Mitigation and Treatment of Radiation-Induced Thoracic Injury With a Cyclooxygenase-2 Inhibitor, Celecoxib

Hunter, Nancy; Valdecanas, David R.; Liao, Zhongxing; Milas, Luka; Mason, Kathy

doi:10.1016/j.ijrobp.2012.04.025

Cited by 28 publications

(19 citation statements)

References 19 publications

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“…The production of PGE2 is associated with oxidative DNA damage and genomic instability that may be prolonged for some days after exposure to radiation (Chai et al, 2012). However, it has been revealed that selective inhibition of COX-2, some months after irradiation, can mitigate the risk of pneumonitis in animal models (Hunter et al, 2013). Increasing NF-κB and COX-2 levels is considered as one of the main mechanisms involved in the appearance of inflammation and pain in some organs, such as gastrointestinal system (El-Ghazaly, Nada, El-Hazek, & Khayyal, 2010;Ghasemi, Danesh, Yazdani-Charati, & Hosseinimehr, 2018;Khayyal, El-Ghazaly, El-Hazek, & Nada, 2009).…”

Section: Radiation-induced Normal Tissue Toxicity: Role Of Nf-κbmentioning

confidence: 99%

NF‐κB targeting for overcoming tumor resistance and normal tissues toxicity

Mortezaee

Najafi

Farhood

et al. 2019

Journal Cellular Physiology

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Radiotherapy and chemotherapy are two famous modalities in tumor‐targeted therapy that lead to systemic and local toxicities for normal tissues. Moreover, several studies have confirmed that exposure of the tumor to radiation or chemotherapy drugs stimulate some signaling pathways in the tumor microenvironment (TME), leading to resistance of cancer cells to apoptosis, as well as promoting angiogenesis and tumor growth. Nuclear factor kappa B (NF‐κB) plays a central role in the regulation of inflammatory responses in both normal tissues and tumors via the release of several cytokines, regulation of prostaglandins, reduction/oxidation (redox) reactions, angiogenesis, and cell death. Upregulation of NF‐κB in normal tissues causes an appearance of inflammatory reactions and oxidative stress, whereas it regulates angiogenesis and suppresses apoptosis, leading to resistance to subsequent doses of radiation or chemotherapy. Selective inhibition of NF‐κB in experimental studies has shown promising results for tumor sensitization via apoptosis induction, inhibition of angiogenesis, and increasing delay of tumor growth. The use of some agents for NF‐κB inhibition has been shown to alleviate radiation/chemotherapy toxicities in normal cells/ tissues. In this current review, we explained the pivotal role of NF‐κB in both normal tissue toxicity and tumor resistance. We also discussed the promising strategies for overcoming these problems with regard to chemotherapy and radiotherapy.

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Section: Radiation-induced Normal Tissue Toxicity: Role Of Nf-κbmentioning

confidence: 99%

NF‐κB targeting for overcoming tumor resistance and normal tissues toxicity

Mortezaee

Najafi

Farhood

et al. 2019

Journal Cellular Physiology

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“…When started immediately or 40 d after irradiation, the decrease in pneumonitis was not as robust. 50 In clinical cases, those that did not use statins or acetylsalicylic acid following radiation therapy for prostate cancer had early biochemical failure and worse outcomes. 130 Acetylsalicylic acid reduced rates of distant metastases and improved overall survival.…”

Section: Resultsmentioning

confidence: 99%

Novel Indications for Commonly Used Medications as Radiation Protectants in Spaceflight

McLaughlin¹,

Donoviel²,

Jones³

2017

Aerospace Medicine and Human Performance

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Background In the space environment, the traditional radioprotective principles of time, distance, and shielding become difficult to implement. Additionally, the complex radiation environment inherent in space, the chronic exposure timeframe, and the presence of numerous confounding variables complicate the process of creating appropriate risk models for astronaut exposure. Pharmaceutical options hold tremendous promise to attenuate acute and late effects of radiation exposure in the astronaut population. Pharmaceuticals currently approved for other indications may also offer radiation protection, modulation, or mitigation properties along with a well-established safety profile. Currently there are only three agents which have been clinically approved to be employed for radiation exposure, and these only for very narrow indications. This review identifies a number of agents currently approved by the U.S. Food and Drug Administration (FDA) which could warrant further investigation for use in astronauts. Specifically, we examine preclinical and clinical evidence for statins, nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), metformin, calcium channel blockers, β adrenergic receptor blockers, fingolimod, N-acetylcysteine, and pentoxifylline as potential radiation countermeasures.

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“…The data presented in Figure 4 already show how the survival times can vary dramatically on changing radiation dose and that these can encompass more than one type of pathology. For those studies in which radiation mitigators have so far been tested, only three, involving investigations on methylprednisolone in CF1 mice, 123,124 D-penicillamine in Sch(ICR)BR mice, 125 and celecoxib in C3Hf/Kam mice 126 have employed more than one radiation dose level. A full appreciation of any modifying effect can be accomplished in experimental study designs that deliver graded radiation doses for each arm for construction of dose-response relationships.…”

Section: Implications For Selecting the Best Models In The Pre-clinicmentioning

confidence: 99%

A survey of changing trends in modelling radiation lung injury in mice: bringing out the good, the bad, and the uncertain

Dabjan

Buck

Jackson

et al. 2016

Laboratory Investigation

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Within this millennium there has been resurgence in funding and research dealing with animal models of radiationinduced lung injury to identify and establish predictive biomarkers and effective mitigating agents that are applicable to humans. Most have been performed on mice but there needs to be assurance that the emphasis on such models is not misplaced. We therefore considered it timely to perform a comprehensive appraisal of the literature dealing with radiation lung injury of mice and to critically evaluate the validity and clinical relevance of the research. A total of 357 research papers covering the period of 1970-2015 were extensively reviewed. Whole thorax irradiation (WTI) has become the most common treatment for studying lung injury in mice and distinct trends were seen with regard to the murine strain, radiation dose, intended pathology investigated, length of study, and assays. Recently, the C57BL/6 strain has been increasingly used in the majority of these studies with the notion that they are susceptible to pulmonary fibrosis. Nonetheless, many of these investigations depend on animal survival as the primary end point and neglect the importance of radiation pneumonitis and the anomaly of lethal pleural effusions. A relatively large variation in survival times of C5BL/6 mice is also seen among different institutions pointing to the need for standardization of radiation treatments and environmental conditions. An analysis of mitigating drug treatments is complicated by the fact that the majority of studies are limited to the C57BL/6 strain with a premature termination of the experiments and do not establish whether the treatment actually prevents or simply delays the progression of radiation injury. This survey of the literature has pointed to several improvements that need to be considered in establishing a reliable preclinical murine model of radiation lung injury. The lethality end point should also be used cautiously and with greater emphasis on other assays such as non-invasive lung functional and imaging monitoring in order to quantify specific pulmonary injury that can be better extrapolated to radiation toxicity encountered in our own species.Laboratory Investigation (2016) 96, 936-949;

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Mitigation and Treatment of Radiation-Induced Thoracic Injury With a Cyclooxygenase-2 Inhibitor, Celecoxib

Cited by 28 publications

References 19 publications

NF‐κB targeting for overcoming tumor resistance and normal tissues toxicity

NF‐κB targeting for overcoming tumor resistance and normal tissues toxicity

Novel Indications for Commonly Used Medications as Radiation Protectants in Spaceflight

A survey of changing trends in modelling radiation lung injury in mice: bringing out the good, the bad, and the uncertain

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