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 2-Iodohexadecanal (2-IHDA) prevents tumor growth. However, the mechanism of action is far from clear.
This study suggests that 2-IHDA, by increasing the expression of its target genes, it may decrease the expression of metastasis promoter PMP22 (fig. 1).
Fig1. Mechanistic insights into 2-Iodohexadecanal (2-IHDA) functions as an anti-metastasis agent
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Thereby, it may inhibit migration, invasion and metastasis of cancer cells. Thus, pharmacological formulations encompassing “2-IHDA or its analogs 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.
Amount: $2
Undisclosed information: How 2-IHDA decreases the expression of metastasis promoter PMP22
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# Research cooperation
References:
Citation: Boominathan, L., Molecular therapy for Metastatic cancers: 2-Iodohexadecanal (2-IHDA) decreases the expression of PPM22 and inhibits migration, invasion and metastasis of cancer cells via up regulation of its target gene, 6/March/2017, 9.34 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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