Blood Res 2016; 51(3):
Published online September 23, 2016
https://doi.org/10.5045/br.2016.51.3.157
© The Korean Society of Hematology
Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology (POSTECH), Pohang, Korea.
Correspondence to : G-One Ahn, Ph.D. Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology (POSTECH), POSTECH Biotech Center, Rm 127, 77 Cheongam-ro, Nam-gu, Pohang 37673, Korea. goneahn@postech.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Recent advancement in the radiotherapy technology has allowed conformal delivery of high doses of ionizing radiation precisely to the tumors while sparing large volume of the normal tissues, which have led to better clinical responses. Despite this technological advancement many advanced tumors often recur and they do so within the previously irradiated regions. How could tumors recur after receiving such high ablative doses of radiation? In this review, we outlined how radiation can elicit anti-tumor responses by introducing some of the cytokines that can be induced by ionizing radiation. We then discuss how tumor hypoxia, a major limiting factor responsible for failure of radiotherapy, may also negatively impact the anti-tumor responses. In addition, we highlight how there may be other populations of immune cells including regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages (TAMs) that can be recruited to tumors interfering with the anti-tumor immunity. Finally, the impact of irradiation on tumor hypoxia and the immune responses according to different radiotherapy regimen is also delineated. It is indeed an exciting time to see that radiotherapy is being combined with immunotherapy in the clinic and we hope that this review can add an excitement to the field.
Keywords Radiotherapy, Cancer, Immune system, Hypoxia
Blood Res 2016; 51(3): 157-163
Published online September 23, 2016 https://doi.org/10.5045/br.2016.51.3.157
Copyright © The Korean Society of Hematology.
Hoibin Jeong, Seoyeon Bok, Beom-Ju Hong, Hyung-Seok Choi, and G-One Ahn*
Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology (POSTECH), Pohang, Korea.
Correspondence to: G-One Ahn, Ph.D. Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology (POSTECH), POSTECH Biotech Center, Rm 127, 77 Cheongam-ro, Nam-gu, Pohang 37673, Korea. goneahn@postech.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Recent advancement in the radiotherapy technology has allowed conformal delivery of high doses of ionizing radiation precisely to the tumors while sparing large volume of the normal tissues, which have led to better clinical responses. Despite this technological advancement many advanced tumors often recur and they do so within the previously irradiated regions. How could tumors recur after receiving such high ablative doses of radiation? In this review, we outlined how radiation can elicit anti-tumor responses by introducing some of the cytokines that can be induced by ionizing radiation. We then discuss how tumor hypoxia, a major limiting factor responsible for failure of radiotherapy, may also negatively impact the anti-tumor responses. In addition, we highlight how there may be other populations of immune cells including regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages (TAMs) that can be recruited to tumors interfering with the anti-tumor immunity. Finally, the impact of irradiation on tumor hypoxia and the immune responses according to different radiotherapy regimen is also delineated. It is indeed an exciting time to see that radiotherapy is being combined with immunotherapy in the clinic and we hope that this review can add an excitement to the field.
Keywords: Radiotherapy, Cancer, Immune system, Hypoxia
Diagram outlining how ionizing radiation (IR) of tumors leads to anti-tumor responses and how tumor hypoxia can interfere such loop.
Abbreviations: DCs, dendritic cells; HMGB1, high mobility group protein box 1; ATP, adenosine triphosphate; HSPs, heat shock proteins; HIF-1, hypoxia-inducible factor-1; PD-L1, programmed death-ligand 1; VEGF, vascular endothelial growth factor; VEGFR-1, vascular endothelial growth factor receptor-1; CXCL-12, C-X-C motif chemokine ligand 12; CXCR-4, C-X-C motif chemokine receptor-4; MDSCs, myeloid-derived suppressor cells; TAMs, tumor-associated macrophages; MMP, matrix metalloproteinase; S100A8, S100 calcium-binding protein A8; IL-1β, interleukin-1β; IL-6, interleukin-6; TNF-α, tumor necrosis factor-α.
Table 1 . Effects of hypoxia on immune cells of the tumor microenvironment..
Abbreviations: BMDC, bone marrow-derived cell; CXCL-12, C-X-C motif chemokine ligand 12; DC, dendritic cell; PD-L1, programmed death-ligand 1; IL-10, interleukin-10; TAM, tumor-associated macrophage; VEGFR-1, vascular endothelial growth factor receptor-1..
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Diagram outlining how ionizing radiation (IR) of tumors leads to anti-tumor responses and how tumor hypoxia can interfere such loop.
Abbreviations: DCs, dendritic cells; HMGB1, high mobility group protein box 1; ATP, adenosine triphosphate; HSPs, heat shock proteins; HIF-1, hypoxia-inducible factor-1; PD-L1, programmed death-ligand 1; VEGF, vascular endothelial growth factor; VEGFR-1, vascular endothelial growth factor receptor-1; CXCL-12, C-X-C motif chemokine ligand 12; CXCR-4, C-X-C motif chemokine receptor-4; MDSCs, myeloid-derived suppressor cells; TAMs, tumor-associated macrophages; MMP, matrix metalloproteinase; S100A8, S100 calcium-binding protein A8; IL-1β, interleukin-1β; IL-6, interleukin-6; TNF-α, tumor necrosis factor-α.