The inhibition of cancer cell stickiness by somatostatin

We employed a test model, which we had developed for the investigation of platelet adhesiveness and aggregation in vivo. Our experiments demonstrated that somatostatin is not only able to dose-dependently inhibit the stickiness of i.v. injected Walker 256 carcinosarcoma cells to the vascular endothe...

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Bibliographic Details
Published in:Research in experimental medicine 1983-01, Vol.182 (1), p.1-6
Main Authors: GASTPAR, H, ZOLTOBROCKI, M, WEISSGERBER, P. W
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Carcinoma 256, Walker - pathology
Cell Adhesion - drug effects
Dose-Response Relationship, Drug
General aspects (metabolism, cell proliferation, established cell line...)
Medical sciences
Platelet Adhesiveness - drug effects
Platelet Aggregation - drug effects
Rats
Rats, Inbred Strains
Somatostatin - pharmacology
Tumor cell
Tumors
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Summary:We employed a test model, which we had developed for the investigation of platelet adhesiveness and aggregation in vivo. Our experiments demonstrated that somatostatin is not only able to dose-dependently inhibit the stickiness of i.v. injected Walker 256 carcinosarcoma cells to the vascular endothelium of the rat mesentery and the drastic, immediate reduction of platelet count in venous blood, but also to significantly reduce the rate of instantly occurring terminal tumor cell embolism of the lung. These actions may be explained as being mediated via an inhibition of platelet adhesion and aggregation to circulating cancer cells. Because some oral antidiabetics showed a similar but weaker effect in our test system (Gastpar et al. 1982), it should be examined as to whether the in vivo inhibition of platelet adhesiveness and aggregation of the investigated compounds are mediated by a somatostatin release from the pancreas.
ISSN:0300-9130
1433-8580
DOI:10.1007/BF01852280