 11 (1992), S. 353-375 
    Details
    ISSN: 1573-7233
    Keywords: adhesion molecules ; metastasis ; organ preference ; endothelial cells ; subendothelial matrix
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cancer metastasis poses the greatest challenge to the eradication of malignancy. The majority of clinical and experimental evidence indicates that metastasis is a non-random, organ-specific process. Tumor cell interaction with endothelium and subendothelial matrix constitutes the most crucial factor in determining the organ preference of metastasis. A plethora of cell surface adhesion molecules, which encompass four major families (i.e., integrins, cadherins, immunoglobulins and selectins) and many other unclassified molecules, mediate tumor-host interactions. Adhesion molecules and adhesion processes are involved in most, if not all, of the intermediate steps of the metastatic cascade. Decreased E-cadherin expression and increased CD44 expression are clearly correlated with the acquisition of the invasive capacity of primary tumor cells. Similarly, altered expression pattern of many other adhesion molecules such as upregulated expression of the laminin receptors and depressed expression of fibronectin receptors (α5β1) appears to be involved in tumor cell invasion into the subendothelial matrix. Tumor cell-endothelium interactions involve several well-defined sequential steps that can be analyzed by the ‘Docking and Locking’ hypothesis at the molecular level. Tumor cell-matrix interactions are determined by the repertoire of adhesion receptors of tumor cells and the unique composition of organ-specific matrices. Our experimental data, together with others', suggest that the integrin αIIbβ3 is one of the major players in these tumor-host interactions. Tumor-host interaction is a dynamic process which is constantly modulated by a host of factors including various cytokines, growth factors and arachidonate metabolites such as 12(S)-HETE. Delineation of the molecular mechanisms of tumor-host interactions may provide additional means to intervene in the metastatic process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01307187
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  • 7
    Electronic Resource
    Electronic Resource
    Fatty acid modulation of tumor cell-platelet-vessel wall interaction (1992)
    Springer
    Cancer and metastasis reviews 11 (1992), S. 389-409 
    Details
    ISSN: 1573-7233
    Keywords: 12(S)-HETE ; 13(S)-HODE ; TXA2 ; PGI2 ; platelet ; vessel wall ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Prostaglandins and other eicosanoids have been studied extensively in their physical, biochemical, biophysical and pharmacological aspects. However, studies on their role in tumor progression, especially metastases are relatively recent. Following a brief overview of the history of discovery and metabolism of eicosanoids and other fatty acids, we discuss the functions of these fatty acids (with emphasis on prostacyclin, thromboxane A2, 12-hydroxyeicosatetraenoic acid and 13-hydroxyoctadecadienoic acid) in cell transformation, tumor promotion and particularly in tumor cell metastasis. The relation between these monohydroxy fatty acids and tumor cell metastasis is discussed from three different perspectives, i.e., their effects on tumor cells, on platelets and on endothelial cells. The mechanism of these effects are then addressed at cell adhesion molecule, motility, protease, cell cytoskeleton, protein kinase and eicosanoid receptor levels. Finally, regulation of three key enzymes which generate eicosanoids (phospholipase, prostaglandin endoperoxide synthase and lipoxygenase) is explored.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01307189
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibition of tumor cell-platelet interactions and tumor metastasis by the calcium channel blocker, nimodipine (1984)
    Springer
    Clinical & experimental metastasis 2 (1984), S. 61-72 
    Details
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nimodipine, a dihydropyridine calcium channel blocker, was evaluated in vitro for its ability to inhibit platelet aggregation induced by B 16 amelanotic melanoma (B16a) and Walker 256 carcinosarcoma (W256) cells, and for its ability to inhibit platelet-enhanced B16a and W256 adhesion to rat microvascular endothelial cells. Nimodipine produced a dose-dependent inhibition of tumor-cell-induced platelet aggregation (TCIPA). Platelets enhanced tumor cell adhesion to endothelium both in the presence and absence of overt platelet aggregation. However, the greatest enhancement of adhesion occurred under aggregatory conditions. Nimodipine at a dose of 40 µg/ml inhibited platelet-enhanced adhesion to endothelium under aggregatory and nonaggregatory conditions. Nimodipine was tested in vivo for its ability to inhibit both ‘experimental’ and spontaneous metastasis. Nimodipine produced a 46 per cent inhibition of lung colony formation at a dose of 5 mg/kg body-weight. Over a dose range of 0·1–80 mg/kg, nimodipine produced a significant dose-dependent inhibition in the formation of lung metastases from a subcutaneous tumor. The in vitro results demonstrate that a dihydropyridine calcium channel blocker can inhibit tumor cell-platelet-endothelial cell interactions. The in vivo results suggest that these compounds may be a new class of antimetastatic agent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00132307
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  • 9
    Electronic Resource
    Electronic Resource
    Degradation of laminin by human tumor cathepsin B (1989)
    Springer
    Clinical & experimental metastasis 7 (1989), S. 461-468 
    Details
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cathepsin B activity, including that of a plasma membrane-associated cathepsin B, has been linked to tumor malignancy. As cathepsin B at the tumor cell surface has been hypothesized to play a role in the focal degradation of basement membrane during the metastatic cascade, we have examined the ability of human tumor cathepsin B to degrade laminin, an adhesive glycoprotein found exclusively in the basement membrane. We report that at pH 6·5 and 7·0 tumor cathepsin B degraded by specific, limited proteolysis both subunits of native laminin. The disappearance of both subunits and the appearance of lower Mr protein bands could be observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Accumulation of degradation products was also observed using gel filtration chromatography and a fluorescamine assay. The proteolysis of laminin by tumor cathepsin B could be inhibited by an active site titrant for cysteine proteinases or stefin B, an endogenous low-Mr cysteine proteinase inhibitor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01753666
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  • 10
    Electronic Resource
    Electronic Resource
    Involvement of a cathepsin B-like cysteine proteinase in platelet aggregation induced by tumor cells and their shed membrane vesicles (1983)
    Springer
    Clinical & experimental metastasis 1 (1983), S. 297-307 
    Details
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Murine 15091A mammary adenocarcinoma cells and membrane vesicles spontaneously shed from these tumor cells in culture can induce aggregation of washed human platelets. A spectrum of proteinase inhibitors was tested for their ability to inhibit 15091A induced platelet aggregation. Of the inhibitors tested the most effective were those selective for cysteine proteinases. The effect of the spectrum of proteinase inhibitors on 15091A induced platelet aggregation was compared to the effect on cathepsin B-like cysteine proteinase activity in homogenates of 15091A tumor cells and their spontaneously shed vesicles. The results suggest that there is a correlation between activity of a cathepsin B-like proteinase in 15091A cells and vesicles and the ability of these cells and vesicles to induce aggregation of washed human platelets.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00121192
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