Tumor radiosensitivity (SF2) is a prognostic factor for local control in head and neck cancers

Björk‐Eriksson, Thomas; West, Catharine M L; Karlsson, Ewa; Mercke, Claes

doi:10.1016/s0360-3016(99)00373-9

Cited by 112 publications

(74 citation statements)

References 20 publications

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“…This conclusion also concurs with seminal studies of Malaise et al (1987) and Deacon et al (1984), updated by Steel (1996) in which they provide considerable evidence that the radiosensitivity of tumours is most reliably measured at 2 Gy. The clinical studies of West and colleagues would support this proposition (West et al, 1997;Bjork-Eriksson et al, 2000).…”

Section: Discussionmentioning

confidence: 96%

“…West and colleagues have shown that biopsies from cervix and head and neck tumours can be used to predict for an individual patient's response to radiotherapy using clonogenic cell survival following exposure to 2 Gy X-irradiation (West et al, 1997;Bjork-Eriksson et al, 2000). The main disadvantages of this assay are that a minimum of 4 weeks is required to obtain a result, and about 30% of excised tumours failed to grow in soft agar; success of this method in other tumour types has been elusive.…”

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confidence: 99%

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Potential use of the alkaline comet assay as a predictor of bladder tumour response to radiation

et al. 2003

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Bladder tumours show a variable response to radiotherapy with only about 50% showing good local control; currently there is no test to predict outcome prior to treatment. We have used five bladder tumour cell lines (T24, UM-UC-3, TCC-SUP, RT112, HT1376) to investigate the potential of the alkaline comet assay (ACA) to predict radiosensitivity. Radiation-induced DNA damage and repair were compared to clonogenic survival. When the five cell lines were irradiated and initial DNA damage was plotted against cell survival, at all doses (0 -6 Gy), a significant correlation was found (r 2 ¼ 0.9514). Following 4 Gy X-irradiation, all cell lines, except T24, showed a correlation between SF2 vs half-time for repair and SF2 vs residual damage at 5, 10, 20 and 30 min. The T24 cell line showed radioresistance at low doses (0 -2 Gy) and radiosensitivity at higher doses (4 -6 Gy) using both cell survival and ACA end points, explaining the lack of correlation observed for this cell line. These data indicate that initial DNA damage and residual damage can be used to predict for radiosensitivity. Our data suggest that predictive tests of radiosensitivity, appropriate to the clinical situation, may require the use of test doses in the clinical range.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

Potential use of the alkaline comet assay as a predictor of bladder tumour response to radiation

et al. 2003

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“…These three groups are composed of radiosensitive tumors

false(SF 2 < 0.4 false)

, semisensitive tumors

false(SF 2 = 0.4 false)

, and radioresistant tumors

false(SF 2 > 0.4 false)

. The value of 0.4 has been determined based on the clinical study by Bjork‐Eriksson et al (16) In addition, it was assumed that the SF2 value for normal tissue is constant

false(SF 2 = 0.4 false)

. The values of α/β ratios for tumor cells and normal cells were considered to be 10 Gy and 2.5 Gy, respectively (17) .…”

Section: Methodsmentioning

confidence: 99%

Is grid therapy useful for all tumors and every grid block design?

Gholami

Nedaie

Longo

et al. 2016

J Applied Clin Med Phys

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Grid therapy is a treatment technique that has been introduced for patients with advanced bulky tumors. The purpose of this study is to investigate the effect of the radiation sensitivity of the tumors and the design of the grid blocks on the clinical response of grid therapy. The Monte Carlo simulation technique is used to determine the dose distribution through a grid block that was used for a Varian 2100C linear accelerator. From the simulated dose profiles, the therapeutic ratio (TR) and the equivalent uniform dose (EUD) for different types of tumors with respect to their radiation sensitivities were calculated. These calculations were performed using the linear quadratic (LQ) and the Hug‐Kellerer (H‐K) models. The results of these calculations have been validated by comparison with the clinical responses of 232 patients from different publications, who were treated with grid therapy. These published results for different tumor types were used to examine the correlation between tumor radiosensitivity and the clinical response of grid therapy. Moreover, the influence of grid design on their clinical responses was investigated by using Monte Carlo simulations of grid blocks with different hole diameters and different center‐to‐center spacing. The results of the theoretical models and clinical data indicated higher clinical responses for the grid therapy on the patients with more radioresistant tumors. The differences between TR values for radioresistant cells and radiosensitive cells at 20 Gy and 10 Gy doses were up to 50% and 30%, respectively. Interestingly, the differences between the TR values with LQ model and H‐K model were less than 4%. Moreover, the results from the Monte Carlo studies showed that grid blocks with a hole diameters of 1.0 cm and 1.25 cm may lead to about 19% higher TR relative to the grids with hole diameters smaller than 1.0 cm or larger than 1.25 cm (with 95% confidence interval). In summary, the results of this study indicate that grid therapy is more effective for tumors with radioresistant characteristics than radiosensitive tumors.PACS number(s): 87.55.‐x

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“…This 'intrinsic' radiosensitivity differs largely between tumour types and is at least partly due to the different sensitivity of the respective tumour cells Deacon et al, 1984;Fertil and Malaise, 1985). It was further shown that within one type of tumours, the outcome of the individual patients after radiotherapy was reflected by the in vitro radiosensitivity (SF2) of their tumour cells (West et al, 1993(West et al, , 1995Stausbol-Gron and Overgaard, 1999;Björk-Eriksson et al, 2000).…”

mentioning

confidence: 99%

Radiosensitivity of human tumour cells is correlated with the induction but not with the repair of DNA double-strand breaks

2003

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Nine human tumour cell lines (four mammary, one bladder, two prostate, one cervical, and one squamous cell carcinoma) were studied as to whether cellular radiosensitivity is related to the number of initial or residual double-strand breaks (dsb). Cellular sensitivity was measured by colony assay and dsb by means of constant-and graded-field gel electrophoresis (CFGE and GFGE, respectively). The nine tumour cell lines showed a broad variation in cellular sensitivity (SF2 0.17 -0.63). The number of initial dsb as measured by GFGE ranged between 14 and 27 dsb/Gy/diploid DNA content. In contrast, normal fibroblasts raised from skin biopsies of seven individuals showed only a marginal variation with 18 -20 dsb/Gy/diploid DNA content. For eight of the nine tumour cell lines, there was a significant correlation between the number of initial dsb and the cellular radiosensitivity. The tumour cells showed a broad variation in the amount of dsb measured 24 h after irradiation by CFGE, which, however, was not correlated with the cellular sensitivity. This residual damage was found to be influenced not only by the actual number of residual dsb, but also by apoptosis and cell cycle progression which had impact on CFGE measurements. Some cell line strains were able to proliferate even after exposure to 150 Gy while others were found to degrade their DNA. Our results suggest that for tumour cells, in contrast to normal cells, the variation in sensitivity is mainly determined by differences in the initial number of dsb induced.

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Tumor radiosensitivity (SF2) is a prognostic factor for local control in head and neck cancers

Cited by 112 publications

References 20 publications

Potential use of the alkaline comet assay as a predictor of bladder tumour response to radiation

Potential use of the alkaline comet assay as a predictor of bladder tumour response to radiation

Is grid therapy useful for all tumors and every grid block design?

Radiosensitivity of human tumour cells is correlated with the induction but not with the repair of DNA double-strand breaks

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