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Through the study, it has been possible to identify new molecular targets that could enhance the immune response.
Researchers from the University of California, San Diego School of Medicine and UC San Diego Moores Cancer Center, with collaborators from the La Jolla Institute for Immunology and elsewhere in United States, have further elucidated how ovarian cancer tumors defy immunotherapy, identifying new molecular targets that could enhance the immune response, as published in the magazine 'PNAS'.
Ovarian cancer is the fifth leading cause of cancer death among women and the majority of these cases are high-grade serous ovarian cancer tumors, according to the American Cancer Society.
High-grade serous ovarian cancer is lethal in part because It is usually resistant to chemotherapy. Immunotherapy, a therapeutic approach that uses a person's immune system to fight disease, has shown promise in many types of cancer, but approaches to use immunotherapy have not yet shown success in this type of tumor.
One immunotherapy approach targets proteins called checkpoint receptors that They act as brakes on the activation of the immune system. Checkpoint receptor inhibitors release this brake, allowing the immune system to attack cancer cells. However, for immunotherapy to work effectively against this tumor, treatments must also deactivate the protective environment created by cancer cells.
"Ovarian cancer is one of the biggest challenges in oncology," says Schlaepfer. "Tumors can develop without obvious symptoms. The most common sign of ovarian cancer is abdominal swelling when the disease is advanced, which is when most women are diagnosed.
Ozmadenci and his colleagues found that activation of a key signaling protein within tumors, called focal adhesion kinase (FAK), regulated the expression of a protein called CD155 that binds to the checkpoint receptor called TIGIT on cells. immunological. In effect, the tumor builds a safe environment for cancer cells to grow and evade immune detection, in part maintaining high levels of CD155 as a shield against immune attack.
In a preclinical model of aggressive ovarian cancer, researchers found that an oral anti-FAK drug reduced CD155 and other checkpoint proteins. When used in conjunction with an immunotherapy that blocked TIGIT, a greater immune response was seen against ovarian cancer cells. This, in turn, resulted in smaller tumors and longer survival.
"Several companies are testing FAK inhibitors and others have TIGIT checkpoint receptor inhibitor antibodies in clinical trials," says Schlaepfer. "In high-grade serous ovarian cancer, where Elevated levels of CD155 and active FAK are common, "Our results provide compelling support for targeting FAK and TIGIT as part of a novel immune-boosting therapeutic strategy."
Source: Heraldo de Aragón
