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REVIEW article
Front. Oncol.
Sec. Cancer Immunity and Immunotherapy
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1552750
This article is part of the Research Topic Colorectal Cancer Immunotherapy and Immune Mechanisms View all articles
The Influence of the Microbiome on Radiotherapy and DNA Damage Responses
Provisionally accepted- 1 Texas Tech University Health Sciences Center, Lubbock, Texas, United States
- 2 University of Texas MD Anderson Cancer Center, Houston, United States
Colorectal cancer (CRC) is one of the most prevalent cancers in terms of diagnosis and mortality. Radiotherapy (RT) remains a mainstay of CRC therapy. As RT relies on DNA damage to promote tumor cell death, the activity of cellular DNA damage repair pathways can modulate cancer sensitivity to therapy. The gut microbiome has been shown to influence intestinal health and is independently associated with CRC development, treatment responses and outcomes. The microbiome can also modulate responses to CRC RT through various mechanisms such as community structure, toxins and metabolites. In this review we explore the use of RT in the treatment of CRC and the molecular factors that influence treatment outcomes. We also discuss how the microbiome can promote radiosensitivity versus radioprotection to modulate RT outcomes in CRC. Understanding the molecular interaction between the microbiome and DNA repair pathways can assist with predicting responses to RT. Once described, these connections between the microbiome and RT response can also be used to identify actionable targets for therapeutic development.
Keywords: Radiotherapy, microbiome, colorectal cancer, DNA Damage, DNA Repair
Received: 29 Dec 2024; Accepted: 24 Feb 2025.
Copyright: © 2025 Sheikh and Curran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Michael Andrew Curran, University of Texas MD Anderson Cancer Center, Houston, United States
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