Defeating Resistant Lung Cancer Using CRISPR

    New groundbreaking research from ChristianaCare's Gene Editing Institute has revealed that CRISPR gene editing can disable the NRF2 gene in lung cancer cells (a key culprit in chemotherapy resistance. When NRF2 is overactive, tumors become a lot more resilient to standard drugs, but by knocking it out using CRISPR/Cas9, researchers were able to restore the cancer cells' sensitivity to chemotherapy and slow tumor growth.

    One of the most promising areas of this work is how precisely the team targeted the resistance mechanism. They were able to lock in on a tumor-specific mutation called R34G and NRF2 while using lipid-nanoparticles (LNPs) to deliver CRISPR safely into tumors in animal models. Amazingly, editing only 20% to 40% of the tumor cells was enough to boost the effectiveness of chemotherapy, a promising insight given that editing each individual cancer cell is not realistic in real-world treatment.

    Thus research could alter the way individuals think about cancer treatment, Rather than creating entirely new therapies, scientists are using gene editing to make existing chemotherapy more effective. Because NRF2 is implicated in resistance across a variety of solid tumors (not only lung cancer), this approach has the potential to benefit several patients. It is still early, but the precision, the targeted delivery, and the dramatic resensitization of tumors all look toward a powerful new weapon in the fight against drug-resistant cancer.

Genetic mutants can survive on a High-Sugar Diets

Researchers from the University of Southern California may have found a way to suppress obesity that is the result of a high sugar diet. So far, they have done research on the worm, Caenorhabditis elegans and also human cells in a petri dish. He found a genetic pathway that has been found to be the same in almost all animals.

Caenorhabditis elegans

They found that the worms that have a genetic mutant with a hyperactive SKN-1 gene can be fed a very high-sugar diet without gaining weight. While the worms without that gene, ballooned up on the same diet. This high-sugar diet that the worms were eating is equivalent to a “western diet,” which is high-fat and high-sugar foods like burgers, fries, and soda.

In humans, the Nrf2 gene is equivalent to the SKN-1 gene in the C. elegans. Therefore, they think the findings from the C. elegans research can translate to humans.  Pharmaceutical companies are already working to develop small-molecule drugs that will target the Nrf2 gene, it hopes to produce more anti-oxidants and slow down the aging process.

As interesting as this research sounds and how helpful it may be for people that consume high-sugar diets frequently, I don’t see how this could be healthy for the human body. The article did state that when the Nrf2 function is increased it has shown to be linked to aggressive cancers. Researchers would have to figure out how to activate Nrf2 in only specific tissues before humans can take advantage of this obesity suppression medication.

If this were to actually work without causing harm to the human body, I think it could potentially prevent other health issues related to a poor diet and obesity. However, I think this medication could also be abused and not used in the correct manner. It would have to be a prescription drug only available to people whom truly needed help loosing weight.  I chose this article because I think this research could have a positive effect in the future if they are able to figure out how to activate the Nrf2 gene in humans in the correct manner to help with obesity issues.

  

This Article: High-sugar diet no problem for genetic mutants