TY - JOUR
T1 - Targeting the tumor microenvironment in radiation oncology
T2 - Proceedings from the 2018 ASTRO–AACR Research workshop
AU - McGee, Heather M.
AU - Jiang, Dadi
AU - Soto-Pantoja, David R.
AU - Nevler, Avinoam
AU - Giaccia, Amato J.
AU - Woodward, Wendy A.
N1 - Publisher Copyright:
© 2019 American Association for Cancer Research.
PY - 2019
Y1 - 2019
N2 - The development of cancer and their response to radiation are intricately linked to the tumor microenvironment (TME) in which they reside. Tumor cells, immune cells, and stromal cells interact with each other and are influenced by the microbiome and metabolic state of the host, and these interactions are constantly evolving. Stromal cells not only secrete extracellular matrix and participate in wound contraction, but they also secrete fibroblast growth factors (FGF) molecules, which mediate macrophage differentiation. Tumor-associated macrophages migrate to hypoxic areas and secrete vascular endothelial growth factor (VEGF) to promote angiogenesis. The microbiome and its byproducts alter the metabolic milieu by shifting the balance between glucose utilization and fatty acid oxidation, and these changes subsequently influence the immune response in the TME. Not only does radiation exert cell-autonomous effects on tumor cells, but it influences both the tumor-promoting and tumor-suppressive components in the TME. To gain a deeper understanding of how the TME influences the response to radiation, the American Society for Radiation Oncology and the American Association of Cancer Research organized a scientific workshop on July 26–27, 2018, to discuss how the microbiome, the immune response, the metabolome, and the stroma all shift the balance between radiosensitivity and radioresistance. The proceedings from this workshop are discussed here and highlight recent discoveries in the field, as well as the most important areas for future research.
AB - The development of cancer and their response to radiation are intricately linked to the tumor microenvironment (TME) in which they reside. Tumor cells, immune cells, and stromal cells interact with each other and are influenced by the microbiome and metabolic state of the host, and these interactions are constantly evolving. Stromal cells not only secrete extracellular matrix and participate in wound contraction, but they also secrete fibroblast growth factors (FGF) molecules, which mediate macrophage differentiation. Tumor-associated macrophages migrate to hypoxic areas and secrete vascular endothelial growth factor (VEGF) to promote angiogenesis. The microbiome and its byproducts alter the metabolic milieu by shifting the balance between glucose utilization and fatty acid oxidation, and these changes subsequently influence the immune response in the TME. Not only does radiation exert cell-autonomous effects on tumor cells, but it influences both the tumor-promoting and tumor-suppressive components in the TME. To gain a deeper understanding of how the TME influences the response to radiation, the American Society for Radiation Oncology and the American Association of Cancer Research organized a scientific workshop on July 26–27, 2018, to discuss how the microbiome, the immune response, the metabolome, and the stroma all shift the balance between radiosensitivity and radioresistance. The proceedings from this workshop are discussed here and highlight recent discoveries in the field, as well as the most important areas for future research.
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U2 - 10.1158/1078-0432.CCR-18-3781
DO - 10.1158/1078-0432.CCR-18-3781
M3 - Article
C2 - 30723144
AN - SCOPUS:85065786534
SN - 1078-0432
VL - 25
SP - 2969
EP - 2974
JO - Clinical Cancer Research
JF - Clinical Cancer Research
IS - 10
ER -