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• W2149669698 abstract "The validity of the linear-quadratic (LQ) model for calculating isoeffect doses in radiation therapy has been intensively debated in recent issues of the International Journal of Radiation Oncology, Biology, Physics ( 1 Glatstein E. The Omega on alpha and beta. Int J Radiat Oncol Biol Phys. 2011; 81: 319-320 Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar , 2 Chapman J.D. Gillespie C.J. The power of radiation biophysics—let’s use it. Int J Radiat Oncol Biol Phys. 2012; 84: 309-311 Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar , 3 Brenner D.J. Rainer K.S. Peters L.J. et al. We forget at our peril the lessons built into the α/β model. Int J Radiat Oncol Biol Phys. 2012; 82: 1312-1314 Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar ). The LQ model is simple and convenient, and by far it has been the most useful means for isodose calculation in treating tumors with conventional fractionated radiation therapy ( 2 Chapman J.D. Gillespie C.J. The power of radiation biophysics—let’s use it. Int J Radiat Oncol Biol Phys. 2012; 84: 309-311 Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar , 3 Brenner D.J. Rainer K.S. Peters L.J. et al. We forget at our peril the lessons built into the α/β model. Int J Radiat Oncol Biol Phys. 2012; 82: 1312-1314 Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar , 4 Fowler J.F. The linear-quadratic formula and progress in fractionated radiotherapy. Br J Radiol. 1989; 62: 679-694 Crossref PubMed Scopus (1744) Google Scholar ). The LQ model solely depends on the expected incidence of direct interactions of radiation with specific cellular targets (ie, DNA strands). Because the LQ survival curve continuously bends downward with increasing radiation dose, many assume that the LQ calculation will inherently overestimate cell death caused by high-dose-per-fraction radiation therapy. Interestingly, however, clinical results have shown that the LQ model actually underestimates tumor control by stereotactic body radiation therapy (SBRT) or stereotactic radiosurgery (SRS) ( 5 Kirkpatrick J.P. Meyer J.J. Marks L.B. The linear-quadratic model is inappropriate to model high dose per fraction effects in radiosurgery. Semin Radiat Oncol. 2008; 18: 240-243 Abstract Full Text Full Text PDF PubMed Scopus (358) Google Scholar ), indicating that mechanism(s) in addition to DNA strand breaks and/or chromosome aberrations may be involved in response of tumors to SBRT or SRS. Therefore, it has been hypothesized that SBRT or SRS may cause significant vascular damage in tumors, leading to indirect cell death ( 5 Kirkpatrick J.P. Meyer J.J. Marks L.B. The linear-quadratic model is inappropriate to model high dose per fraction effects in radiosurgery. Semin Radiat Oncol. 2008; 18: 240-243 Abstract Full Text Full Text PDF PubMed Scopus (358) Google Scholar , 6 Kocher M. Treuer H. Voges J. et al. Computer simulation of cytotoxic and vascular effects of radiosurgery in solid and necrotic brain metastases. Radiother Oncol. 2000; 54: 149-156 Abstract Full Text Full Text PDF PubMed Scopus (87) Google Scholar ). We have recently reviewed previous studies on the radiation-induced vascular damage in tumors and pointed out the potentially important role of indirect/necrotic cell death due to the vascular damage in tumor control with SBRT and SRS ( 7 Park H.J. Griffin R.J. Hui S. et al. Radiation-induced vascular damage in tumors: Implications of vascular damage in ablative hypofractionated radiotherapy (SBRT and SRS). Radiat Res. 2012; 177: 311-327 Crossref PubMed Scopus (354) Google Scholar ). We further discussed the radiobiological principles of SBRT and SRS in relation to radiation-induced vascular damage and resultant indirect cell death ( 8 Song C.W. Park H.J. Griffin R.J. et al. Radiobiology of stereotactic radiosurgery and stereotactic body radiation therapy. in: Levitt S.H. Technical Basis of Radiation Therapy. Springer-Verlag, Berlin2012: 51-61 Google Scholar ). Interestingly, some 35 years ago we (C.W.S. and S.H.L.) realized that irradiation of rodent tumors with 10-20 Gy in a single dose caused severe vascular injury, leading to necrotic cell death in significant fractions of tumor cells 2 to 3 days after the treatment ( 9 Clement J.J. Song C.W. Levitt S.H. Changes in functional vascularity and cell number following x-irradiation of a murine carcinoma. Int J Radiat Oncol Biol Phys. 1976; 1: 671-678 Abstract Full Text PDF PubMed Scopus (34) Google Scholar , 10 Clement J.J. Takanka N. Song C.W. Tumor reoxygenation and postirradiation vascular changes. Radiology. 1978; 127: 799-803 Crossref PubMed Scopus (45) Google Scholar ). Figure 1 summarizes the observations we made on the effects of 10 Gy (1000 rads) of x-rays in a single dose on the clonogenic surviving cells in Walker 256 rat tumors ( 10 Clement J.J. Takanka N. Song C.W. Tumor reoxygenation and postirradiation vascular changes. Radiology. 1978; 127: 799-803 Crossref PubMed Scopus (45) Google Scholar ). The surviving cell fraction, as measured with an in vivo–in vitro excision method, was approximately 2.6 × 10−2 when tumors were explanted immediately after irradiation, and it progressively decreased to 5 × 10−3 when explanted 2 days after irradiation. We attributed the decrease in viability of tumor cells over 2 days after irradiation with a single dose of 10 Gy to indirect cell death due to vascular damage. In support of this hypothesis, the functional vascularity in Walker tumors 2 days after 10-Gy irradiation was also found to be decreased by approximately 50% ( 10 Clement J.J. Takanka N. Song C.W. Tumor reoxygenation and postirradiation vascular changes. Radiology. 1978; 127: 799-803 Crossref PubMed Scopus (45) Google Scholar ). In our recent studies with FSaII fibrosarcoma of C3H mice, the surviving fraction several days after 20-Gy irradiation in a single exposure was more than 2 logs less than that observed immediately after irradiation (data not shown). Here again, it would be reasonable to attribute the massive additional loss of tumor cell viability that developed over several days after 20-Gy irradiation in a single exposure to indirect/necrotic cell death as a consequence of vascular damage. Indeed, such indirect cell death by high-dose-per-fraction radiation therapy will not be accounted for in the original LQ model, as well as in other modified-LQ models. Therefore, we propose that caution should be exercised in applying and interpreting results when using the original LQ model and other modified-LQ models for SBRT and SRS with radiosurgical doses per fraction. The rapid adoptions of SBRT and SRS in radiation oncology, and the excellent clinical results obtained, further highlights the notion that we need better models to account for all mechanisms of action play in modern day radiation therapy application." @default.
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• W2149669698 title "Radiobiology of Stereotactic Body Radiation Therapy/Stereotactic Radiosurgery and the Linear-Quadratic Model" @default.
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