Combinatorial therapy for Metastatic cancers: A pharmaceutical mixture encompassing Docosahexaenoic acid (DHA) and Aspirin (ASA) increases the expression of tumor/metastatic suppressors GRHL3 and Long ncRNA GAS5 , inhibits cell cycle progression, and suppresses migration, invasion and metastasis of cancer cells via up regulation of its target gene, 21/February/2018, 6.00 am
Molecular therapy for autoimmune diabetes (TIDM): Ursodeoxycholic acid increases PD-L1 expression, increases Tregs function, promotes immune tolerance, increases pancreatic β-cell proliferation and regeneration, increases insulin secretion, improves insulin sensitivity, increases energy utilization, and reverses TIDM, via up regulation of its target gene, 20/February/2018,12.41 am
February 19, 2018
Combinatorial therapy for blood-stage Plasmodium infection: A therapeutic mix encompassing Ketorolac (Trade name: Toradol, Acular, Sprix] and Aspirin (anti-inflammatory drugs) decreases the expression of CTLA-4, PD-L1 and LAG-3, promotes CD4+ T-cell function, increases secretion of protective antibodies, promotes and clear blood-stage malaria via up regulation of its target gene, 21/February/2018, 6.13 am
February 21, 2018From significance of the study to Public health relevance:
Given that: (i) each year nearly 14 million people are diagnosed with cancer globally, and little more than half of them will die; (ii) cancer deaths globally are expected to be doubled by 2030; (iii) most of the cancer patients die due to metastasis; (iv) cancer treatment causes the highest economic loss compared to all the known causes of death worldwide, there is an urgent need to find: (i) bio-molecules that drive metastatic process; and the the way to prevent their expression; (ii) a way to activate immune system to combat cancer (Cancer immunotherapy); (ii) a cheaper alternative to the existing expensive anticancer drugs; (ii) a side-effect-free natural product-based drug; (iii) increase the therapeutic index of anticancer drugs; and (iv) a way to effectively treat and prevent metastatic progression and relapse of advanced/drug-resistant cancers.
Research findings to Therapeutic opportunity:
This study suggests, for the first time, that a pharmaceutical mixture(DHAASA) encompassing Docosahexaenoic acid (DHA) and Aspirin (ASA), by regulating the expression of its target genes, it may increase the expression of tumor/metastatic suppressors GRHL3 and Long ncRNA GAS5 (fig. 1).
Thereby, it may: (a) inhibit cell cycle progression; and (b) suppress migration, invasion and metastasis of cancer cells. [easy_payment currency=”USD”]
Given the mechanism of action of DHAASA , it may be an ideal anti-metastatic agent to (i) increase the expression of metastasis suppressor genes in tumors; (ii) inhibit the progression of metastatic tumors; and (ii) enhance the efficacy of Cancer therapy.
Taken together, this study suggests that oncologists may consider treating terminally ill metastatic cancer patients with Docosahexaenoic acid (DHA) and Aspirin (ASA) , as it may stall the progression of advanced metastatic cancers.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D
Amount: $5
Undisclosed mechanistic information: How a pharmaceutical mixture encompassing Docosahexaenoic acid (DHA) and Aspirin (ASA) increases the expression of tumor/metastatic suppressors GRHL3 and Long ncRNA GAS5
Fig1. Mechanistic insights into how a therapeutic mix encompassing Docosahexaenoic acid (DHA) and Aspirin (ASA) functions as an anti-metastasis agent. Docosahexaenoic acid (DHA) and Aspirin (ASA) increase the expression of tumor/metastatic suppressors GRHL3 and Long ncRNA GAS5 via up regulation of their target genes
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References:
Citation: Boominathan, L., Combinatorial therapy for Metastatic cancers: A pharmaceutical mixture encompassing Docosahexaenoic acid (DHA) and Aspirin (ASA) increases the expression of tumor/metastatic suppressors GRHL3 and Long ncRNA GAS5 , inhibits cell cycle progression, and suppresses migration, invasion and metastasis of cancer cells via up regulation of its target gene, 21/February/2018, 6.00 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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