Background: Classical tumor treatments can fail: surgeries, radiation and chemotherapy not always elongate the life span. Less destructive treatments are possible nowadays. To find and analyse the efficiency of alternate treatments, long term case reports are essential. Aim: To determine long term analyses of Amanita treatment in patients with different tumor types. Methods: Patients are treated with Amanita alone, as long as the tumor growth of cells can be retarded. Other anti tumor therapies are applied in addition, when the retardation of the tumor growth is not sufficiently manageable with Amanita alone. The treatments with Amanita are supported by application of Terebinthina laricina in intervals to eliminate Borrelia. Results: The state of a patient with a thyroid-carcinoma and a rectum-carcinoma can be stabilized for ten years with Amanita alone, until her age of 90 years. The patient cannot further tolerate uptake of Amanita. Thyroid cells start to grow, rectum-carcinoma cells grow slower. The disease state of a patient with prostate-carcinoma can be stabilized with Amanita alone for six years. Other therapies are applied from then on in intervals in addition for further six years. No chemotherapy or radiation is applied. The patient died at the age of 84 with metastases. A patient with B-cell chronic lymphatic leukemia is treated with Amanita as sole antitumor therapy for eleven years. After that period, no further antitumor treatment is necessary, the patient lives now with high but stable leukocyte count for two years after the end of the Amanita therapy. Conclusions: Amanita can inhibit tumor growth of different tumor types for a long period of time, elongation of the life span is possible. A synergistic effect of anti-Borrelia treatment is observed. Occasionally the tumor growth of cells stops without further anti tumor therapy, and no correlation with the origin can be identified.

With the definition of four gene classes, all differences between tumor cells and normal cells can be explained. Proliferative mutations induce a shortcut, forcing the cell to divide. They allow replication without control, induce somatic pairing defects of chromosomes and genome instability. Intact Tumor Supressors or mutant Switch Functions can inhibit this process. Oncogene mutations optimize the growth of the cells.

Aims: Amanita phalloides contains alpha-amanitin, inhibiting RNApolymeraseII. Due to overexpression of switch genes in tumor cells, RNApolymeraseII is used to full extent there. Partial inhibition with amanitin influences tumor cell but not normal cell activity. A patient with diagnosed prostate cancer was treated successfully for six years with Amanita alone, prostate specific antigen levels increased slowly. However, the necessary dose for stabilization of the level increased during this time. To circumvent further habituation or resistance, other therapeutics were applied in intervals. Presentation of Case: Inhibitors of 5-alpha-reductase were applied in intervals of pausing Amanita. They can further stabilize the prostate antigen level, but tumor cells became resistant to this drug after a few months. The patient suffered under severe side effects. Melatonin was applied in one interval together with Amanita. It shows no additional side effect, but no additional advantage for the patient occurs. Discussion and Conclusion: Amanita is the drug for long term stabilization of a tumor patient. Fast occurrence of resistance was never observed so far. 5-alpha-reductase inhibitors can be Case Report Riede; BJMMR, 17(5): 1-6, 2016; Article no.BJMMR.27895 2 applied in shorter intervals, with speedy development of resistance. Melatonin has no advantageous effect for this patient. Consequent monitoring for all therapy steps is recommended.

Objectives: Amanita phalloides contains amanitin, inhibiting RNA polymerase II. Partial inhibition with amanitin influences tumor cell - but not normal cell - activity. A patient with diagnosed B-cell chronic lymphatic leukemia was treated successfully for eight years with Amanita phalloides . However, the necessary dose for stabilization of the disease increased during this time. In addition thrombocyte levels decreased, indicating bone marrow affection. Therefore additional regimen was necessary. Methods: Chelidonium

ABSTRACT Background: To date, Chronic Lymphocytic Leukemia (CLL) has been viewed as a malignant disease with tumor growth of cells. This hypothesis should be reviewed. Methods: A patient diagnosed with CLL is treated with Amanita phalloides, containing amanitin, inhibiting specifically tumor cell activity without affecting normal cells. Despite initial leukocyte cell count decrease, further therapy fails after eight months. He suffers from severe symptoms of inflammation, not specific for CLL. Additional Borrelia infection is diagnosed and Terebinthina laricina is applied. Results: Herxheimer reaction occurs some weeks later, accompanied by continuous leukocyte cell count drop to normal range within four months, even after stopping Amanita therapy. All symptoms of borreliosis and CLL vanished. Conclusion: CLL might be induced by a Borrelia-infection. This should be considered in diagnostic and therapeutic regimen. Keywords: Amanita phalloides; Terebinthina laricina; CLL; lyme disease; Borrelia infection. Case Study

