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Researchers May Have Discovered How to Stop Secondary Tumors

October 03, 2016
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In a recent breakthrough in breast cancer research, a study may have found a way to stop the spread of secondary tumors during metastasis. The culprit? Scientists at the Institute of Cancer Research in London and the German Cancer Research Center in Heidelberg believe it relates to pericytes. Typically, cancers that are not detected early on will metastasize, a process where the body develops secondary tumors in the bloodstream. The majority of deaths by cancer are caused by these secondary growths. Not much is known about how cancerous cells get in the bloodstream, and scientists haven’t had a proper answer for the process. This breakthrough may have found the solution. The study, published by the journal Cancer Research, points to pericytes because it is wrapped around blood vessels and transfers molecules into the bloodstream. Pericytes also produce endosialin, a protein believed to affect how cancerous cells in tumors spread through the bloodstream. To test the effect of endosialin, researchers analyzed mice and in vitro samples. First, normal mice were compared to mice genetically engineered to lack endosialin. The primary breast cancer tumor growth was identical, but the genetically engineered rat experienced far less metastasis and secondary tumors. The endosialin proteins were affecting the primary tumor alone. Scientists discovered that instead of moving to the secondary tumors, endosialin proteins were staying at the primary tumor site to transfer cancerous cells into the bloodstream. The more endosialin found, the more cancerous cells were spread. This was confirmed when the endosialin-deficient mice had far less cancer cells identified in the bloodstream. Through further in vitro studies, researchers realized that when pericytes create the endosialin, the two communicate through cell-to-cell contact and let the cancerous cells into the blood vessel walls. This is the first time scientists have been able to identify how cancer cells transfer and spread in the bloodstream. To prove that endosialin may produce the same results in humans, researchers also examined humans and their in vitro samples. After testing both samples, women who suffered metastasis had much higher numbers of endosialin proteins than those who haven’t had metastasis. Endosialin ended up having a similar role in cancerous cell growth for humans and mice. These results are pivotal for breast cancer research, because it suggests that targeting endosialin proteins may reduce mortality rates of secondary tumors. Rather than being reactive in cancer treatments, doctors can be proactive by eliminating or hindering the protein’s spread in the bloodstream. Additionally, if endosialin indicates a higher risk of secondary tumors, doctors can test for high levels of the protein as an identifier for metastasis. This could result in early discoveries and save more lives. As this is one of the first studies to identify how cancerous cells enter the bloodstream, it offers an opportunity to build upon its discoveries. Now, scientists can look into how endosialin proteins can be reduced or potentially blocked from allowing cancer to spread. New and deeper research will need to be conducted, but the potential results can be life changing for victims of breast cancer.
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