- June 20, 2016
- Posted by: emobile
- Category: Researcher's Corner
Emobileclinic Researchers’ corner
Researchers from the Beatson Institute in Glasgow, United Kingdom, have submitted that CXCR2 protein plays significant role in the management of pancreatic cancer. This finding published in the Cancer Cell Journal reveals that the protein helps to avoid pancreatic cancer and then exploit the immune system.
In the last four decades, the survival rate for many cancers has improved dramatically, with the exception of pancreatic cancer whose survival remains pitifully low as the vast majority of patients do not live more than 5 years after diagnosis. The Researchers at the Beatson Institute have been investigating a protein called CXCR2 for some years. The team recently discovered that CXCR2 plays a role in cancer – helping to drive tumor growth in mice with skin and bowel cancer. So they decided to investigate its role in pancreatic cancer.
First, the researchers analyzed tumor tissue from pancreatic cancer patients who had undergone surgery. They found high levels of CXCR2 on immune cells in the tumor surroundings. They also discovered that higher levels of CXCR2 correlated with worse outcomes for patients. Prof. Owen Sansom, explains that “the mice lacking CXCR2 still developed pancreatic cancer and survived just as long as the others. But, remarkably, their tumors did not spread.”
Following closer examination, the team found in the mice lacking CXCR2 that immune system cells called T cells known to be involved in attacking cancer cells had broken through the protective shield and invaded the tumors. In another set of experiments in mice with late stage pancreatic cancer, the researchers showed those treated with an experimental drug that blocks CXCR2 survived longer than untreated mice.
The team also found the CXCR2 inhibitor had a more powerful effect when combined with a chemotherapy drug called gemcitabine – the current gold standard of care for pancreatic cancer. The combination stopped the tumors spreading, and on closer inspection, the team again saw that the T cells had broken through the protective shield and invaded the tumors.
Finally, the researchers tried to work out why CXCR2 appears to have such a key role in helping tumors spread. They concluded it has to do with two types of immune cell: neutrophils and myeloid-derived suppressor cells. CXCR2 acts as a type of homing device for these cells, helping them navigate to sites of injury or tissue damage.When the immune system spots the injury or damage, it sends out alarm molecules into the bloodstream to summon neutrophils to start containing and fixing the problem. The neutrophils use their CXCR2 receptors to pick up the navigation direction from the alarm molecules. Also, while less clear-cut, it appears the myeloid-derived suppressor cells also use CXCR2 to guide them to the site of the damage, except their role is to switch the process off again when the problem is fixed.