A new study shows that tumors can become resistant to drugs over time by learning to steal normal blood vessels from surround tissue. This is a process that researchers call vessel co-option.
The process of new blood vessel growth is important to cancers to grow. Several anti-angiogenic drugs have been developed to combat it. Unfortunately, cancers often become resistant to these drugs, through mechanisms, which until now were poorly understood.
The study shows that it could be possible to treat cancers by designing new therapies that block both vessel co-option and angiogenesis. These may be more effective than existing treatments which only bloc angiogenesis.
Researchers used mice to examine how a type of liver cancer called hepatocellular carcinoma can become resistant to an anti-angiogenic drug called sorafenib.
Researchers discovered that tumors which responded to treatment, initially relied mainly on growing their own blood vessels, but developed resistance to treatment by actively stealing the normal pre-existing blood vessels of the liver instead.
This study may have implications not only for the treatment of live cancer, but also for other cancer types including metastatic breast cancer and metastatic bowel cancer. Researchers are currently investigating the implication of this research for these other cancer type.
Researchers also found that the switch to vessel co-option was reversible. Once treatment was stopped, the tumors switched back to using angiogenesis. This finding provides a potential explanation as to why some patients can respond again to the same anti-angiogenic drug after they have a “treatment holiday.”
At the moment there are no existing drugs that target vessel co-option therefore, researchers also carried out experiments to identify how vessel co-option works. They discovered that the cancer cells increase their ability to move when they co-opt vessels. This suggests that targeting cancer cell movement might be used to block vessel co-option.
This is the first study that shows that cancer can adapt to treatment by actively co-opting blood vessels from nearby tissues as a mechanism of drug resistance.
Hopefully these findings will lead to the development of new drug types that target vessel co-option.
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