Inhibitory protein reduces radioactive bone defect in experimental animal models

  A new study may provide new clues to alleviate the terrible side effects that cancer patients experience during radiotherapy. Radiation therapy puts cancer patients at risk of losing bone density, which can cause fractures at the irradiated site. This study uses neutralizing antibodies of bone-specific proteins to inhibit protein activity, thereby reducing radioactive bone defects in animal models.

  Radiotherapy uses high-energy ionizing radiation to destroy cell DNA to damage cancer cells, thereby inducing cell apoptosis. There are approximately two million patients in the United States each year, of which more than 50% are cancer patients. These cancer patients need to receive radiotherapy alone or in combination with drug chemotherapy, surgery and targeted drug therapy at certain stages of their illness.

  Although the target cells of radiotherapy are tumor cells, the process of radiotherapy still causes damage to surrounding healthy tissues. Although this side effect has been improved through computer-assisted guidance, radiation therapy still exposes cancer patients to the risk of bone density loss, causing them to suffer fractures at the radiation site for their entire lives.

  New research from the University of Pennsylvania School of Medicine and Philadelphia Children’s Hospital may have found a way to reduce this terrible side effect: inhibiting protein activity through neutralizing antibodies of bone-specific proteins, thereby reducing radioactive bone defects in animal models. Ling Qin, MD, associate professor of plastic surgery at the University of Pennsylvania School of Medicine, and corresponding author of the papers and journals, said: "Our research shows that activating the Wnt/β-catenin signaling pathway can overcome radiation-induced DNA damage and osteoblast death. "The clinical significance of this study is that it demonstrates an antibody (Scl-Ab) that can block bone sclerostin, a circulating factor that can inhibit bone formation, thereby reducing osteoporosis caused by radiotherapy." The research team will Their findings are published in the Journal of Bone & Mineral Research.

  Other research centers are conducting phase II clinical trials of Romosozumab (Scl-Ab). They used Romosozumab (Scl-Ab) to treat general osteoporosis. As a result, it showed a good effect. This encouraged the research team to explore whether the weekly Scl-Ab antibody treatment can prevent radiation-induced small Rat osteoporosis. They found that Scl-Ab blocked the deterioration or foaming of trabecular bone after radiotherapy by partially preserving the number and activity of osteoblasts. Scl-Ab accelerates the DNA repair of bone cells after radiation by reducing the number of DNA double-strand break markers and increasing DNA repair proteins, and prevents osteoblasts from transforming to radiation-induced apoptosis!

  By applying cell lineage tracing technology, the research team found that radiation turned bone progenitor cells into fat cells, thereby blocking their proliferation ability, but did not induce cell death. Scl-Ab treatment can partially block cell lineage transformation, but has no effect on the loss of cell proliferation potential.