On the eve of Mahatma Gandhi Birth Anniversary
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Dr L Boominathan PhD
Director & CSO, GBMD
From Significance of the study to Public health relevance:
Given that: (1) cancer suppressor p53 is mutated in more than 50% of human cancers of different tissue origin; (2) p53 pathway is altered in about 80% of tumors.; (3) our understanding is incomplete in terms of molecular targets and the oncogenic/malignant pathways involved in mutant p53-overexpressing tumors; (4) cancer causes the highest economic loss compared to all the known causes of death worldwide; and (5) cancer causes the considerable economic loss worldwide, there is an urgent need to find: (i) a cheaper alternative to the existing expensive drugs; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and stall metastatic progression and relapse of mutant p53-overexpressing human cancers.
From therapeutic strategy to Research Findings:
(i) Therapeutic strategy:
This study suggests a therapeutic strategy for stalling the progression of p53-deficient/deleted or mutant-p53 expressing metastatic cancers. By activating tumour suppressor p53’s unmutated “homologous protein such as TAp73/p63” in p53-deficient or mutant-p53 expressing metastatic cancer cells, one can stall their progression.
(ii) Research findings:
This study suggests that Act1 (Adaptor for IL-17 receptors) may function as a tumor suppressor gene in mutant p53 expressing human cancers.
This study suggests that Mibolerone, by increasing the expression of its target gene, it may increase the expression of tumor/metastasis suppressors genes, such as TPM1, CCM3/KRIT1, p53, TA-p73, p53, INK4a/ARF and others. Thereby, it may inhibit the migration and invasion of metastatic cancer cells expressing mutant-p53 (figure1).
Given the ability of Act1 (Adaptor for IL-17 receptors) to induce the expression of a number of tumor/metastasis suppressor genes, it may be used, either alone or in combination with other anticancer drugs, to inhibit the progression of p53-mutated invasive metastatic tumors. Taken together, this study suggests, for the first time, that oncologists may consider treating metastatic cancer patients with activators of Act1 (Adaptor for IL-17 receptors), as it may stall the progression of advanced metastatic cancers. (figure 2).
Details of the research findings:
Idea Proposed/Formulated by Dr L Boominathan Ph.D.
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
Undisclosed mechanistic information: How Act1 (Adaptor for IL-17 receptors) increases the expression of tumor suppressor genes, such as ANP32A, VHL, p53, p53, TAp63, TAp73, INK4a/ARF and others, in mutant p53 expressing cancer cells?
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Citation: Boominathan, L., Awakening the sleeping/cancer-protecting angels in mutant p53-expressing human tumors: Act1 (Adaptor for IL-17 receptors) increases the expression of tumor suppressors genes, such as ANP32A, VHL, p53, p53, TAp63, TAp73, INK4a/ARF, and others, induces regression of p53-mutated human tumors, via down-regulation of its target gene, 2/October/2018, 11.56 pm, Genome-2-Biomedicine Discovery center (GBMD), http://genomediscovery.org
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