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A study led by investigators from Massachusetts General Hospital (MGH) and the University of Cyprus reveals details of a way the dangerous brain tumors called glioblastomas resist the effects of antiangiogenic drugs designed to cut off their blood supply. In their report published in PNAS, the researchers describe how the tumors can spread along existing blood vessels in normal tissue, a process called vessel co-option that can lead to compression of those vessels, reducing the oxygen supply to adjacent tissues and actually stimulating angiogenesis.



"The treatments designed to starve tumors by pruning away blood vessels have provided little or no survival benefits to patients with glioblastoma, says Rakesh K. Jain, Ph.D., director of the Edwin L. Steele Laboratories for Tumor Biology in the MGH Department of Radiation Oncology and senior author of the PNAS report. "Because of its ability to circumvent a tumor's need to develop a new blood supply, vessel co-option can confer resistance to antiangiogenic therapy. Unfortunately this mode of tumor progression is difficult to target because the underlying mechanisms are not fully understood."



To get a better understanding of how cancer cells interact with the vasculature during co-option, Jain and his team followed tumor progression in mouse models of glioblastoma. Using advanced imaging technology they found that treating existing glioblastomas with the antiangiogenic drug cediranib increased the spread of tumor cells along existing blood vessels and away from the primary tumor mass. They also presented evidence that this process causes the compression of co-opted vessels by tumor cells, which can trigger hypoxia-induced angiogenesis.



Read more at: https://medicalxpress.com/news/2019-01-reveals-brain-tumors-effects-antiangiogenic.html


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