Phosphorus-32, a Clinically Available Drug,Inhibits Cancer Growth by Inducing DNA Double-Strand Breakage |
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| Authors: | Yulan Cheng Ana P Kiess Joseph M Herman Martin G Pomper Stephen J Meltzer John M Abraham |
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| Institution: | 1. Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.; 2. Department of Radiation Oncology and Molecular Radiation, The Johns Hopkins University School of Medicine, Baltimore, Maryland.; 3. Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.; ACTREC, Tata Memorial Centre, INDIA, |
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| Abstract: | Radioisotopes that emit electrons (beta particles), such as radioiodine, can effectively kill target cells, including cancer cells. Aqueous 32PPO4] is a pure beta-emitter that has been used for several decades to treat non-malignant human myeloproliferative diseases. 32PPO4] was directly compared to a more powerful pure beta-emitter, the clinically important 90Y isotope. In vitro, 32PPO4] was more effective at killing cells than was the more powerful isotope 90Y (P ≤ 0.001) and also caused substantially more double-stranded DNA breaks than did 90Y. In vivo, a single low-dose intravenous dose of aqueous elemental 32P significantly inhibited tumor growth in the syngeneic murine cancer model (P ≤ 0.001). This effect is exerted by direct incorporation into nascent DNA chains, resulting in double-stranded breakage, a unique mechanism not duplicatable by other, more powerful electron-emitting radioisotopes. 32PPO4] should be considered for human clinical trials as a potential novel anti-cancer drug. |
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