The Elimination of Low-Dose Hyper-radiosensitivity by Transfer of Irradiated-Cell Conditioned Medium Depends on Dose Rate

Edin, Nina Frederike Jeppesen; Sandvik, Joe Alexander; Olsen, Dag Rune; Pettersen, Erik O.

doi:10.1667/rr1143.1

Cited by 11 publications

(41 citation statements)

References 46 publications

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“…Hence, HRS-negative H460 cells showed increased clonogenic inhibition than apoptosis when compared with HRS-positive H-157 cells. However, UKY-29 and A549 cells harboring HRS did not show significant induction of apoptosis following LDFRT, thus supporting the previous observations that apoptosis may be indicative of HRS but is not a prerequisite for HRS (37,38). Furthermore, in H460 cells, significant differences in the expression of genes related to apoptosis were not observed with any of the treatments when compared with the untreated group (Supplementary Table 6).…”

Section: Discussionsupporting

confidence: 85%

Low-Dose Fractionated Radiation Potentiates the Effects of Cisplatin Independent of the Hyper-Radiation Sensitivity in Human Lung Cancer Cells

Gupta

Koru‐Sengul

Arnold

et al. 2011

Molecular Cancer Therapeutics

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In this study, the role of hyper-radiation sensitivity (HRS) in potentiating the effects of cisplatin by low-dose fractionated radiation (LDFRT) was evaluated in four human non-small cell lung cancer cell lines. Presence of HRS and cisplatin enhancement ratio (CER) by LDFRT/2 Gy was assessed using colony-forming and apoptotic assays. Cell-cycle disturbances were studied by flow cytometry. Expression of genes involved in apoptosis was assessed using real-time reverse transcriptase PCR arrays. H-157 cells showed a distinct HRS region, followed by UKY-29 and A549 cells, whereas it was absent in H460 cells, which when lack HRS showed maximum CER with LDFRT (4 Â 0.5 Gy) both by clonogenic inhibition and by apoptosis compared with single fraction of 2 Gy whereas the most radioresistant A549 cells had the least CER, with no significant differences between LDFRT or 2 Gy. Interestingly, in H-157 cells, a more pronounced CER was observed with LDFRT when assessed by apoptosis but clonogenic inhibition-CER was higher with 2 Gy than with LDFRT. Excluding H-157 cells, the CER by LDFRT was inversely proportional to radioresistance [(determined by D 0 , the dose to reduce survival by 67% from any point on the linear portion of the survival curve or surviving fraction (SF) at 2 Gy (SF 2 )] of the cells. LDFRT alone or in combination with cisplatin induced larger number of proapoptotic genes than 2 Gy or cisplatin þ 2 Gy in cells showing HRS when compared to H460 cells that lack HRS. These findings indicate that chemopotentiation by LDFRT is correlated more with the intrinsic radiation sensitivity of the non-small lung cancer cells than the HRS phenomenon whereas the mode of cell killing is both through apoptosis and clonogenic inhibition. Mol Cancer Ther; 10(2); 292-302. Ó2011 AACR.

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Section: Discussionsupporting

confidence: 85%

Low-Dose Fractionated Radiation Potentiates the Effects of Cisplatin Independent of the Hyper-Radiation Sensitivity in Human Lung Cancer Cells

Gupta

Koru‐Sengul

Arnold

et al. 2011

Molecular Cancer Therapeutics

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“…In previous studies (Edin et al 2007, Edin et al 2009, T-47D breast cancer cells were found to display a pronounced low-dose hyper-radiosensitivity when irradiated acutely (40 Gy/h) with 60 Co g-rays. Surprisingly, irradiating the cells with a priming dose of 0.3 Gy at the low dose-rate (LDR) of 0.3 Gy/h was found to eliminate HRS permanently, i.e., the cells did not show a HRS response to subsequent acute irradiation given up to 14 months (with continuous culturing of the cells) after the LDR priming dose (Edin et al 2009).…”

Section: Introductionmentioning

confidence: 92%

“…Surprisingly, irradiating the cells with a priming dose of 0.3 Gy at the low dose-rate (LDR) of 0.3 Gy/h was found to eliminate HRS permanently, i.e., the cells did not show a HRS response to subsequent acute irradiation given up to 14 months (with continuous culturing of the cells) after the LDR priming dose (Edin et al 2009). If the priming dose of 0.3 Gy was given as an acute irradiation (i.e., at a dose-rate of 40 Gy/h), HRS was eliminated only transiently (less than 24 h) (Edin et al 2007).…”

Section: Introductionmentioning

confidence: 99%

“…It appears that different mechanisms are activated depending on dose-rate (Edin et al 2007, Edin et al 2009). This was corroborated by experiments demonstrating that medium harvested from flasks of irradiated cells and transferred to unirradiated cells eliminated HRS in the recipient cells, but this occured if the irradiation was delivered at the low dose-rate only.…”

Section: Introductionmentioning

confidence: 99%

“…The ability of the medium to eliminate HRS in recipient cells was present even 14 months after the LDR priming, but the recipient cells recovered HRS within 2 weeks after the medium transfer. When the medium transferred from LDR primed cells was diluted, the effect on HRS was reduced (Edin et al 2009). …”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of the elimination of low dose hyper-radiosensitivity in T-47D cells by low dose-rate priming

Edin¹,

Olsen²,

Stokke³

et al. 2009

International Journal of Radiation Biology

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Integrated Modelling of Cell Responses after Irradiation for DNA-Targeted Effects and Non-Targeted Effects

Matsuya

Sasaki

Yoshii

et al. 2018

Sci Rep

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Intercellular communication after ionizing radiation exposure, so-called non-targeted effects (NTEs), reduces cell survival. Here we describe an integrated cell-killing model considering NTEs and DNA damage along radiation particle tracks, known as DNA-targeted effects (TEs) based on repair kinetics of DNA damage. The proposed model was applied to a series of experimental data, i.e., signal concentration, DNA damage kinetics, cell survival curve and medium transfer bystander effects (MTBEs). To reproduce the experimental data, the model considers the following assumptions: (i) the linear-quadratic (LQ) function as absorbed dose to express the hit probability to emit cell-killing signals, (ii) the potentially repair of DNA lesions induced by NTEs, and (iii) lower efficiency of repair for the damage in NTEs than that in TEs. By comparing the model results with experimental data, we found that signal-induced DNA damage and lower repair efficiency in non-hit cells are responsible for NTE-related repair kinetics of DNA damage, cell survival curve with low-dose hyper-radiosensitivity (HRS) and MTBEs. From the standpoint of modelling, the integrated cell-killing model with the LQ relation and a different repair function for NTEs provide a reasonable signal-emission probability and a new estimation of low-dose HRS linked to DNA repair efficiency.

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The Elimination of Low-Dose Hyper-radiosensitivity by Transfer of Irradiated-Cell Conditioned Medium Depends on Dose Rate

Cited by 11 publications

References 46 publications

Low-Dose Fractionated Radiation Potentiates the Effects of Cisplatin Independent of the Hyper-Radiation Sensitivity in Human Lung Cancer Cells

Low-Dose Fractionated Radiation Potentiates the Effects of Cisplatin Independent of the Hyper-Radiation Sensitivity in Human Lung Cancer Cells

Mechanisms of the elimination of low dose hyper-radiosensitivity in T-47D cells by low dose-rate priming

Integrated Modelling of Cell Responses after Irradiation for DNA-Targeted Effects and Non-Targeted Effects

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