From 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:
A number of studies suggest that Prodigiosin functions as an anticancer agent. However, the mechanism of action is far from clear.
This study suggests that Prodigiosin, by increasing the expression of its target genes, it may decrease the expression of metastasis promoter PMP22 (figs. 1-3).
Thereby, it may inhibit migration, invasion and metastasis of cancer cells. Thus, pharmacological formulations encompassing “Prodigiosin or its analogues either alone or in combination with other anticancer drugs” may be used to inhibit the progression of invasive tumors.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D.
Undisclosed information: How Prodigiosin decreases the expression of metastasis promoter PMP22
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
# Research cooperation
Citation: Boominathan, L., Molecular therapy for Metastatic cancers: Prodigiosin decreases the expression of PPM22 and inhibits migration, invasion and metastasis of cancer cells via up regulation of its target gene, 3/March/2017, 5.57 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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