For many patients around the world, lung cancer is one of the most serious and frightening diseases. It is often found late, grows quickly, and can be very hard to treat.
One of the biggest challenges in cancer treatment is something called “drug resistance.” This happens when cancer cells stop responding to medicines that once worked. Chemotherapy that used to slow or shrink a tumor suddenly becomes useless, allowing the cancer to keep growing and spreading.
Now, exciting new research from ChristianaCare’s Gene Editing Institute is giving fresh hope. Scientists there have shown that turning off a single gene inside lung cancer cells can make these cells sensitive to chemotherapy again. The discovery was published in the journal Molecular Therapy Oncology and is the result of more than ten years of careful work.
The key player in this study is a gene called NRF2. In healthy cells, this gene helps protect the body from stress and damage. It turns on protective systems when the cell is in danger, such as when it is exposed to toxins or harmful chemicals. This is normally a good thing.
But in some cancers, including many lung cancers, the NRF2 gene becomes overactive. When that happens, the cancer cells become extra strong and start to defend themselves against chemotherapy. Instead of being destroyed by the drugs, they survive, adapt, and keep growing.
The research team decided to see what would happen if they could switch this gene off inside the cancer cells. They used a powerful tool called CRISPR, which works like precise molecular scissors that can cut and change DNA.
By using CRISPR, they were able to remove or “knock out” the NRF2 gene in lung cancer cells that had a special mutation known as R34G. This mutation is commonly found in a type of lung cancer called lung squamous cell carcinoma, which makes up about 20 to 30 percent of lung cancer cases.
Lung squamous cell carcinoma is a fast‑growing form of non‑small cell lung cancer. Each year, more than 190,000 people in the United States receive a lung cancer diagnosis, and many of those cases are difficult to treat because the tumors become resistant to standard drugs.
When the scientists turned off the NRF2 gene in the cancer cells, they noticed something remarkable. The cells became sensitive to common chemotherapy drugs again. Medications like carboplatin and paclitaxel, which had stopped working before, were suddenly able to damage and kill the cancer cells.
In animal studies that were designed to copy how tumors grow in the human body, the tumors that received this gene‑editing treatment grew more slowly and responded much better to chemotherapy than untreated tumors.
Even more impressive was the fact that the researchers did not need to edit every single cancer cell. They found that changing only 20 to 40 percent of the tumor cells was enough to make a big difference. The tumors shrank and became weaker, proving that this kind of treatment could still work even if every single cancer cell cannot be reached.
To deliver the CRISPR tool safely, the scientists used tiny fat‑based particles called lipid nanoparticles. These particles can carry the CRISPR system into the cancer cells without using viruses, which can sometimes be risky.
When they checked the results, they found that the gene editing was very accurate. It mainly targeted the mutated NRF2 gene, and there were very few changes in other parts of the DNA. This level of precision is extremely important for future medical use.
Although this study focused on one type of lung cancer, the researchers explained that NRF2 is also overactive in other cancers, including cancers of the liver, esophagus, and head and neck. This means that the same gene‑editing approach might one day be used to help patients with several different kinds of tumors that no longer respond to treatment.
Senior researchers on the project explained that this discovery could change the way doctors think about treating resistant cancers.
Instead of always trying to invent new drugs, scientists may be able to make existing treatments work again by changing the cancer cells themselves. This could lower costs, reduce side effects, and give patients more time and better quality of life.
In analysing the findings, this study stands out because it tackles one of the hardest problems in cancer care: resistance to treatment. By showing that a single overactive gene can be responsible for blocking chemotherapy, and that this gene can be safely switched off, the research opens a new path forward.
It does not claim to be a cure yet, and more studies, including human clinical trials, will be needed to test safety and effectiveness. However, the logic behind the results is strong, and the success in both cell and animal models provides a solid foundation for the next steps.
Overall, this work suggests that the future of cancer treatment may not only rely on stronger medicines, but also on smarter and more precise ways to change how cancer cells behave.
If this method proves to be safe and effective in people, it could one day help thousands of patients whose cancers no longer respond to current treatments. It is a powerful example of how science, patience, and advanced technology can come together to create new hope in the fight against a devastating disease.
If you care about cancer, please read studies that a low-carb diet could increase overall cancer risk, and vitamin D supplements could strongly reduce cancer death.
For more information about health, please see recent studies about how drinking milk affects the risks of heart disease and cancer and results showing higher intake of dairy foods linked to higher prostate cancer risk.
Copyright © 2025 Knowridge Science Report. All rights reserved.
