Comparison of radiosensitization by 41°C hyperthermia during low dose rate irradiation and during pulsed simulated low dose rate irradiation in human glioma cells

Raaphorst, G. P.; Ng, Cheng E.; Shahine, Bilal

doi:10.1016/s0360-3016(98)00565-3

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…US apparatus and intensity measurement. The US apparatus C 4 To whom correspondence should be addressed. E-mail: kondot@ms.toyama-mpu.ac.jp (ES-1, OG Giken Co., Ltd., Okayama), described in a previous paper, 15) with a resonance frequency of 1 MHz was used in all the sonication experiments.…”

Section: Methodsmentioning

confidence: 99%

“…1) Enhancing the therapeutic effects of hyperthermia by other methods is a welcome advance in this field. [2][3][4][5][6][7][8][9] An example is the use of the so-called thermal sensitizers. [6][7][8][9] Thermal sensitizers are agents that may not have much value in therapy when used alone, but can enhance the therapeutic effect of hyperthermia when used in conjunction with it.…”

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confidence: 99%

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Ultrasound‐induced killing of monocytic U937 cells enhanced by 2,2′‐azobis(2‐amidinopropane) dihydrochloride

et al. 2004

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To determine the effect of 2,2′ ′ ′ ′-azobis(2-amidinopropane) dihydrochloride (AAPH) on ultrasound (US)-induced cell killing, human monocytic leukemia cells (U937) were incubated at various temperatures (25.0, 37.0 and 40.0°C) for 1 min in air-saturated phosphate-buffered solution (PBS) containing 50 mM AAPH before exposure to nonthermal 1 MHz US for 1 min at an intensity of 2.0 W/cm 2 . Cell viability was determined by means of the Trypan blue dye exclusion test immediately after sonication. Apoptosis was measured after 6-h incubation post-sonication by flow cytometry. Free radicals generated by AAPH, a temperature-dependent free radical generator, or US or both were also investigated using electron paramagnetic resonance (EPR) spin trapping. The results showed that US-induced cell lysis and apoptosis were enhanced in the presence of AAPH regardless of the temperature at the time of sonication. At 40.0°C, US alone induced increased cell killing, while AAPH alone is capable of inducing significant but minimal apoptosis at this temperature. Although free radicals were increased in the combined treatment, this increase did not correlate well with cell killing. The mechanism of enhancement points to the increased uptake of the agent during sonication rather than potentiation by AAPH. These findings suggest the clinical potential of temperature-dependent free radical generators in cancer therapy with therapeutic US. ombinations of cancer therapy modalities have long been of interest as an approach to improve the outcome of treatment, since single modalities have not always been suffiently effective. However, combinations of established modalities, though they may potentially enhance cancer eradication, are also often accompanied by increased risk and complications in the procedure. Therefore, unconventional but safe methods should be considered to attain effective and safe combination therapies.Hyperthermia is now earning wide acceptance in cancer therapy.1) Enhancing the therapeutic effects of hyperthermia by other methods is a welcome advance in this field.2-9) An example is the use of the so-called thermal sensitizers.6-9) Thermal sensitizers are agents that may not have much value in therapy when used alone, but can enhance the therapeutic effect of hyperthermia when used in conjunction with it. These type of agents are now drawing attention not only in the field of hyperthermia, but also in free radical research 8,10) and especially research related to apoptosis. [11][12][13] Among the heat sensitizers, 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH) and 2,2′-azobis(2,4-dimethylvaleronitrile) (AMVN) are well known. A water-soluble, temperaturedependent free radical initiator, AAPH, has been shown to sensitize Chinese hamster V79 cells to thermal killing 6) and to enhance hyperthermia-induced apoptosis of U937, 8) CaSki and HeLa cells.11) This was attributed to the temperature-dependent generation of carbon-centered free radicals. Although free radicals are generated by AAPH at 37°C, the compound is not to...

