The capacity of immune system to control and shape cancer, that is, cancer immunoediting, is the result of three processes, which function either independently or in sequence: elimination (cancer immunosurveillance, in which immune system functions as an extrinsic tumour suppressor in naive hosts); equilibrium (expansion of transformed cells is held in check by immune system); and escape (tumour cell variants with dampened immunogenicity or with the capacity to attenuate immune responses grow into clinically apparent cancers). The current belief about treating cancer is that tumour cells need to be eradicated as quickly as possible, so as to halt tumour growth and spread, and to prevent or delay the death of the patient, but considering cancer as a fatal disease is not always appropriate. In this study we used a cell line model, BB1 cells, to explain latency or dormancy of the tumour. This cell line was isolated from mammary carcinoma of transgenic FVB/neuT mice and it showed its tumorigenicity when inoculated in syngeneic FVB/neuT mice. Herein we use a murine model (FVB wild type mice) where BB1 tumour cells were injected subcutaneously into the backs of the animal and then monitored for tumour development. The results of this study show the capacity of immune system to destroy and shape cancer and also to control cancer for long time periods by a process called ''equilibrium''. Furthermore, we showed that ''equilibrium'' is a component of cancer immunoediting because tumour cells in equilibrium are highly immunogenic, whereas those that spontaneously exit equilibrium condition and become growing tumours have attenuated immunogenicity. These results place this process temporally between elimination and escape.

CANCER IMMUNE TOLERANCE, IMMUNOSURVEILLANCE AND IMMUNOEDITING: USE OF A STABILIZED TUMOURIGENIC CELL LINE FROM HER-2/neu TRANSGENIC MICE AS TUMOUR DORMANCY MODEL

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2008-07-01

Abstract

The capacity of immune system to control and shape cancer, that is, cancer immunoediting, is the result of three processes, which function either independently or in sequence: elimination (cancer immunosurveillance, in which immune system functions as an extrinsic tumour suppressor in naive hosts); equilibrium (expansion of transformed cells is held in check by immune system); and escape (tumour cell variants with dampened immunogenicity or with the capacity to attenuate immune responses grow into clinically apparent cancers). The current belief about treating cancer is that tumour cells need to be eradicated as quickly as possible, so as to halt tumour growth and spread, and to prevent or delay the death of the patient, but considering cancer as a fatal disease is not always appropriate. In this study we used a cell line model, BB1 cells, to explain latency or dormancy of the tumour. This cell line was isolated from mammary carcinoma of transgenic FVB/neuT mice and it showed its tumorigenicity when inoculated in syngeneic FVB/neuT mice. Herein we use a murine model (FVB wild type mice) where BB1 tumour cells were injected subcutaneously into the backs of the animal and then monitored for tumour development. The results of this study show the capacity of immune system to destroy and shape cancer and also to control cancer for long time periods by a process called ''equilibrium''. Furthermore, we showed that ''equilibrium'' is a component of cancer immunoediting because tumour cells in equilibrium are highly immunogenic, whereas those that spontaneously exit equilibrium condition and become growing tumours have attenuated immunogenicity. These results place this process temporally between elimination and escape.
lug-2008
Orlando, Fiorenza
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11581/401885
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