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We have shown that up regulating our patented and patent-pending genes kills human cancer cells in pre-clinical experiments performed with cell lines derived from tumors. We isolated and identified these genes in human cells.
As discussed elsewhere, the immune system targets abnormal cells to die as part of its surveillance system to ensure good health. Tumors arise when these abnormal cells are unable to die due to mutations in their genetically triggered apoptosis "pathways". There are two major apoptosis pathways triggered by the immune system: the DNA damage pathway and the death receptor pathway. We have demonstrated that our genes induce apoptosis in human cancer cell lines through both of these pathways.
In a DNA damage pathway model, we found that when our genes were up regulated in a human carcinoma cell line, virtually 100% of the cancer cells were killed. This pathway contains the well-studied tumor killing gene p53, which promotes apoptosis, as well as the bcl-2 gene, which suppresses apoptosis. Our findings indicate that Factor 5A activates the DNA damage pathway by both up-regulating the expression of p53 and by down-regulating the expression of bcl-2.
On the basis of these findings, we conducted live animal tumor studies to elucidate further the role of our genes and the mechanisms of their action. In our initial mouse studies, the treated mice had a 92% reduction in tumor load. Coincident with this tumor load reduction was an 88% reduction in VEGF, a growth factor which increases vascularization of tumors which aids their growth.
These data led to a mouse longevity study which employed tumor-forming B16F0 melanoma cancer cells. Two control groups of nine mice each received placebo treatments and a test group of ten mice received eIF-5A1 intratumorally every other day. The median survival of the control mice was 7 days post-treatment, whereas the mice that received eIF-5A1 treatment had a median survival of 25 days post-treatment (P< 0.001). The enhanced survival time of the eIF-5A1 -treated mice equates to 3.5 fold or a 250% increase compared to the control mice. Tumor regression, and even remission in one of the treated mice, was seen.
Please click here to see two of the mice from this study.
If you have more technical questions or interests, please contact us directly at info@senesco.com.
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