Stanford researchers, led by Dr. Lingyin Li, have published a study revealing the role of the enzyme ENPP1 in breast cancer progression. ENPP1 breaks down cGAMP, a molecule vital for activating the STING pathway in the immune system, which fights cancer. High levels of ENPP1 in tumors correlate with poor prognosis, while lower levels are associated with better responses to immunotherapy. The study suggests that targeting ENPP1 could enhance immunotherapy effectiveness and that ENPP1 levels could serve as a biomarker for treatment response. This breakthrough has significant implications for the development of new cancer treatments and has sparked interest among pharmaceutical companies in finding ENPP1 inhibitors.
Researchers at Stanford University and the Arc Institute have discovered that a protein called ENPP1 acts as an on/off switch for breast cancer metastasis and resistance to immunotherapy. High levels of ENPP1 are associated with poor patient response to immunotherapy and increased metastasis. The findings could lead to the development of more effective immunotherapies and improved prediction of patient response to existing treatments. ENPP1 inhibitors are already in clinical development, and the researchers believe that ENPP1 may play a critical role in other "cold" tumors as well.
Researchers at Stanford University and the Arc Institute have discovered that a protein called ENPP1 acts as an on/off switch for breast cancer metastasis and resistance to immunotherapy. High levels of ENPP1 are associated with poor patient response to immunotherapy and increased metastasis. The findings could lead to the development of more effective immunotherapies and help clinicians predict patient response to existing treatments. ENPP1 inhibitors are already in clinical development, and the researchers believe that ENPP1 may play a critical role in other "cold" tumors as well.
