What they say:
A recent study from the Department of Cell Biology, University of Texas Southwestern Medical Center, Texas 75390, USA shows that XPO1 can be pharmacologically targeted in KRAS-mutant lung cancer. This study was published in the 28 September 2016 issue of Nature by Prof Michael A.White, Kim, and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for KRAS-mutant lung cancer: UBTD1 (Ubiquitin domain containing 1) decreases the expression of XPO1, increases the level of NFKBIA, inhibits NFKB transcriptional activity and suppresses the progression of KRAS-mutant lung cancer via up regulation of its target gene
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From Significance of the study to Public health relevance:
Given that: (1) 20-30% of people with lung cancer have mutations in k-ras gene; (2) out of 1.82 million people diagnosed with lung cancer in 2012, 1.56 million people died; (3) most of the k-ras mutation-containing lung tumors are not amenable to radiation therapy; (4) there are no effective anti-ras therapy available at present; (5) lung cancer is one of the most frequent cancer in men; (6) lung cancer is more common in developed countries than in developing countries; and (7) the global economic cost spent for lung cancer treatment is enormous, there is an urgent need to find: (a) a newer and effective treatment for K-ras mutated lung cancers; (b) a cheaper alternative to the existing expensive non-specific drugs; and (c) a Natural product-based side-effect-free drug.
What is known?
Prof. Michael A. White’s research team has recently shown that inhibition of XPO expression in lung cancer inhibits the progression of K-ras mutated lung cancer through down-regulation of NFKB transcriptional activity.
From Research findings to Therapeutic opportunity:
On the foundation of this interesting finding, this study suggests a Natural product-based anti-cancer therapy for K-ras mutated human cancers. UBTD1, by increasing the expression of its target gene, it may decrease the expression of XPO1. Thereby, it may: (1) increase the levels of NFKBIA, (2) inhibit NFKB transcriptional activity; and (3) suppress the progression of KRAS-mutant lung cancer. Thus, by treating lung cancer patients with UBTD1 activators, one may prevent the progression of Kras-mediated lung cancer. Together, this study suggests that pharmacological formulations encompassing “UBTD1 activators” may be used to inhibit the progression of Kras-mediated lung cancer.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D.
Amount: $100#
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Undisclosed mechanistic information: How UBTD1 decreases the expression of XPO1?
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References
Citation: Boominathan, L., Molecular therapy for KRAS-mutant lung cancer: UBTD1 (Ubiquitin domain containing 1) decreases the expression of XPO1, increases the level of NFKBIA, inhibits NFKB transcriptional activity and suppresses the progression of KRAS-mutant lung cancer via up regulation of its target gene, 27/November/2016, 8.03 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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