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This doctoral thesis is about an animal experimental study in which tumour cachexia was caused by inoculating Yoshida AH-130 hepatomas into rats.
The signals pointing to and involved in the development of tumour cachexia are not yet fully understood. A developed tumour leads to a continuous inflammation reaction, during which characteristically an APR develops because of the production of cytocines by T1 helper cells such as, for example TNF, IL-1, IL-6, IFN and CNTF.
The status caused by the tumour leads to a chronic inflammation and cachexia in cancer patients. Investigated were the effects of medication with EPO and TPM cytoprotective substances on the behaviour of an induced tumour cachexia. Moreover, the combined administration of EPO and TPM with the 1-adrenoceptor inhibitor bisoprolol was studied identically. It could be shown that the administration of EPO or TPM can counteract the cachexia associated with the tumour.
Positive effects on maintaining heart function and an improvement in the general condition were also proven. Well-known adverse reactions of a therapy with EPO like an increased risk of thrombosis, high blood pressure or polycythemia do not appear under a treatment with TPM. The best results were given by the two substances in the high combination with bisoprolol; TPM, which has no haemotopoetic characteristics, was shown to be superior to EPO. Administration of EPO and TPM, especially in combination with bisoprolol, could reduce a cachexia and influence the illness progression positively in rats with a Yoshida AH-130 hepatoma. Further investigative studies should be undertaken to determine the best dosage.