Monday, November 10, 2014 9:45:52 PM
Cellceutix Makes Breakthrough in Cancer Research by Activating p53, the "Guardian Angel of the Human Genome"
All text and Title from Cellceutix Website News Release!
Cellceutix announced that research on Kevetrin™, the Company’s flagship compound against cancers, has demonstrated the potential for a major breakthrough in cancer research by exhibiting an activation of p53 in both wild and mutant types of p53. p53, often referred to as the “Guardian Angel Gene” or the “Guardian Angel of the Human Genome” due to its crucial role in controlling cell mutations, is a tumor suppressor protein that is encoded by the TP53 gene in humans and has been widely regarded as possibly holding a key to the future of cancer therapies.
p53 has been shown to play critical roles in the homeostatic health of the human body by activating proteins required to repair DNA and plays a major role in the life cycle of cells by inducing cell cycle arrest and apoptosis to maintain cellular and genetic stability.
In more than 50 percent of all human carcinomas, p53 is limited in its anti-tumor activities by mutations in the protein itself. Currently, there are greater than 10 million people with tumors that contain inactivated p53, while a similar number have tumors in which the p53 pathway is partially abrogated by inactivation of other signaling components. This has left cancer researchers with the grand challenge of searching for therapies that could restore the protein’s protective function, which Kevetrin appears to be doing the majority of the time.
Extensive pre-clinical research on Kevetrin has resulted in a compilation of promising data showing a wide therapeutic index through the re-activation of p53. Importantly, Kevetrin has been proven to be non-genotoxic (does not damage DNA). Research has shown Kevetrin to outperform current chemotherapies in testing against multiple cancer lines, including breast, lung, head and neck, colon, prostate, pancreatic and leukemia. Kevetrin is presently in Phase 1 clinical trials for solid tumors at Harvard Cancer Center’s Dana-Farber Cancer Institute and partner Beth Israel Deaconess Medical Center, recognized among the world’s most prominent cancer research centers.
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Below excerpt from Cellceutix PR 11-11-14
Cellceutix has also recently been informed of additional research data from the Company’s Phase 1 trial of Kevetrin for solid tumors being conducted at Harvard’s Dana-Farber Cancer Institute and Beth Israel Deaconess Medical Center. The trial is currently enrolling patients in the ninth cohort. Preliminary data show that 50 percent of patients treated with Kevetrin through the eighth cohort demonstrated enhancement in p21 expression in peripheral blood cells, and that these observations appeared dose-related. The biomarker p21 is tightly controlled by the tumor suppressor protein p53, which is often referred to as the “Guardian Angel Gene” because of its crucial role in controlling cell mutations. Initial comparisons between early and latter cohorts support Cellceutix’s expectations that p53 activation is dependent on extent of exposure to Kevetrin. These results support the hypothesis that Kevetrin has pharmacological activity in patients
CTIX $CTIX
All text and Title from Cellceutix Website News Release!
Cellceutix announced that research on Kevetrin™, the Company’s flagship compound against cancers, has demonstrated the potential for a major breakthrough in cancer research by exhibiting an activation of p53 in both wild and mutant types of p53. p53, often referred to as the “Guardian Angel Gene” or the “Guardian Angel of the Human Genome” due to its crucial role in controlling cell mutations, is a tumor suppressor protein that is encoded by the TP53 gene in humans and has been widely regarded as possibly holding a key to the future of cancer therapies.
p53 has been shown to play critical roles in the homeostatic health of the human body by activating proteins required to repair DNA and plays a major role in the life cycle of cells by inducing cell cycle arrest and apoptosis to maintain cellular and genetic stability.
In more than 50 percent of all human carcinomas, p53 is limited in its anti-tumor activities by mutations in the protein itself. Currently, there are greater than 10 million people with tumors that contain inactivated p53, while a similar number have tumors in which the p53 pathway is partially abrogated by inactivation of other signaling components. This has left cancer researchers with the grand challenge of searching for therapies that could restore the protein’s protective function, which Kevetrin appears to be doing the majority of the time.
Extensive pre-clinical research on Kevetrin has resulted in a compilation of promising data showing a wide therapeutic index through the re-activation of p53. Importantly, Kevetrin has been proven to be non-genotoxic (does not damage DNA). Research has shown Kevetrin to outperform current chemotherapies in testing against multiple cancer lines, including breast, lung, head and neck, colon, prostate, pancreatic and leukemia. Kevetrin is presently in Phase 1 clinical trials for solid tumors at Harvard Cancer Center’s Dana-Farber Cancer Institute and partner Beth Israel Deaconess Medical Center, recognized among the world’s most prominent cancer research centers.
*****
Below excerpt from Cellceutix PR 11-11-14
Cellceutix has also recently been informed of additional research data from the Company’s Phase 1 trial of Kevetrin for solid tumors being conducted at Harvard’s Dana-Farber Cancer Institute and Beth Israel Deaconess Medical Center. The trial is currently enrolling patients in the ninth cohort. Preliminary data show that 50 percent of patients treated with Kevetrin through the eighth cohort demonstrated enhancement in p21 expression in peripheral blood cells, and that these observations appeared dose-related. The biomarker p21 is tightly controlled by the tumor suppressor protein p53, which is often referred to as the “Guardian Angel Gene” because of its crucial role in controlling cell mutations. Initial comparisons between early and latter cohorts support Cellceutix’s expectations that p53 activation is dependent on extent of exposure to Kevetrin. These results support the hypothesis that Kevetrin has pharmacological activity in patients
CTIX $CTIX
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