The relative biological effectiveness of proton and ion beams

Jäkel, Oliver

doi:10.1016/j.zemedi.2008.06.012

Cited by 29 publications

(8 citation statements)

References 42 publications

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“…Although a generic RBE of 1.1 is generally applied to clinical use (Wambersie 1999, there are many uncertainties regarding proton RBE (Wambersie 2004, Jäkel 2008. For the evaluation of RBE value, the endpoints that have been applied include loss of clonogenicity, apoptosis induction in in vitro studies (Matsumura et al 1999, Kagawa et al 2002, Moertel et al 2004, Oya et al 2008, and crypt disappearance in in vivo studies (Uzawa et al 2007).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, their biological characteristics have been analysed primarily in comparison to photons (Belli et al 1993, Ando et al 2001, Belli et al 2001, Kagawa et al 2002, Moertel et al 2004, Baek et al 2008. Although the relative biological effectiveness (RBE) values of protons range between small limits, proton RBE can differ according to energy and depth (Gerweck and Kozin 1999, Paganetti 2005, Jäkel 2008. RBE values can also differ according to the endpoints or tissues in terms of alpha/beta (a/b) values (Paganetti et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Induction of in situ DNA double-strand breaks and apoptosis by 200 MeV protons and 10 MV X-rays in human tumour cell lines

Gerelchuluun

Hong

Sun

et al. 2010

International Journal of Radiation Biology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Induction of in situ DNA double-strand breaks and apoptosis by 200 MeV protons and 10 MV X-rays in human tumour cell lines

Gerelchuluun

Hong

Sun

et al. 2010

International Journal of Radiation Biology

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“…Both primary and secondary delta ray tracks from heavy ion radiation is highly ionizing and will cause significant damage to the cells they traverse (Curtis et al 1992, Brooks et al 2001a) with short term as well as long term consequences. Of major short term concern are injury to rapidly proliferating cells in the gastrointestinal (GI) tract and bone marrow (BM), because of the prediction that astronauts could receive enough HZE dose from GCR and solar particle events (SPE) to perturb these tissues in long-term missions (Jakel 2008). Also, in the short term, exposure to ionizing radiation (IR) decreases host immune defense via its effects on the GI tract and BM, thus enhancing the risk of developing local and systemic infection due to endogenous as well as exogenous microorganisms (Brook et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Accelerated hematopoietic toxicity by high energy⁵⁶Fe radiation

Datta

Suman

Trani

et al. 2011

International Journal of Radiation Biology

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Purpose There is little information on the relative toxicity of highly charged (Z) high-energy (HZE) radiation in animal models compared to γ or x-rays, and the general assumption based on in vitro studies has been that acute toxicity is substantially greater. Methods C57BL/6J mice were irradiated with 56Fe ions (1 GeV/nucleon), and acute (within 30 d) toxicity compared to that of γ rays or protons (1 GeV). To assess relative hematopoietic and gastrointestinal toxicity, the effects of 56Fe ions were compared to γ rays using complete blood count (CBC), bone marrow granulocyte-macrophage colony forming unit (GM-CFU), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay for apoptosis in bone marrow, and intestinal crypt survival. Results Although onset was more rapid, 56Fe ions were only slightly more toxic than γ rays or protons with lethal dose (LD)50/30 (a radiation dose at which 50% lethality occurs at 30-day) values of 5.8, 7.25, and 6.8 Gy respectively with relative biologic effectiveness for 56Fe ions of 1.25 and 1.06 for protons. Conclusions 56Fe radiation caused accelerated and more severe hematopoietic toxicity. Early mortality correlated with more profound leukopenia and subsequent sepsis. Results indicate that there is selective enhanced toxicity to bone marrow progenitor cells, which are typically resistant to γ rays, and bone marrow stem cells, because intestinal crypt cells did not show increased HZE toxicity.

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“…Comparison of the biological effects of different radiation qualities is usually being performed in terms of relative biological effectiveness (RBE). 6 In radiotherapy, the RBE is not only of highest interest for cell killing but also for late effects such as cancerogenesis ( 149 ). For the various biological endpoints, the RBE can depend on many factors, such as LET, dose rate, dose fractionation, radiation dose, and type of the irradiated cells or tissues.…”

Section: Influence Of Linear Energy Transfer On Transcription Factor mentioning

confidence: 99%

Transcription Factors in the Cellular Response to Charged Particle Exposure

et al. 2016

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Charged particles, such as carbon ions, bear the promise of a more effective cancer therapy. In human spaceflight, exposure to charged particles represents an important risk factor for chronic and late effects such as cancer. Biological effects elicited by charged particle exposure depend on their characteristics, e.g., on linear energy transfer (LET). For diverse outcomes (cell death, mutation, transformation, and cell-cycle arrest), an LET dependency of the effect size was observed. These outcomes result from activation of a complex network of signaling pathways in the DNA damage response, which result in cell-protective (DNA repair and cell-cycle arrest) or cell-destructive (cell death) reactions. Triggering of these pathways converges among others in the activation of transcription factors, such as p53, nuclear factor κB (NF-κB), activated protein 1 (AP-1), nuclear erythroid-derived 2-related factor 2 (Nrf2), and cAMP responsive element binding protein (CREB). Depending on dose, radiation quality, and tissue, p53 induces apoptosis or cell-cycle arrest. In low LET radiation therapy, p53 mutations are often associated with therapy resistance, while the outcome of carbon ion therapy seems to be independent of the tumor’s p53 status. NF-κB is a central transcription factor in the immune system and exhibits pro-survival effects. Both p53 and NF-κB are activated after ionizing radiation exposure in an ataxia telangiectasia mutated (ATM)-dependent manner. The NF-κB activation was shown to strongly depend on charged particles’ LET, with a maximal activation in the LET range of 90–300 keV/μm. AP-1 controls proliferation, senescence, differentiation, and apoptosis. Nrf2 can induce cellular antioxidant defense systems, CREB might also be involved in survival responses. The extent of activation of these transcription factors by charged particles and their interaction in the cellular radiation response greatly influences the destiny of the irradiated and also neighboring cells in the bystander effect.

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The relative biological effectiveness of proton and ion beams

Cited by 29 publications

References 42 publications

Induction of in situ DNA double-strand breaks and apoptosis by 200 MeV protons and 10 MV X-rays in human tumour cell lines

Induction of in situ DNA double-strand breaks and apoptosis by 200 MeV protons and 10 MV X-rays in human tumour cell lines

Accelerated hematopoietic toxicity by high energy⁵⁶Fe radiation

Transcription Factors in the Cellular Response to Charged Particle Exposure

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The relative biological effectiveness of proton and ion beams

Cited by 29 publications

References 42 publications

Induction of in situ DNA double-strand breaks and apoptosis by 200 MeV protons and 10 MV X-rays in human tumour cell lines

Induction of in situ DNA double-strand breaks and apoptosis by 200 MeV protons and 10 MV X-rays in human tumour cell lines

Accelerated hematopoietic toxicity by high energy56Fe radiation

Transcription Factors in the Cellular Response to Charged Particle Exposure

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Accelerated hematopoietic toxicity by high energy⁵⁶Fe radiation