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Ultrasound‐induced killing of monocytic U937 cells enhanced by 2,2′‐azobis(2‐amidinopropane) dihydrochloride

et al. 2004

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“…A second study of 10 human glioblastoma cell lines in vitro resulted in the mean lethal dose D 0 ¼ 1.670.5 (Taghian et al, 1992(Taghian et al, , 1995 and a third study of 11 human glioblastoma cell lines in vitro resulted in a mean inactivation dose of D 0 ¼ 2.070.6 (Allam et al, 1993). Radiation survival curves for U373MG and U87MG human glioma cells, under the condition of high-dose rate up to 10 Gy resulted in the mean lethal dose values of 1.0 and 0.7 Gy, respectively (Wilkins et al, 1996;Raaphorst et al 1999). The results obtained in our study from three new GBM cell cultures yielded the mean lethal (nonproliferating) dose D 0 in the order of 6 -8 Gy.…”

Section: Radiation Sterilisation Of Brain Tumour Cells C Bauréus-kochmentioning

confidence: 99%

“…Other previously documented studies of the intrinsic cellular radiation sensitivity of noninfected human glioblastoma cell lines have mostly used irradiation at absorbed dose levels below 12 Gy (Malaise et al, 1986;Taghian et al, 1992;Allam et al, 1993;Taghian et al, 1995;Wilkins et al, 1996;Budach et al, 1997;Raaphorst et al 1999). The first study of five human glioma cell lines resulted in the mean lethal dose D 0 ¼ 1.470.4 Gy (Malaise et al, 1986).…”

Section: Radiation Sterilisation Of Brain Tumour Cells C Bauréus-kochmentioning

confidence: 99%

Radiation sterilisation of cultured human brain tumour cells for clinical immune tumour therapy

et al. 2004

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The aim is to investigate the radiosensitivity of noninfected cultured human glioma cells to ascertain that intracutaneously administered cells are viable enough to produce interferon-g but not able to proliferate. Cell cultures were established from five patients undergoing brain tumour surgery. By karyotyping, we found four malignant (three glioblastoma multiforme (GBM), one giant cell glioma) and one normal. The cells were irradiated with 137 Cs-g rays at absorbed dose levels of 0, 20, 40, 60, 80, 100 and 120 Gy.

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“…A similar question pertains to PDR brachytherapy, which is of interest scientifically and clinically although wide spread clinical implementation is now in doubt. Separate reports using rat 9L cells 21 and human glioma cells 22 in vitro demonstrated that LDMH was as effective in sensitizing PDR as LDR. Also very interesting were observations indicating that sensitization of an HDR scheme of five fractions of 5 Gy each over 3 days increased linearly with increasing duration of LDMH 23 .…”

Section: Long Duration Hyperthermia and Low Dose-rate Brachytherapy: mentioning

confidence: 99%

Long duration mild temperature hyperthermia and brachytherapy

Armour

Raaphorst

2004

International Journal of Hyperthermia

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Combining long duration mild temperature hyperthermia (LDMH) and low dose-rate (LDR) brachytherapy to enhance therapeutic killing of cancer cells was proposed many years ago. The cellular and tumour research that supports this hypothesis is presented in this review. Research describing LDMH interaction with pulsed brachytherapy and high dose-rate brachytherapy using clinically relevant parameters are compared with LDMH/LDR brachytherapy. The mechanism by which LDMH sensitizes LDR has been established as the inhibition of sublethal damage repair. The molecular mechanisms have been shown to involve DNA repair enzymes, but the exact nature of these processes is still under investigation. The relative differences between LDMH interactions with human and rodent cells are presented to help in the understanding of possible roles of LDMH in clinical application. The role of LDMH in modifying tumour blood flow and its possible role in LDR sensitization of tumours is also presented. The positive aspects of LDMH-brachytherapy for clinical application are sixfold; (1) the thermal goals (temperature, time and volume) are achievable with currently available technology, (2) the hyperthermia by itself has no detectable toxic effects, (3) thermotolerance appears to play a minor if any role in radiation sensitization, (4) TER of around 2 can be expected, (5) hypoxic fraction may be decreased due to blood flow modification and (6) simultaneous chemotherapy may also be sensitized. Combined LDMH and brachytherapy is a cancer therapy that has established biological rationale and sufficient technical and clinical advancements to be appropriately applied. This modality is ripe for clinical testing.

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Comparison of radiosensitization by 41°C hyperthermia during low dose rate irradiation and during pulsed simulated low dose rate irradiation in human glioma cells

Cited by 11 publications

References 20 publications

Ultrasound‐induced killing of monocytic U937 cells enhanced by 2,2′‐azobis(2‐amidinopropane) dihydrochloride

Ultrasound‐induced killing of monocytic U937 cells enhanced by 2,2′‐azobis(2‐amidinopropane) dihydrochloride

Radiation sterilisation of cultured human brain tumour cells for clinical immune tumour therapy

Long duration mild temperature hyperthermia and brachytherapy

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