Fluidity of cellular membranes is essential for life. Two possibilities are known to keep human membranes fluid: unsaturated fatty acids and cholesterol. Whereas liver cells can synthesize cholesterol, unsaturated fatty acids are essential. Life style in Western civilization leads to deprivation of essential fatty acids, to elevated serum-cholesterol-levels and to autoimmunity. Here the hypothesis is presented, and explains the relationship: deprivation of essential fatty acids lead to imminent quasi-crystallization of the membrane. Serum cholesterol-levels are elevated. Incorporation of cholesterol into membranes enhancing fluidity again, is able to repair the effect. At saturation, repair fails. Quasi-crystallization occurs. Proteins tilt into another conformation. This has not been learned during the "self" recognition process of the immune system during the embryonic phase. Immune system attacks the new conformation as "non-self", autoimmunity emerges.

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.

Molecular events that cause tumor formation upregulate a number of HOX genes, called switch genes, encoding for RNApolymeraseII transcription factors. Thus, RNApolymeraseII is used to full extent in tumor cells but not in somatic cells. Amanita phalloides contains amanitin, inhibiting RNApolymeraseII. Application of Amanita phalloides influences tumor cell (but not normal cell) activity. Dilutions of Amanita phalloides are applied to a patient with both, colon carcinoma and thyroid carcinoma. Monitoring tumormarkers, different doses of Amanita are applied. After two years of stabilization, somatic investigations and imaging methods reveal complete remission. Change of dietary practice with the addition of daily 70 gram sugar lead to increase of tumormarker values. Following dietary without sugar and reduced carbohydrates decrease tumormarker values. With sugar, tumor activity increase despite Amanita tumor therapy, therefore, poor carbohydrate diet supports the therapy

C-propeptide, ABSTRACT The nucleotide sequence of a segment of the chick al type III collagen gene which codes for the C-propeptide was determined and compared with the corresponding sequence in the al type I and a2 type I collagen genes. the a2 I gene coding information the C-propeptide of the collagen gene in four exons. Similarly, the amino proximal exon contains sequences for both the carboxy terminal end of the a-helical segment of collagen and for the beginning of the C-propeptide in both genes. There-fore, this organization of exons must have been established before these two collagen genes arose by duplication of a connon ancestor. and

The central biochemical events in tumor induction are not completely understood. In a novel cell biochemical approach some questions are answered here. A proliferative mutation allows replication shortcuts to the S-phase in the cell cycle. The repair system is involved in tumor formation, and many tumor cells cannot be brought to apoptosis induction. This study illuminates the biochemical pathways of these features. Mutational translocations within the gene ALL-1 might cause human acute leukemia. In those leukemic cell lines, replication starts immediately after mitosis. Mutations thus, allow replication without control, defining ALL-1 as the proliferative gene. Cells metabolize their DNA continuously. The repair system is constantly active. Cells are blind to DNA damage by methylating agents and then replicate and repair their DNA. Induction of apoptosis fails. Thus, chemotherapy resistance is intrinsic. Tumor induction occurs by a mutation that allows replication and turns on the repair system.

Lyme disease antibiotic therapy regimens are recommended by the Centres for Disease Control and Prevention, the Infectious Disease Society of America, and the National Institutes of Health. Alternative approaches consist of prolonged antibiotic treatment however Lyme disease often results in persistent Borrelia burgdorferi infection. Continuous antibiotic therapy results in low lymphocyte levels thus cannot be applied for long term without harm. Objectives: Alternative approaches for treatment of Lyme borreliosis are required, which successfully reduce or erase bacteria without affecting the human cells. Terebinthina laricina, an alcoholic extract of Larix decidua resin was selected for a pilot study to treat a patient with neuroborreliosis. Results: After six weeks of treatment, the patient shows a strong Herxheimer reaction. No disease progression occurs, within weeks she recovers from most of the Lyme disease specific symptoms. Elispot results indicate no bacterial activity. Conclusion: This new principle of Lyme disease treatment shows high potential to provide a smooth medical treatment for neuroborreliosis.

