黑色素瘤 z-bo 2020-10-28 437

　　The treatment of targeted BRAF-MEK inhibitors is an effective treatment for patients with advanced melanoma that cannot be surgically removed or spread to other parts of the body. However, many patients are resistant to this therapy, which usually leads to further metastasis. Researchers at the Mofit Cancer Center have helped develop this combination and are currently working to better understand the causes of this resistance, hoping to find a solution. EphA2 is a tyrosine kinase receptor that helps maintain a stable environment for normal cells. However, EphA2 is usually overexpressed in many cancers and plays an important role in its growth. Its exact function depends on the signaling path: classic and non-classical. The classical pathway inhibits the growth of cancer cells and acts as a tumor suppressor. Non-classical methods have the opposite effect and promote tumor survival and metastasis.

　　The Moffitt team worked with scientists at the Sanford Burnham Prebys Institute of Medical Discovery to study the non-classical method of EphA2. Researchers used mass analysis-based integrated proteomics technology to map the signal network driven by non-classical EphA2 and found that this signal can enhance the metastatic potential of cancer cells.

　　The research team established a mouse model using melanoma cells transfected by the non-classical route EphA2-S897E. This further confirmed this finding and found that the number of metastases to the lung was significantly higher.

　　Keiran Smalley said: "A better understanding of the treatment resistance of BRAF and BRAF-MEK inhibitors and the reasons for further metastasis will allow us to have a better understanding of the escape process and treatment support. Patients with melanoma have developed new treatment strategies."