Researchers have discovered a clever survival trick used by melanoma cells that helps them resist treatment. This new insight could lead to better ways to treat this deadly skin cancer and improve patient survival.
Melanoma is the most dangerous type of skin cancer and is often caused by changes (mutations) in a gene called BRAF. These changes make cancer cells grow out of control.
To fight this, doctors often use drugs called BRAF inhibitors, such as vemurafenib, which can stop the cancer’s growth—at least at first. But in many cases, the cancer finds a way to survive and starts growing again, leading to treatment failure.
Until now, most scientists believed that cancer cells escaped these drugs by changing their genes over time. But the new study, done by researchers at the Institute for Systems Biology and MIT, shows something different.
They found that melanoma cells don’t need to wait for genetic changes. Instead, they can quickly adapt to the drug—within just a few hours or days. This means that cancer cells can start fighting back before the treatment has even had a chance to work fully.
This early adaptation is not permanent. It doesn’t come from a mutation in the DNA. Rather, it’s a flexible, reversible change in how the cells behave. The research team used advanced tools to track how the cancer cells respond to treatment at different time points.
They discovered that even though the usual cancer-causing pathway (called the BRAF-ERK pathway) was shut down by the drug, the cancer cells didn’t give up. Instead, they turned on a different backup pathway, known as the SRC family kinase (SFK) pathway.
This backup pathway helps the cells survive during treatment and may give them time to develop more long-lasting resistance later on.
One of the biggest clues the researchers found was a connection between this backup pathway and a type of stress inside the cells called reactive oxygen species (ROS).
These are harmful molecules that build up when cells are stressed—such as when they’re being attacked by a drug. In melanoma cells, higher ROS levels led to increased SFK activity, which helped the cells survive. But once the drug was removed, everything went back to normal, showing how temporary and flexible this escape plan really is.
This discovery gave the scientists an idea. What if they could block both the main cancer pathway and the backup SFK pathway at the same time? They tested this by combining a BRAF inhibitor with a drug called dasatinib, which blocks the SFK pathway.
The results were encouraging. In lab tests and animal models, the combination therapy reduced cancer cell survival and slowed down tumor growth more effectively than BRAF inhibitors alone. Interestingly, dasatinib by itself didn’t have much effect. But when used alongside the BRAF inhibitor, it helped stop the cancer’s escape plan.
“This approach may help keep the treatment working for longer,” said Dr. Wei Wei, an associate professor at ISB and one of the lead researchers.
The team also pointed out that rising ROS and SFK activity could serve as biomarkers—warning signs that doctors could watch for to know which patients might benefit most from this type of combined treatment.
Review and Analysis
This study uncovers a key reason why melanoma treatments often stop working so quickly, even before long-term resistance takes hold. By showing that cancer cells can adapt early and non-genetically, the research challenges the traditional view that resistance always comes from DNA mutations.
The work also offers a new treatment strategy: combine BRAF inhibitors with an SFK inhibitor like dasatinib to block this early escape. This could delay or prevent resistance, giving patients a longer-lasting response to therapy.
However, more studies and clinical trials are needed before this approach can be used widely. Scientists need to confirm that the combination is safe and effective for real patients. They also need to find out whether the same trick is used in other types of cancer.
Still, this research offers hope. It shows that catching cancer’s moves early—and stopping them before they become permanent—could be a powerful new way to outsmart drug resistance and improve treatment outcomes for people with melanoma.
If you care about skin health, please read studies about top signs of diabetic skin disease, and Mediterranean diet could help lower the skin cancer risk.
For more health information, please see recent studies about eating fish linked to higher risk of skin cancer, and results showing how to combat the effects of aging on your skin.
The research findings can be found in Cell Systems.
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