C-propeptide, ABSTRACT The nucleotide sequence of a segment of the chick al type III collagen gene which codes for the C-propeptide was determined and compared with the corresponding sequence in the al type I and a2 type I collagen genes. the a2 I gene coding information the C-propeptide of the collagen gene in four exons. Similarly, the amino proximal exon contains sequences for both the carboxy terminal end of the a-helical segment of collagen and for the beginning of the C-propeptide in both genes. There-fore, this organization of exons must have been established before these two collagen genes arose by duplication of a connon ancestor. and

Molecular events that cause tumor formation up regulate a number of HOX genes, called switch genes, coding for RNA polymerase II transcription factors. Thus, in tumor cells RNA polymerase II is more active than in other somatic cells. Amanita phalloides contains Amanitin, inhibiting RNA polymerase II. Partial inhibition with Amanitin influences tumor cell - but not normal cell - activity. Objectives: To enlarge treatment spectrum, dilutions of Amanita phalloides, are applied to prostate cancer patients. Monitoring prostate specific antigen, different doses of Amanitin are used. Results: Within a period of up to five years, prostate specific antigen values can be stabilized. Somatic investigations and imaging methods reveal remission in all three cases. No prostate cancer associated symptoms, nor liver damage occur. When pausing the therapy, PSA levels always increase, even after five years. Conclusion: This new principle of tumor therapy shows high potential to provide a smooth medical treatment. Treatment should exceed the period of five years.

Molecular events that cause tumor formation enhance a number of HOX genes, called switch genes, coding for RNApolymeraseII transcription factors. Thus, in tumor cells, RNApolymeraseII is more active than in other somatic cells. Amanita phalloides contains amanitin which inhibits RNApolymeraseII. Partial inhibition with amanitin influences tumor cell - but not normal cell - activity. To widen the treatment spectrum, dilutions of Amanita phalloides, containing amanitin, are applied to a patient with mammary duct cancer. For monitoring tumormarkers, different doses of amanitin are applied. The former duplication time of tumor growth represented three months; however within a period of 18 months the patient can be stabilized without further growth of the tumor. There are also no severe symptoms, no liver damage and no continuous erythrocyte deprivation. This new principle of tumor therapy shows high potential to provide a medical treatment.

BACKGROUNDMolecular events that cause tumor formation upregulate a number of HOX genes, called switch genes, coding for RNA polymerase II transcription factors. Thus, in tumor cells, RNA polymerase II is more active than in other somatic cells. Amanita phalloides contains amanitin, inhibiting RNA polymerase II. Partial inhibition with amanitin influences tumor cell--but not normal cell--activity.OBJECTIVESTo widen the treatment spectrum, homeopathic dilutions of Amanita phalloides, containing amanitin, were given to a patient with leukemia. Monitoring the leukemic cell count, different doses of amanitin were given.RESULTSThe former duplication time of leukemic cells was 21 months. Within a period of 21 months, the cell count is stabilized to around 10(5)/μL. No leukemia-associated symptoms, liver damage, or continuous erythrocyte deprivation occur.CONCLUSIONSThis new principle of tumor therapy shows high potential to provide a gentle medical treatment.

Drosophila tumor forming lines (malignant brain tumor, lethal giant larvae, discs large, brain tumor, and tumor suppressor gene) exhibit incomplete somatic pairing of specific regions in the salivary gland chromosomes, indicating that excessive cell proliferation correlates with somatic pairing defects in Drosophila. Alleles of malignant brain tumor enhancing the frequency of cell divisions exhibit melanizing tumors in the larvae. The giant chromosomes are defective in somatic pairing, indicating that a functional component of the chromosomes is influenced. Genes at different sites are affected, but the similarity of the phenotypes and complex complementation pattern reveals that their functions are interrelated. In the brain of malignant brain tumor recombinants and mutants in proliferative genes, polytene cells appear; wildtype does not amplify DNA in brain tissue cells. Thus, mutant proliferative genes induce the S-phase and allow replication of DNA.

The Drosophila melanogaster strain Malignant Brain Tumor reveals temperature-sensitive transformation of the larval brain tissue. Genetic analysis shows that three gene defects, spzMBT, yetiMBT, and tldMBT, cooperatively induce brain tumor formation. Whereas spz and tld belong to the genes inducing differentiation patterns in the embryo, yeti induces cell overgrowth. spzMBT-, yetiMBT-, and tldMBT-containing animals are larval lethal, whereas Malignant Brain Tumor is kept as a homozygous strain at a permissive temperature. This reveals that this tumor-forming strain is the result of a number of adaptive mutation events.