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

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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

price-100[easy_payment currency=”USD”]


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?

For purchase and payment details, you may reach us at admin@genomediscovery.org

# Research cooperation


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

Web: http://genomediscovery.org or newbioideas.com 

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