Carcinogenesis: A multihit, multistage phenomenon

 

UPDATE: Cancer is a disease of the mitochondria. Infection of mitochondria by the Rife BX BY virus (DNA sequenced to be bacillus licheniformis) which causes the cell to flip into anerobic energy generation cycle. If a carcinogen is present the cell starts to mutate. After four steps the cell moves into uncontrollable growth. See Tripping Over the Truth by Travis Christofferson.

 

These bacillus licheniformis organisms can be seen in a 25000x microscope and are photographed in detail in this video. They grow much faster in a solution with carbohydrates, which explains why ketogenic diets help. The researchers using the high power microscopes assert that all saccharides much be removed from the diet of cancer patients, or they are at risk of death from these microbes.

 

The cancer microbes have many strains and frequencies for all identified strains can be found on this web site. Eliminating these microbes has eliminated cancer cells in some researchers with biopsied tumors. From microscopic photos it can be determine that these microbes cause malfunction of heart cells. This is combination with nanobacteria clogging arteries seems to be the root of heart disease.

 

If these organisms infect liver cell mitochondria they can cause fatty liver syndrome. If they infect pancreas mitochondria they can cause diabetes.

 

The multihit research can be found in: Sutherland, Jeff and Bailar, John. The multihit model of carcinogenesis: etiologic implications for colon cancer. J Chronic Dis 1984;37(6):465-80.

 

While this work built on the research of many of the leading scientists earlier in the 20th century, it marked the beginning of a turning point in the conventional wisdom about carcinogenesis. This can be seen in more recent research, for example:

Owens DM, Wei S, Smart RC. A multihit, multistage model of chemical carcinogenesis. Carcinogenesis, Vol. 20, No. 9, 1837-1844, September 1999

Abstract: Carcinogenesis involves the accumulation of genetic changes within a single cell. Tumor promotion functions in the initial clonal expansion of an initiated cell but is generally not considered to influence later stages. To investigate whether tumor promotion can influence later stages of carcinogenesis we developed a two-hit 7,12-dimethylbenz[a]anthracene (D) protocol designed to enrich for keratinocytes that contain at least two D-induced genetic alterations. FVB/N mice were initiated with D and promoted with 12-O-tetradecanoylphorbol-13-acetate (T) or treated with acetone (A) vehicle for 6 weeks. At 7 weeks after the start of promotion, but before visible papilloma development, groups of mice were treated with a second dose of D or A and 1 week later T promotion was resumed. D/T/A/T mice developed 2.8 papillomas/mouse and D/A/D/T mice demonstrated an additive tumor response and developed 5.8 papillomas/mouse. Importantly, D/T/D/T mice developed 12.4 papillomas/mouse, thereby demonstrating a synergistic tumor response compared with D/A/D/T and D/T/A/T mice. D/T/D/T papillomas exhibited increases in suprabasal S phase cells and keratin 13 expression when compared with D/T/A/T papillomas. D/T/D/T mice developed squamous cell carcinomas (SCCs) 10 weeks earlier than D/T/A/T mice and demonstrated a 96% malignancy incidence and 1.71 SCC/mouse compared with D/T/A/T mice, which demonstrated a 28% malignancy incidence and 0.32 SCC/mouse. Greater than 90% of D/T/A/T and D/T/D/T papillomas and SCCs contained mutant Ha-ras, while a normal Ha-ras allele persisted in all cases, indicating that a gene other than the remaining normal allele of Ha-ras was a target gene for the second D hit. These data demonstrate that: (i) promotion between the first and second hits has a profound outcome on carcinogenesis, presumably by increasing the probability that a second hit will occur in a previously initiated cell; (ii) continued promotion after the second hit is required for full expression of malignancy; (iii) the classic initiation–promotion protocol can be extended to a multihit, multistage model.