Mitochondrial metabolism: a predictive biomarker of radiotherapy efficacy and toxicity.

Farzad Taghizadeh-Hesary, Mohammad Houshyari, Mohammad Farhadi
Author Information
  1. Farzad Taghizadeh-Hesary: ENT and Head and Neck Research Center and Department, The Five Senses Health Institute, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. farzadth89@gmail.com.
  2. Mohammad Houshyari: Clinical Oncology Department, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  3. Mohammad Farhadi: ENT and Head and Neck Research Center and Department, The Five Senses Health Institute, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Abstract

INTRODUCTION: Radiotherapy is a mainstay of cancer treatment. Clinical studies revealed a heterogenous response to radiotherapy, from a complete response to even disease progression. To that end, finding the relative prognostic factors of disease outcomes and predictive factors of treatment efficacy and toxicity is essential. It has been demonstrated that radiation response depends on DNA damage response, cell cycle phase, oxygen concentration, and growth rate. Emerging evidence suggests that altered mitochondrial metabolism is associated with radioresistance.
METHODS: This article provides a comprehensive evaluation of the role of mitochondria in radiotherapy efficacy and toxicity. In addition, it demonstrates how mitochondria might be involved in the famous 6Rs of radiobiology.
RESULTS: In terms of this idea, decreasing the mitochondrial metabolism of cancer cells may increase radiation response, and enhancing the mitochondrial metabolism of normal cells may reduce radiation toxicity. Enhancing the normal cells (including immune cells) mitochondrial metabolism can potentially improve the tumor response by enhancing immune reactivation. Future studies are invited to examine the impacts of mitochondrial metabolism on radiation efficacy and toxicity. Improving radiotherapy response with diminishing cancer cells' mitochondrial metabolism, and reducing radiotherapy toxicity with enhancing normal cells' mitochondrial metabolism.

Keywords

References

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MeSH Term

Humans
Mitochondria
Radiobiology
Neoplasms
Radiation Oncology
Biomarkers
Radiation Injuries
Radiation Tolerance
Radiotherapy

Chemicals

Biomarkers

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