He and his colleagues at the NCI have identified a biochemical signaling pathway that can profoundly influence what happens to cancer cells and healthy when they are exposed to radiation. In experiments on mice have found that blocking a molecule called thrombospondin-1 binding to its cell surface receptor called CD47, has almost complete protection of normal tissues of both standard and high doses of radiation.?Dr. Isenberg and his team are looking at multiple strategies for the treatment of diseases of pulmonary hypertension, wound healing, sickle cell disease and heart attacks, on the basis of the block of the street thrombospondin-1/CD47,? he has said.
Isenberg, MD, MPH, Associate Professor, Division of Pulmonary Medicine, Allergy and Critical, Pitt School of Medicine. But the radiation itself that kills the cancer cells can also destroy healthy cells, causing side effects such as nausea and vomiting, skin ulcers and rashes, and weakness and fatigue. The long-term exposure to radiation can lead to scar formation and death of normal tissue.
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Fears have been expressed that alternative approaches to healthy cells may inadvertently protect the tumor cells, said the lead author, David D. Roberts, Ph., NCI Center for Cancer Research. But, he added, ?in our experiments, suppression of CD47 robust delay regrowth of tumors in mice treated with radiation.?
Researchers at the University of Pittsburgh School of Medicine and the National Cancer Institute , part of the National Institutes of Health, perhaps in the wake of a Holy Grail of cancer therapy: They found a means not only to protect the health of the tissues against the toxic effects of radiotherapy, but also increase tumor death. The results appear today in Science Translational Medicine.
Researchers are already exploring the role of the signaling pathway in several other areas, said Mark Gladwin, MD, Chief, Division of Pitt Pulmonology, Allergy and Critical Care Medicine and Director of Vascular Medicine Institute, where Dr. Isenberg is a principal investigator.
?We almost could not believe what I see,? said Dr. Isenberg. The cells that may have died of radiation exposure remained viable and functional when pre-treated with drugs that interfere with the way which thrombospondin-1/CD47 ?.
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