The evolution of the disease toward drug resistance is one of the biggest issues facing the oncology community at the moment. As lung cancer remains the deadliest form of malignancy, accounting for almost one-quarter of all cancer-related deaths, now more than ever there is a clear need for improved solutions.
One recent study from scientists at The Gene Editing Institute within Christiana Care Health System opens the possibility of using CRISPR-Cas9 technology to disable certain key proteins in order to make cancer more vulnerable to treatment. The team led by Pawel Bialk already found a suitable candidate in NRF2 (Nuclear Factor Erythroid 2-Related Factor), considered the master regulator of 100–200 target genes involved in cellular responses to oxidative and/or electrophilic stress.
Tests conducted on mouse models confirmed that “knocking out” NRF2 lead to “reduced proliferation phenotype” and increased sensitivity to “chemotherapeutic agents, such as cisplatin and carboplatin”.
As the next objective is to move into human trials, it is important to note that the CRISPR application does not involve directly editing a patient’s genome, only the genes found in the tumor.
CRISPR stands for “Clustered Regularly Interspaced Short Palindromic Repeats” and was originally a defense mechanism found in bacteria that allows them to recognize and slice up the DNA of invading viruses. Researchers have learned to utilize this mechanism, effectively granting them the power to program or eliminate specific sequence of DNA code.
The approach could offer a number of advantages, keeping costs low as patients have better odds of receiving coverage from insurance companies and providing a high level of safety and reliability.
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