4.7 Article

Antiproton induced DNA damage: proton like in flight, carbon-ion like near rest

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SCIENTIFIC REPORTS
卷 3, 期 -, 页码 -

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NATURE PUBLISHING GROUP
DOI: 10.1038/srep01770

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资金

  1. European Union Seventh Framework Programme [262010 - ENSAR]
  2. Department of Education and Learning NI scholarship
  3. Engineering and Physical Sciences Research Council (EPSRC, UK) [EP/H017844/1, EP/I017550/1]
  4. DFG [WE3565-3]
  5. NSF [CBET 0853157]
  6. EU through a Marie Curie Fellowship [PIIF-GA-2009-234814]
  7. Engineering and Physical Sciences Research Council [EP/H017844/1, EP/I017550/1] Funding Source: researchfish
  8. Medical Research Council [G1100014] Funding Source: researchfish
  9. EPSRC [EP/I017550/1, EP/H017844/1] Funding Source: UKRI
  10. MRC [G1100014] Funding Source: UKRI

向作者/读者索取更多资源

Biological validation of new radiotherapy modalities is essential to understand their therapeutic potential. Antiprotons have been proposed for cancer therapy due to enhanced dose deposition provided by antiproton-nucleon annihilation. We assessed cellular DNA damage and relative biological effectiveness (RBE) of a clinically relevant antiproton beam. Despite a modest LET (similar to 19 keV/mu m), antiproton spread out Bragg peak (SOBP) irradiation caused significant residual gamma-H2AX foci compared to X-ray, proton and antiproton plateau irradiation. RBE of similar to 1.48 in the SOBP and, 1 in the plateau were measured and used for a qualitative effective dose curve comparison with proton and carbon-ions. Foci in the antiproton SOBP were larger and more structured compared to X-rays, protons and carbon-ions. This is likely due to overlapping particle tracks near the annihilation vertex, creating spatially correlated DNA lesions. No biological effects were observed at 28-42 mm away from the primary beam suggesting minimal risk from long-range secondary particles.

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