Gene therapy for radioprotection

Everett, William; Curiel, David T.

doi:10.1038/cgt.2015.8

Cited by 15 publications

(7 citation statements)

References 101 publications

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“…Moreover, the evolution of tumor heterogeneity and sub-clones can further differentiate cancer mutation. When radiation is combined with TKI, the secondary gene mutation of tumors may become more complex, demonstrating new challenges for the treatment of tumors [19][20][21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Increase of secondary mutations may be a drug-resistance mechanism for lung adenocarcinoma after radiation therapy combined with tyrosine kinase inhibitor

et al. 2019

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Objective: To investigate changes in the secondary mutations of tumor in a drug-resistance mechanism for lung adenocarcinoma after radiation therapy combined with tyrosine kinase inhibitor (TKI). Methods: Lung adenocarcinoma cell line PC9 in vitro and xenograft model in nude mice were used to observe tumor inhibitory effects and drug-resistance under the effect of radiation therapy combined with erlotinib through apoptosis detection through in vitro survival curve and in vivo growth curve; changes in gene mutations before and after drug-resistance in nude mice xenografts were observed by the next generation sequencing, and the relationship between cancer drug-resistance and radiation therapy combined with TKI was observed. Results: Radiation therapy combined with erlotinib had a more reliable radio-sensitizing effect in vitro and in vivo, however, there were several drug-resistant tumor cells. Meanwhile, radiation therapy combined with erlotinib could significantly increase the number of mutations in tumor genes. The whole genome sequencing showed that the secondary mutation in the combined treatment group significantly increased in comparison with those of the single treatment group and the blank control group. Conclusion: The increase of secondary mutations may be an important drug-resistance mechanism for lung adenocarcinoma after radiation therapy combined with TKI, which provided further space exploration under the combined action of radiation and TKI.

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Section: Discussionmentioning

confidence: 99%

Increase of secondary mutations may be a drug-resistance mechanism for lung adenocarcinoma after radiation therapy combined with tyrosine kinase inhibitor

et al. 2019

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“…As an alternative biological strategy, gene therapy could be combined with cellular therapy by using cellular therapeutic agents as vectors. This would allow a dual approach to radioprotection through both cell-mediated and transgene-mediated mechanisms [163] . On the other hand, nanoparticles are a potential non-biological vector that could be used in radioprotection [164] .…”

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confidence: 99%

Research and Development of Radioprotective Agents: A Mini-Review

Saaya

Katsube

Xie

et al. 2017

International Journal of Radiology

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The research and development (R&D) of radioprotective agents (RAs) have been conducting since seven decades ago, and the safety and protection against undesirable effects of ionizing radiation (IR) has become an important issue especially for the benefit of patients receiving the radiotherapy, in addition to the applications in nuclear industry, military, outer space exploration and accidental exposures. Although the technology advancement makes the radiotherapy a promising better treatment by maximizing the effect of IR to the cancer cells, there are still needs for improvement in minimizing the toxicity to the normal cells. Aiming at providing the new researchers in the radiation protection field with an overall view for R&D of the RAs, this mini-review elucidates in brief a general understanding of the IR and its effects on the cell, the concepts of radiotherapy and therapeutic ratio, the categories of RAs and their mechanisms, and discusses on the strategies and challenge for R&D of the RAs.

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“…Another possibility to mitigate radiation-induced damage of normal tissue is the intracellular stabilization of ROS scavenging enzyme levels, which are inactivated after irradiation due to a ROS burst and infiltration of neutrophils. Administration of DNA-sequences encoding ROS-scavenging enzymes ameliorate radiotherapy-induced cell damage ( 391 ). Ingestion of manganese superoxide dismutase- plasmid liposomes (MnSOD-PL) has been shown to prolong mice survival after total body irradiation without protecting the tumor ( 392 , 393 ).…”

Section: Protecting Normal Tissue During Radiotherapymentioning

confidence: 99%

Metabolic Rewiring in Radiation Oncology Toward Improving the Therapeutic Ratio

2021

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To meet the anabolic demands of the proliferative potential of tumor cells, malignant cells tend to rewire their metabolic pathways. Although different types of malignant cells share this phenomenon, there is a large intracellular variability how these metabolic patterns are altered. Fortunately, differences in metabolic patterns between normal tissue and malignant cells can be exploited to increase the therapeutic ratio. Modulation of cellular metabolism to improve treatment outcome is an emerging field proposing a variety of promising strategies in primary tumor and metastatic lesion treatment. These strategies, capable of either sensitizing or protecting tissues, target either tumor or normal tissue and are often focused on modulating of tissue oxygenation, hypoxia-inducible factor (HIF) stabilization, glucose metabolism, mitochondrial function and the redox balance. Several compounds or therapies are still in under (pre-)clinical development, while others are already used in clinical practice. Here, we describe different strategies from bench to bedside to optimize the therapeutic ratio through modulation of the cellular metabolism. This review gives an overview of the current state on development and the mechanism of action of modulators affecting cellular metabolism with the aim to improve the radiotherapy response on tumors or to protect the normal tissue and therefore contribute to an improved therapeutic ratio.

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Gene therapy for radioprotection

Cited by 15 publications

References 101 publications

Increase of secondary mutations may be a drug-resistance mechanism for lung adenocarcinoma after radiation therapy combined with tyrosine kinase inhibitor

Increase of secondary mutations may be a drug-resistance mechanism for lung adenocarcinoma after radiation therapy combined with tyrosine kinase inhibitor

Research and Development of Radioprotective Agents: A Mini-Review

Metabolic Rewiring in Radiation Oncology Toward Improving the Therapeutic Ratio

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