Biological Principles of Stereotactic Body Radiation Therapy (SBRT) and Stereotactic Radiation Surgery (SRS): Indirect Cell Death
To review the radiobiological mechanisms of stereotactic body radiation therapy stereotactic body radiation therapy (SBRT) and stereotactic radiation surgery (SRS). We reviewed previous reports and recent observations on the effects of high-dose irradiation on tumor cell survival, tumor vasculature,...
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Published in | International journal of radiation oncology, biology, physics Vol. 110; no. 1; pp. 21 - 34 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
01.05.2021
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Abstract | To review the radiobiological mechanisms of stereotactic body radiation therapy stereotactic body radiation therapy (SBRT) and stereotactic radiation surgery (SRS).
We reviewed previous reports and recent observations on the effects of high-dose irradiation on tumor cell survival, tumor vasculature, and antitumor immunity. We then assessed the potential implications of these biological changes associated with SBRT and SRS.
Irradiation with doses higher than approximately 10 Gy/fraction causes significant vascular injury in tumors, leading to secondary tumor cell death. Irradiation of tumors with high doses has also been reported to increase the antitumor immunity, and various approaches are being investigated to further elevate antitumor immunity. The mechanism of normal tissue damage by high-dose irradiation needs to be further investigated.
In addition to directly killing tumor cells, high-dose irradiation used in SBRT and SRS induces indirect tumor cell death via vascular damage and antitumor immunity. Further studies are warranted to better understand the biological mechanisms underlying the high efficacy of clinical SBRT and SRS and to further improve the efficacy of SBRT and SRS. |
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AbstractList | To review the radiobiological mechanisms of stereotactic body radiation therapy stereotactic body radiation therapy (SBRT) and stereotactic radiation surgery (SRS). To review the radiobiological mechanisms of stereotactic body radiation therapy stereotactic body radiation therapy (SBRT) and stereotactic radiation surgery (SRS). We reviewed previous reports and recent observations on the effects of high-dose irradiation on tumor cell survival, tumor vasculature, and antitumor immunity. We then assessed the potential implications of these biological changes associated with SBRT and SRS. Irradiation with doses higher than approximately 10 Gy/fraction causes significant vascular injury in tumors, leading to secondary tumor cell death. Irradiation of tumors with high doses has also been reported to increase the antitumor immunity, and various approaches are being investigated to further elevate antitumor immunity. The mechanism of normal tissue damage by high-dose irradiation needs to be further investigated. In addition to directly killing tumor cells, high-dose irradiation used in SBRT and SRS induces indirect tumor cell death via vascular damage and antitumor immunity. Further studies are warranted to better understand the biological mechanisms underlying the high efficacy of clinical SBRT and SRS and to further improve the efficacy of SBRT and SRS. To review the radiobiological mechanisms of stereotactic body radiation therapy stereotactic body radiation therapy (SBRT) and stereotactic radiation surgery (SRS).PURPOSETo review the radiobiological mechanisms of stereotactic body radiation therapy stereotactic body radiation therapy (SBRT) and stereotactic radiation surgery (SRS).We reviewed previous reports and recent observations on the effects of high-dose irradiation on tumor cell survival, tumor vasculature, and antitumor immunity. We then assessed the potential implications of these biological changes associated with SBRT and SRS.METHODS AND MATERIALSWe reviewed previous reports and recent observations on the effects of high-dose irradiation on tumor cell survival, tumor vasculature, and antitumor immunity. We then assessed the potential implications of these biological changes associated with SBRT and SRS.Irradiation with doses higher than approximately 10 Gy/fraction causes significant vascular injury in tumors, leading to secondary tumor cell death. Irradiation of tumors with high doses has also been reported to increase the antitumor immunity, and various approaches are being investigated to further elevate antitumor immunity. The mechanism of normal tissue damage by high-dose irradiation needs to be further investigated.RESULTSIrradiation with doses higher than approximately 10 Gy/fraction causes significant vascular injury in tumors, leading to secondary tumor cell death. Irradiation of tumors with high doses has also been reported to increase the antitumor immunity, and various approaches are being investigated to further elevate antitumor immunity. The mechanism of normal tissue damage by high-dose irradiation needs to be further investigated.In addition to directly killing tumor cells, high-dose irradiation used in SBRT and SRS induces indirect tumor cell death via vascular damage and antitumor immunity. Further studies are warranted to better understand the biological mechanisms underlying the high efficacy of clinical SBRT and SRS and to further improve the efficacy of SBRT and SRS.CONCLUSIONSIn addition to directly killing tumor cells, high-dose irradiation used in SBRT and SRS induces indirect tumor cell death via vascular damage and antitumor immunity. Further studies are warranted to better understand the biological mechanisms underlying the high efficacy of clinical SBRT and SRS and to further improve the efficacy of SBRT and SRS. |
Author | Cho, L. Chinsoo Sperduto, Paul W. Kim, Mi-Sook Song, Chang W. Grimm, Jimm Marks, Lawrence B. Hui, Susanta Dusenbery, Kathryn E. Glatstein, Eli Emami, Bahman |
Author_xml | – sequence: 1 givenname: Chang W. surname: Song fullname: Song, Chang W. email: songx001@umn.edu organization: Department of Radiation Oncology, University of Minnesota Medical School, Minneapolis, Minnesota – sequence: 2 givenname: Eli surname: Glatstein fullname: Glatstein, Eli organization: Department of Radiation Oncology, University of Pennsylvania, Philadelphia, Pennsylvania – sequence: 3 givenname: Lawrence B. surname: Marks fullname: Marks, Lawrence B. organization: Department of Radiation Oncology, University of North Carolina, Chapel Hill, North Carolina – sequence: 4 givenname: Bahman surname: Emami fullname: Emami, Bahman organization: Department of Radiation Oncology, Loyola University Medical Center, Chicago, Illinois – sequence: 5 givenname: Jimm surname: Grimm fullname: Grimm, Jimm organization: Department of Radiation Oncology and Molecular Radiation Sciences, Johns Hopkins University, Baltimore, Maryland – sequence: 6 givenname: Paul W. surname: Sperduto fullname: Sperduto, Paul W. organization: Minneapolis Radiation Oncology and Gamma Knife Center, University of Minnesota, Minneapolis, Minnesota – sequence: 7 givenname: Mi-Sook surname: Kim fullname: Kim, Mi-Sook organization: Department of Radiation Oncology, Korea Institute of Radiological & Medical Sciences, Seoul, Korea – sequence: 8 givenname: Susanta surname: Hui fullname: Hui, Susanta organization: Department of Radiation Oncology, University of Minnesota Medical School, Minneapolis, Minnesota – sequence: 9 givenname: Kathryn E. surname: Dusenbery fullname: Dusenbery, Kathryn E. organization: Department of Radiation Oncology, University of Minnesota Medical School, Minneapolis, Minnesota – sequence: 10 givenname: L. Chinsoo surname: Cho fullname: Cho, L. Chinsoo organization: Department of Radiation Oncology, University of Minnesota Medical School, Minneapolis, Minnesota |
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