Low dose radiation, inflammation, cancer and chemoprevention

Rashid, Al Maqsudur; Ramalingam, Latha; Moustaid‐Moussa, Naima; Moussa, Hanna

doi:10.1080/09553002.2018.1484194

Cited by 16 publications

(13 citation statements)

References 74 publications

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“…This is supported by the observation that mutation frequencies in cells treated with ultra-hyper-FRT doses may even be lower than in untreated cells (Redpath et al, 2003). Other recent analyses reach different conclusions (Maqsudur Rashid et al, 2019).…”

Section: Discussionmentioning

confidence: 81%

Ultra‐hyper‐fractionated radiotherapy for high‐grade gliomas

Fròsina

Fontana

Verzola

et al. 2021

J of Neuroscience Research

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High-grade gliomas (HGGs; WHO grades III and IV) are invariably lethal brain tumors.Low-dose hyper-radiosensitivity (HRS) of HGG is a well-established phenomenon in vitro. However, possibly linked to the unavailability of accurate animal models of the diseases, this therapeutic effect could not be consistently translated to the animal setting, thus impairing its subsequent clinical development. The purpose of this study was to develop radiotherapeutic (RT) schedules permitting to significantly improve the overall survival of faithful animal models of HGG that have been recently made available. We used primary glioma initiating cell (GIC)-driven orthotopic animal models that accurately recapitulate the heterogeneity and growth patterns of the patients' tumors, to investigate the therapeutic effects of low radiation doses toward HGG. With the same total dose, RT fractions ≤0.5 Gy twice per week [ultra-hyperfractionation (ultra-hyper-FRT)] started at early stages of tumor progression (a condition that in the clinical setting often occurs at the end of the guidelines treatment) improved the effectiveness of RT and the animal survival in comparison to standard fractions. For the same cumulative dose, the use of fractions ≤0.5 Gy may permit to escape one or more tumor resistance mechanisms thus increasing the effectiveness of RT and the overall animal survival. These findings suggest investigating in the clinical setting the therapeutic effect of an ultra-hyper-FRT schedule promptly extending the conventional RT component of the current guideline ("Stupp") therapeutic protocol.

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Section: Discussionmentioning

confidence: 81%

Ultra‐hyper‐fractionated radiotherapy for high‐grade gliomas

Fròsina

Fontana

Verzola

et al. 2021

J of Neuroscience Research

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“…Moreover, exposure of adipose-derived stem cells to LDR(1.4 Gy/min) slows the proliferation rate and causes cell cycle arrest 46 , and exposure to 10 cGy to 50 cGyLDR causes DNA damage in human adipose mesenchymal stem cell nuclei 47 or activation of the NLRP3 inflammasome inhuman lung cells 48 . In adipose cells of breast cancer tissues, LDR can activate inflammatory cytokines, the levels of which are elevated following LDR exposure 49 . Although Vibe N et al found that exposure of L6 cells to 1–2 Gy decreased insulin signalling in radiated preadipocytes 31 , there have been limited cell studies on the effects of LDR on insulin resistance in adipose cells and liver cells.…”

Section: Discussionmentioning

confidence: 99%

Low-dose radiation exaggerates HFD-induced metabolic dysfunction by gut microbiota through PA-PYCR1 axis

et al. 2022

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Co-exposure of High-fat-diet (HFD) behavior and environmental low-dose radiation (LDR) is common among majority occupational workers, but the synergism of this co-exposure in metabolic health is poorly understood. This study aimed to investigate the impact of gut microbiota and its metabolites on the regulation of HFD accompanied by LDR-associated with metabolic dysfunction and insulin resistance. Here, we reported that Parasutterella was markedly elevated in the gut microbiota of mice in co-exposure of HFD and LDR, accompanied by increased pyrrolidinecarboxylic acid (PA) level in both intestine and plasma. Transplantation of fecal microbiota from mice with co-exposure HFD and LDR with metabolic dysfunction resulted in increased disruption of metabolic dysfunction, insulin resistance and increased PYCR1 (Pyrroline-5-carboxylate reductase 1) expression. Mechanistically, intestinal barrier was damaged more serious in mice with co-exposure of HFD and LDR, leading high PA level in plasma, activating PYCR1 expression to inhibit insulin Akt/mTOR (AKT kinase-transforming protein/Serine threonine-protein kinase) signaling pathway to aggravate HFD-induced metabolic impairments. This study suggests a new avenue for interventions against western diet companied with low dose radiation exposure-driven metabolic impairments.

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“…However, if radiation carcinogenesis proceeds through the hosts’ recovery processes from damage in normal tissues, there could be a possibility in the future that it might be possible to develop methods to mitigate radiation-induced carcinogenesis processes. 33 Specific approaches toward this goal may include, for example, controls on the expression of cGAS, 26 GPCR (G protein-coupled receptor), 34 MK2, 35 CD28, 36 PUFA (n-3 polyunsaturated fatty acids), 37 TGFβ and PDGF 38 etc, and in turn, this may be applicable to the processes involved in spontaneous carcinogenesis. It has been reported that the use of, for example, non-steroid anti inflammatory drugs 39,40 or soy isoflavones, 41 might help prevent radiation carcinogenesis, although actual experimental data are still limited.…”

Section: Discussionmentioning

confidence: 99%

A hypothesis: radiation carcinogenesis may result from tissue injuries and subsequent recovery processes which can act as tumor promoters and lead to an earlier onset of cancer

Nakamura

2020

BJR

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Cancer risks from radiation can be observed as an increase in mortality when compared to a control group. However, it is unknown if this increased risk results from the induction of cancer or from an earlier onset of cancer. In mouse studies, it has been repeatedly shown that after an irradiation, the survival curve is shifted toward lower ages, but remains parallel to the control curve, and the extent of the shift in time to lower ages is dose-dependent. This shift is not satisfactorily explained by the induction model which assumes that cancers in the exposed group consist of spontaneous and induced events. Consequently, it seems that this shift could be interpreted to mean that all animals in the exposed group had suffered from life shortening. Under this scenario, however, it turns out that the radiation effects can no longer be interpreted as the result of oncogenic mutations, because these effects would have to involve all tumors, and the effectiveness of radiation changes with the dose. This leads to the speculation that radiation exposures induce a broad range of tissue injuries, and that these injuries are subsequently subjected to longlasting systemic recovery processes which act as promoters for tumor cells. In other words, potential cancer stem cells which were located in the irradiated field can escape oncogenic damage but undergo stimulation later in life toward the development of malignancy from radiation-induced activated microenvironment. This is an unusual form of the non-targeted or bystander effects of radiation. It is worth noting that this model suggests that there could be a path or paths which could be used to intervene in the process of post-exposure carcinogenesis, and that cancer risks at low doses could be described as days or weeks of life lost.

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Low dose radiation, inflammation, cancer and chemoprevention

Cited by 16 publications

References 74 publications

Ultra‐hyper‐fractionated radiotherapy for high‐grade gliomas

Ultra‐hyper‐fractionated radiotherapy for high‐grade gliomas

Low-dose radiation exaggerates HFD-induced metabolic dysfunction by gut microbiota through PA-PYCR1 axis

A hypothesis: radiation carcinogenesis may result from tissue injuries and subsequent recovery processes which can act as tumor promoters and lead to an earlier onset of cancer

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