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Interactions between neoplastic cells with different metastasizing capacity and platelet function.

G Grignani, P Almasio, L Pacchiarini

    European Journal of Cancer & Clinical Oncology
    |April 1, 1983
    PubMed
    Summary
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    More malignant fibrosarcoma cells induce platelet aggregation and serotonin release, suggesting platelets play a role in tumor metastasis development. Aspirin (ASA) inhibited these effects.

    Area of Science:

    • Oncology
    • Hematology
    • Biochemistry

    Background:

    • Cancer metastasis is a complex process involving interactions between tumor cells and the host.
    • Platelets are known to interact with cancer cells, but their precise role in metastasis is not fully understood.

    Purpose of the Study:

    • To investigate the effects of different murine fibrosarcoma (m FS6) sublines with varying metastatic potential on human platelet function.
    • To determine if tumor cell malignancy correlates with platelet aggregation and serotonin release.

    Main Methods:

    • Two sublines (M4 and M9) of m FS6 fibrosarcoma, differing in metastatic potential, were used.
    • Platelet aggregation and serotonin release assays were performed upon incubation with tumor cells or their culture supernatants.
    • The effect of aspirin (ASA) on these interactions was evaluated.

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    Main Results:

    • Highly metastatic M4 cells, but not less metastatic M9 cells, induced irreversible human platelet aggregation and serotonin release.
    • This platelet activation was concentration-dependent and inhibited by preincubation of platelets with ASA.
    • Neoplastic cells released an activity that directly stimulated platelet aggregation and potentiated the response to ADP, with higher activity from more malignant cells.

    Conclusions:

    • Tumor cell malignancy is associated with the ability to activate platelets.
    • Platelet activation by tumor cells, including serotonin release, may be inhibited by aspirin.
    • These findings suggest a significant role for platelets in the development of tumor metastases.