In a new study, researchers found a new drug combo could stop the progression of a particularly aggressive melanoma.
The research was conducted by a team from Boston University.
Damaging effects of ultraviolet light from sunlight and tanning beds can lead to melanoma on the DNA of skin cells.
The damage can activate genes that encourage precancerous cells to grow further into skin cancer. It also can turn off other genes that help stop cancer growth.
It is estimated that about 100,000 people will be diagnosed with melanoma this year and more than 7,000 people will die from the disease.
Previous studies have shown that one type of melanoma is caused by a mutation of a gene called NRAS. It can drive 25% of skin cancers.
Although therapies have been developed to treat melanoma, they are not very effective to treat the disease in people with NRAS mutations.
In the current study, the team found a way to stop the progression of melanoma with NRAS mutations.
They found a method to interrupt the process that mutated NRAS in the growth of skin cancer.
They identified a protein STK19 that can work as an “on” switch for NRAS.
When the researchers disabled the STK19 gene, they found it could reduce its ability to grow skin cancer.
Based on the findings, the team developed a new drug combo to shut down the effect of STK19 on NRAS.
They tested the drug combo in in animals and proved that it could block NRAS activation and prevent melanoma from developing.
The researchers suggest that their approach can be used in the treatment of other difficult-to-cure cancers.
Next, the team wants to test their drug combo clinical trials to see if the STK19 inhibitor can work in humans.
They hope in the near future it available as a targeted therapy to combat NRAS-driven melanomas.
The team also suggests that doctors need to monitor patients with early diagnosis and conduct full-body examinations. This is important for preventing cancer progression and metastasis.
The research was funded by many sources, including Boston University, the National Key R&D Program, and the National Natural Science Foundation of China.
One author of the study is Rutao Cui, a professor of pharmacology and dermatology at the Boston University School of Medicine.
The study is published in Cell.
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