How chemotherapy drugs block blood vessel growth
Researchers at Johns Hopkins University School of Medicine have discovered how an entire class of chemotherapy drugs in common use can block cancer growth. Their findings, published online this week in the Proceedings of the National Academy of Sciences Early Edition, suggests that a subgroup of cancer patients in particular could benefit from these medications.
The anthracycline class of chemotherapy – doxorubicin (Adriamycin), daunorubicin, epirubicin, idarubicin – have been used for four decades to treat many cancers such as leukemia, lymphomas, sarcomas and carcinomas, the standard method of administration was the utilization the highest tolerable dose every few weeks to kill all rapidly growing cells, avoiding exactly copy their genetic material.
“But the late Judah Folkman discovered in 2000 that the so-called metronomic therapy, giving patients low doses of these drugs more often, you can keep in check the growth of cancer by blocking blood vessel formation, but the exact mechanism by which this occurs is not known, “says Gregg L. Semenza, MD, Ph.D., program director in vascular Johns Hopkins Institute for Cell Engineering and member of the McKusick-Nathans Institute of Genetic Medicine. “Now we have shown how this happens and what players are involved, which could help shape the future of clinical trials for patients with certain types of cancer.”
Semenza and his team have long studied as hypoxia inducible factor, or HIF-1 protein helps cells survive in low oxygen conditions. HIF-1 becomes the genes that grow new blood vessels to help oxygen-starved cells like those found in rapidly growing solid tumors survive.
To search for drugs that can prevent the growth of new blood vessels, the team tested more than 3,000 already approved by the FDA Drug Johns Hopkins University Library for their ability to stop the activity of HIF-1. Use of liver cancer cells grown in low oxygen time, the team of the cells treated with each drug in the library and examines whether the drug was bound to HIF-1 genes become.
A drug-daunorubicin reduced HIF-1 in gene-activation capacity by more than 99 percent. They tested other members of the anthracycline drug class and found that doxorubicin, epirubicin and idarubicin also blocked the activity of HIF-1. But a closer examination shows that both drug-treated and untreated cells contained similar amounts.
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