Switch the Tumor Off: From Genes to Amanita Therapy

Isolde Riede^1,

¹Independent Cancer Research, Im Amann, Uberlingen, Germany

Cite this paper:
Isolde Riede. Switch the Tumor Off: From Genes to Amanita Therapy. American Journal of Biomedical Research. 2013; 1(4):93-107. doi: 10.12691/ajbr-1-4-5

Abstract

Tumor formation is due to somatic mutations. Mutant oncogenes and tumor suppressor genes lead to destabilization of the differentiation pattern and to defect cell adhesion. Proliferative genes are the cause of tumor formation, allow replication and thereby shortcut the cell cycle. At least one proliferative mutation is present in every tumor cell. Biochemical characteristics for tumor cells are onset of replication, constitutive onset of the repair system, and cell death defects. A successful tumor therapy inhibits specifically tumor cell activity and not the immune response. Thereby, the immune system is able to recognize and to digest tumor cells. In search of the center of the tumor pathways, switch genes are identified, that influence in trans tumor cell activity. Switch genes are not mutant, but overexpressed in human tumor cells. All switch proteins are RNApolymeraseII transcription factors. Therefore in tumor cells RNApolymeraseII should be used to full extent. Amanita phalloides contains amanitin, inhibiting RNApolymeraseII. Applying Amanita phalloides dilutions lead to reduction of the tumor cell activity, and in cancer patients to stabilization of the disease state, or eventually to remission.

Keywords:
tumor formation oncogenes tumor suppression proliferative genes switch genes Amanita phalloides tumor therapy

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