Triple negative breast cancer is present in about 12% of breast cancer patients. This cancer is characterized by breast cancer cells that lack three surface cell receptors that are found in other breast cancers, and it is typically more aggressive and more likely to relapse. Currently, there are no targeted therapies for triple negative breast cancer.
“Claudin-Low” Breast Cancer
Immunotherapy is designed to harness the power of a patient?s immune system to fight off cancer cells. It is used for a variety of cancers, including triple negative breast cancer, but its efficacy has been limited a certain group of triple negative breast cancer that is known as ?claudin- low? breast cancer. A new study published in the Journal of Clinical Investigation is shedding some light on why certain triple negative breast cancers do not respond to immunotherapy, and what can be done to solve it.
Interestingly, the patients who aren?t being affected by immunotherapy, who are claudin-low, have a heavy presence of immune cells in and near the tumor. With this elevated number of immune cells, researchers would expect that immunotherapy would be more effective, but quite the opposite has been revealed.
Reserachers at UNC Lineberger Comprehensive Cancer Center are explaining this phenomenon through their findings in gene expression analysis, which show that during immunotherapy, specifically checkpoint inhibitors, claudin-low tumor are not being flooded with immune cells that attack cancer, rather, they had a high concentration of regulatory T-cells- a type of immune cell that actually suppresses the body?s defenses. They concluded that s a chemical signal to attract regulatory T-cells is being released from these claudin-low tumors.
Depleting Regulatory T-Cells
In attempt to combat this and clear the path for immunotherapy drugs , researchers tested an investigational approach that would deplete the presence of regulatory T-cells in conjunction with a checkpoint inhibitor that would typically be used in immunotherapy. What they have found is that this combination did actually slow tumor growth. These findings show a crucial part of why immunotherapy isn?t working in these cancers, and how it may potentially be solved.
“I think it’s important for us to try to start segregating out the types of tumors that don’t respond to these treatments at a much granular genomic level, and try to figure out new mechanisms to enhance the response rate to immunotherapy.” said Jonathan Serody, MD, UNC Lineberger member and the Elizabeth Thomas Professor in the UNC School of Medicine.
Researchers hope these findings will underscore the need to study cancers on a genomic level, in order to personalize immunotherapy for each patient?s individual needs.
Last Editorial Review: August 25, 2017
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