Cancer is an adaptable disease and context dependent. More specifically, tumors can respond differently to therapies. Various therapeutic responses are associated with different factors that play a critical role in the regression of tumor growth. Precision medicine is an emerging field in which physicians and scientists work to specialize therapeutic treatments for individual patients. While the use of artificial intelligence and next generation sequencing can help improve individual patient care, scientists are still trying to understand the different mechanisms by which the tumor persists. Scientists are working to learn more about how tumor cells evade detection and progress, and what is necessary to regress tumor expansion. Consequently, researchers are currently investigating the role of various proteins and molecules that influence tumor growth.
A recent article in Cell Reports, by Dr. Philip O. Scumpia and others, demonstrate the impact of a protein, known as IRF1, on tumor progression. Scumpia is an Associate Professor of Medicine and physician at the David Geffen School of Medicine at the University of California Los Angeles (UCLA). His work focuses on the translation of mechanistic findings related to skin diagnoses. More specifically, his work focuses on the role of the immune system associated with wound healing, vaccination, and cancer immunotherapies.
Scumpia and others discovered for the first time that IRF1 plays a critical role in tumor progression dependent on which cell expresses the protein. It was previously known that IRF1 plays an antiviral role in immunity, but it was unclear the role it played in cancer. The discovery that IRF1 function is cell type dependent helps explain conflicting reports in which some state IRF1 has antitumor function, while others report it has pro-tumor function. The report from Scumpia and others helps clarify the contradictory findings previously published.
There are many cancer treatments that have improved patient outcomes. Immunotherapy is one form of cancer treatment that redirects the immune system toward the tumor. As a single agent, immunotherapy is limited to specific cancer types and within subsets of patients. As a result, immunotherapy has been combined with standard-of-care to improve patient survival. Scumpia and others help identify the mechanism behind IRF1, which has the potential to improve immunotherapeutic efficacy.
The team observed the role of IRF1 regulation on the both the tumor and the surrounding cells. Researchers downregulated IRF1 in tumor cells and found that it promoted tumor growth by inhibiting surrounding immune cell function. Additionally, they tested immunotherapy on these IRF1 downregulated cells and found that it increased pro-tumor markers, which are used for immunotherapeutic targets. Alternatively, IRF1 is critical for immune cell development, trafficking, and activation. These findings indicate that reducing IRF1 on tumor cells and increasing them on immune cells could improve tumor regression.
Scumpia and his team discovered that IRF1 expression is cell dependent and could lead to improved immunotherapies. Additionally, researchers demonstrate that IRF1 is a critical protein in the development of cancer. By understanding its role in different cell types, scientists can improve immunotherapeutic regimens and prolong patient survival.
