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.
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