The biochemistry of rapid replication
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50. Genome Replikin Count™ Predicts Increased Lethality of Cancer
April 3, 2012
(From Nature Precedings: doi:10.1038/npre.2012.7143.1 April 2012)

Samuel Bogoch and Elenore S. Bogoch, Foundation for Research on the Nervous System, Boston University School of Medicine, Bioradar UK Ltd, and Replikins Ltd. 36 The Fenway, Boston, MA 02215

Figure 1- Cancer Mortality Increases With Cancer Cell Replikin Count

This communication is one of four submitted together:

Genome Replikin Count™ Predicts Increased Lethality of Resistant Tuberculosis
Genome Replikin Count™ Predicts Increased Lethality of Malaria
Genome Replikin Count™ Predicts Increased Lethality of Cancer
Genome Replikin Count™ Predicts Increased Infectivity/Lethality of Virus

We have found that the concentration of replikins, a new class of peptides in genomic proteins, are quantitatively related to the mortality rate in human cancer of different cell types. No cancer cell genomic structure has previously been reported to be quantitatively related to mortality rate.

Figure 1 shows the relationship between the Replikin Count™ in the Replikin Peak Gene (see Methods) and the percent mortality in human cancer: the higher the Replikin Count, the higher the percent mortality after 5 years. Glioblastoma multiforme and non-small-cell lung cancer, the two cancer cell types with the greatest 5-year mortality rates in 2002 (98% and 91% respectively), are also the cell types which have the highest Replikin Counts (325 and 250 respectively).

The count in Glioblastoma Multiforme is 18 times higher than the counts in prostate and thyroid cancer which have the lowest Replikin Counts (20 and 15 respectively) as well as the lowest 5-year mortality rates (each approximately 2%). The quantitative relationship of Replikin count to mortality is also seen in the figure for other common cancers, which shows some deviations from an 'ideal' curve. For example, gastric cancer has a higher mortality rate than expected from its Replikin Count (ie shifted to the right), possibly because of the known difficulty of early detection of gastric cancer. Breast and urinary bladder cancer have lower mortality rates than expected from their Replikin Counts (ie shifted to the left), possibly because of the improvement in their early detection and prompt treatment.

To obtain these results, all cancer protein sequences published on PubMed were analyzed by histological cancer cell type by ReplikinForecast™ software. The Replikin Peak Gene (RPGene), that area of the gene which contained the highest oncentration of Replikins, the highest Replikin Count, was identified in each cell type. The replikins in each RPGene were counted (Replikin Count = number of replikins per 100 amino acids). The Replikin count of each RPGene then was compared in the different histological cancer cell types as shown in the Figure.

Replikin count has already been shown to be related to rapid replication, disease outbreaks, and host mortality in viruses such as influenza and HIV, bacteria, malaria, and other infectious diseases (see accompanying communications). The relationship between Replikin count and mortality in cancer parallels that found in H5N1 virus in humans and in Taura Syndrome Virus in shrimp.

The autWe speculate that in low mortality cancers, it is possible that the immune system may be adequate to the number of invading units; but that the increased mortality rate in viruses and in cancer may reflect the overwhelming of host immune defenses by markedly increased numbers of viruses or of cancer cells produced in each case by increasing replikin concentration in the up-regulated Replikin Peak Gene. An increase in number of cancer cells per unit time produced by rapid replication has been demonstrated in the laboratory in the case of glioblastoma multiforme brain cancer cells in tissue culture*. The quantitative relationship of Replikin Count to mortality rate has been demonstrated in the laboratory in four strains of lethal Taura Syndrome Virus in shrimp*.

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