Counterattack – a principle of tumour cell metastasation?

  • N Freudenberg1,

    Affiliated with

    • S Göppinger2,

      Affiliated with

      • A Gold1,

        Affiliated with

        • C Galanos3 and

          Affiliated with

          • MA Feudenberg3

            Affiliated with

            Diagnostic Pathology20072(Suppl 1):S25

            DOI: 10.1186/1746-1596-2-S1-S25

            Published: 14 March 2007

            Aims

            The aim of the present study was to investigate whether tumour cell supernatants of 4 different malignant tumour cell lines with different aggressive behaviour show comparable pathobiological reactions.

            Methods

            Mature mouse (C57/Bl6) macrophages were incubated with the a.m. different tumour cell supernatants and followed by the investigation of apoptosis factors using immunocytochemistry. In addition, the experiments were performed with Fas-knock-out mouse macrophages and PCR in order to investigate the involvement of the Fas/FasL system.

            Results

            All tumour cell supernatants investigated induced a significant increase of apoptototic activities in macrophages compared with control groups. Interestingly, the tumour cell supernatants showed differences in their intensities of apoptosis-inducing effects on the macrophages one to each other. The Fas/FasL system has been identified as one of the involved factors from tumours which induce apotoses in macrophages.

            Conclusion

            Our observation of the induction of apoptoses in macrophages due to so far undefined tumour cell factors supports the counterattack hypothesis which supposes the active destruction of the tumoricidal cell system by neoplastic cells. For now, the counterattack is an exciting new way for research in tumour immunology and probably offers a therapeutic potential.

            Authors’ Affiliations

            (1)
            Institut für Pathologie der Universität Freiburg
            (2)
            Institut für Pathologie der Universität Heidelberg
            (3)
            Max-Planck-Institut für Immunbiologie Freiburg

            Copyright

            © Freudenberg et al 2007

            This article is published under license to BioMed Central Ltd.

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