Release date: 2017-08-28
Breast cancer remains the leading cause of cancer-related deaths among women in the United States. Early detection and targeted therapy improve overall patient outcomes, but these factors also profoundly affect prognosis. The so-called "three-negative" breast cancer, which lacks estrogen, progesterone and human epidermal growth factor 2 (HER2) hormone receptor expression, cannot be targeted by existing hormonal therapies, and patient survival is poor. The claudin-low subtype of triple-negative breast cancer is characterized by a poorly specific prognosis and a significantly higher rate of immune cell infiltration in the tumor microenvironment. Although observations indicate that immune infiltration in breast cancer subtypes is inversely associated with patient outcome, the link has not been established.
Researchers at the Jon Serody Laboratory at the Lineberger Cancer Center at UNC Chapel Hill attempted to determine how tumor-infiltrating immune cells contribute to breast tumor growth and response to immunotargeting therapy. Their recent work published in JCI reported that low-density breast tumors contain large amounts of regulatory T cells (Tregs), an immune cell that suppresses the activity of the immune system. In a mouse model of breast cancer, checkpoint inhibition therapy (immunotargeted therapy) does not reduce the growth of tight junction protein tumors. Studies have determined that during checkpoint inhibition therapy, an increase in Treg interferes with immune targeting, thereby providing protection for tightly linked tumors. Consistent with this mechanism, checkpoint inhibition treatment delays tumor growth in these mice when Tregs are depleted.
These findings suggest that interfering with Treg recruitment to tumors is a potential strategy to improve targeted therapy for triple-negative breast cancer. In addition, they support the notion that determining the immune profile of a breast cancer subtype can more effectively and quickly apply an effective treatment, which may improve the patient's prognosis.
Source: Noble
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