Studies on tumor-cell induced platelet aggregation in human lung cancer cell lines

Heinmoller, E and Weinel, RJ and Heidtmann, HH and Salge, U and Seitz, R and Schmitz, I and Muller, KM and Zirngibl, H (1996) Studies on tumor-cell induced platelet aggregation in human lung cancer cell lines. JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY, 122 (12). pp. 735-744. ISSN 0171-5216,

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Abstract

We investigated the ability of human lung cancer cells of different histological subtypes to cause platelet aggregation. Tumor-cell-induced platelet aggregation (TCIPA) was studied in vitro in 13 human lung cancer cell lines [small-cell lung cancer (SCLC), squamous-cell lung cancer, large-cell lung cancer, adenocarcinoma and alveolar-cell lung cancer]. Three tumor cell lines failed to aggregate platelets in platelet-rich plasma, whereas platelet aggregation was induced by 12 cell lines when added to washed platelets and minimal amounts of platelet-poor plasma (0.5% v/v). The thrombin antagonist hirudin inhibited TCIPA in non-small-cell lung cancer cell lines (NSCLC). In SCLC, TCIPA was fully abolished only when the ADP scavenger apyrase was added to hirudin. Thus ADP and thrombin generation by these tumor cell lines are responsible for platelet aggregation. The ability to activate platelets independently of coagulation factors VII and X was demonstrated for 8 cell lines. Electron-microscopically, direct tumor-cell/platelet contact was found to be the initiating mechanism of TCIPA in SCLC, whereas tumor-cell/platelet contacts in NSCLC could only be observed at the peak of the aggregation curve. Lung cancer cells activate platelets in vitro by generation of thrombin and/or ADP.

Item Type: Article
Uncontrolled Keywords: THROMBIN GENERATION; COLON ADENOCARCINOMA-26; MONOCLONAL-ANTIBODIES; CULTURED INVITRO; SQUAMOUS-CELL; GROWTH-FACTOR; IIB-IIIA; ACTIVATION; CARCINOMA; MEMBRANE; coagulation; lung cancer; platelet aggregation
Depositing User: Dr. Gernot Deinzer
Last Modified: 19 Oct 2022 08:34
URI: https://pred.uni-regensburg.de/id/eprint/51296

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