A number of existing anti-cancer treatments involve boosting the body’s own ability to notice and destroy tumors. Although these treatments have met with a fair level of success, a distinct number of patients don’t respond to the therapy. A study by a group of Swedish researchers published in the Journal of the National Cancer Institute may have pinpointed why.
Under these therapies, the body’s T-cells are directed toward the tumor and ideally destroy or shrink it. In order to reach the tumor, the cells enter through the blood vessels created to nourish it. Sometimes, those blood vessels contain what are termed myeloid-derived suppressor cells (MDSCs). These cells, as their name partially implies, suppress the killer ability of T-cells. Although normally an important part of regulating the body’s immune system, in certain cases, MDSCs can sometimes hinder more than help.
It was previously discovered that high levels of MDSCs correlate with inferior patient responses to immune-focused therapy. The MDSCs are drawn to the tumor by signal molecules the tumor secretes, identified as IL-6. The researchers’ goal was to understand the mechanism behind the IL-6 secretion.
The research eventually focused on a form of cells called pericytes, one of the cells found in the tumor blood vessels. Although the reason for this wasn’t determined, the team found that pericytes had an inverse correlation with IL-6. That is, the more pericytes there were, the less IL-6 was secreted.
What all of this means is that the team’s findings can be used to improve existing cancer treatments. By devising means to improve the number of pericytes—or by discovering the cause of the pericyte/IL-6 link and manipulating the mechanism—the prevalence of MDSCs can be reduced and overall therapy effectiveness boosted.
Source for Today’s Article:
Hong, J.W., et al., “Role of Tumor Pericytes in the Recruitment of Myeloid-Derived Suppressor Cells,” Journal of the National Cancer Institute 2015; 107(10): djv209, doi:10.1093/jnci/djv209, http://jnci.oxfordjournals.org/content/107/10/djv209.abstract.