Optimizing radiotherapy protocols using computer automata to model tumour cell death as a function of oxygen diffusion processes

Paul‐Gilloteaux, Perrine; Potiron, Vincent; Delpon, G.; Supiot, S.; Chiavassa, S.; Pâris, François; Costes, Sylvain V.

doi:10.1038/s41598-017-01757-6

Cited by 28 publications

(35 citation statements)

References 53 publications

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“…Hypoxic niches protect cancer cells from radiation-induced killing since oxygen is a critical determinant of cell response to radiation ( 151 ). A certain degree of reoxygenation can be achieved in some tumors after radiation by a process where the surviving hypoxic tumor cells become better oxygenated due to the aerobic population being killed.…”

Section: Metabolic Targeting Of Gscsmentioning

confidence: 99%

Glioblastoma Stem-Like Cells, Metabolic Strategy to Kill a Challenging Target

et al. 2019

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Over the years, substantial evidence has definitively confirmed the existence of cancer stem-like cells within tumors such as Glioblastoma (GBM). The importance of Glioblastoma stem-like cells (GSCs) in tumor progression and relapse clearly highlights that cancer eradication requires killing of GSCs that are intrinsically resistant to conventional therapies as well as eradication of the non-GSCs cells since GSCs emergence relies on a dynamic process. The past decade of research highlights that metabolism is a significant player in tumor progression and actually might orchestrate it. The growing interest in cancer metabolism reprogrammation can lead to innovative approaches exploiting metabolic vulnerabilities of cancer cells. These approaches are challenging since they require overcoming the compensatory and adaptive responses of GSCs. In this review, we will summarize the current knowledge on GSCs with a particular focus on their metabolic complexity. We will also discuss potential approaches targeting GSCs metabolism to potentially improve clinical care.

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Section: Metabolic Targeting Of Gscsmentioning

confidence: 99%

Glioblastoma Stem-Like Cells, Metabolic Strategy to Kill a Challenging Target

et al. 2019

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“…Finally, the fact that the damage to healthy tissue is significantly lower than in photon therapy permits dose escalation and hypofractionation (fewer, but higher-dose irradiations for the same total dose received by the tumor), which may lead to a greater therapeutic advantage [7] and potentially tumor reoxygenation for better cell killing by increasing blood vessel leakage [9]. However, using higher individual doses may also change the long-term risk of increased damage to healthy tissue [5].…”

Section: The Superior Energy Deposition and Tissue Relative Biologicamentioning

confidence: 99%

Comparing Photon and Charged Particle Therapy Using DNA Damage Biomarkers

Ray

Cekanaviciute

Paulino-Lima

et al. 2018

International Journal of Particle Therapy

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Treatment modalities for cancer radiation therapy have become increasingly diversified given the growing number of facilities providing proton and carbon-ion therapy in addition to the more historically accepted photon therapy. An understanding of high-LET radiobiology is critical for optimization of charged particle radiation therapy and potential DNA damage response. In this review, we present a comprehensive summary and comparison of these types of therapy monitored primarily by using DNA damage biomarkers. We focus on their relative profiles of dose distribution and mechanisms of action from the level of nucleic acid to tumor cell death.

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“…179 IR resulted in acute hypoxia in the tumor due to transient changes in blood flow and this acute hypoxia increased radioresistance in the tumor. 180,181 Higher radiosensitivity of normoxic compared with hypoxic cells is most likely due tofixation of ROS under normoxic conditions. 182,183 Preclinical studies support that hypoxia leads to a radioresistant and metastatic phenotype of prostate tumors.…”

Section: Predictive Markers Of Resistance To Radiotherapymentioning

confidence: 99%

Profiles of Radioresistance Mechanisms in Prostate Cancer

et al. 2018

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Radiation therapy (RT) is commonly used for the treatment of localized prostate cancer (PCa). However, cancer cells often develop resistance to radiation through unknown mechanisms and pose an intractable challenge. Radiation resistance is highly unpredictable, rendering the treatment less effective in many patients and frequently causing metastasis and cancer recurrence. Understanding the molecular events that cause radioresistance in PCa will enable us to develop adjuvant treatments for enhancing the efficacy of RT. Radioresistant PCa depends on the elevated DNA repair system and the intracellular levels of reactive oxygen species (ROS) to proliferate, self-renew, and scavenge anti-cancer regimens, whereas the elevated heat shock protein 90 (HSP90) and the epithelial-mesenchymal transition (EMT) enable radioresistant PCa cells to metastasize after exposure to radiation. The up-regulation of the DNA repairing system, ROS, HSP90, and EMT effectors has been studied extensively, but not targeted by adjuvant therapy of radioresistant PCa. Here, we emphasize the effects of ionizing radiation and the mechanisms driving the emergence of radioresistant PCa. We also address the markers of radioresistance, the gene signatures for the predictive response to radiotherapy, and novel therapeutic platforms for targeting radioresistant PCa. This review provides significant insights into enhancing the current knowledge and the understanding toward optimization of these markers for the treatment of radioresistant PCa.

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Optimizing radiotherapy protocols using computer automata to model tumour cell death as a function of oxygen diffusion processes

Cited by 28 publications

References 53 publications

Glioblastoma Stem-Like Cells, Metabolic Strategy to Kill a Challenging Target

Glioblastoma Stem-Like Cells, Metabolic Strategy to Kill a Challenging Target

Comparing Photon and Charged Particle Therapy Using DNA Damage Biomarkers

Profiles of Radioresistance Mechanisms in Prostate Cancer

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