Radiosensitization of two murine tumours with mild temperature hyperthermia and carbogen breathing

Griffin, Robert J.; Okajima, Kaoru; Ogawa, Atsushi; Song, Chang W.

doi:10.1080/095530099139467

Cited by 34 publications

(3 citation statements)

References 17 publications

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“…Studies have shown that heat-induced changes in tumour oxygenation parallel the changes in tumour blood flow [17, 31–34]. Under physiological conditions, blood flow is tightly regulated by vasodilating factors that stimulate endothelial cells to release nitric oxide (NO), which then causes relaxation of the vascular smooth muscle and subsequent increased blood flow.…”

Section: Discussionmentioning

confidence: 99%

Tumour thermotolerance, a physiological phenomenon involving vessel normalisation

Dings

Loren

Zhang

et al. 2011

International Journal of Hyperthermia

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The purpose of this study was to delineate the mechanisms by which stromal components of cancer may induce tumour thermotolerance and exploit alterations in stromal and tumour physiology to enhance radiation therapy. The vascular thermoresponse was monitored by daily one-hour 41.5°C heatings in two murine solid tumour models, SCK murine mammary carcinoma and B16F10 melanoma. A transient increase was seen in overall tumour oxygenation for 2–3 days, followed by a progressive decline in tumour pO2 upon continued daily heatings. Vascular thermotolerance was further studied by treating tumours with different heating strategies, i.e. (1) a single 60 min 41.5°C treatment; (2) two consecutive daily treatments of 41.5°C for 60 min; (3) a single 60 min 43°C treatment or (4) two days of 41.5°C for 60 min followed by treatment with 43°C for 60 min on the third day. Pre-heating tumours with mild temperature hyperthermia induced vascular thermotolerance, which was accompanied by evidence of vessel normalisation, i.e. a decrease in microvessel density and an increase in pericyte coverage. Rational scheduling of fractionated radiation during heat-induced increases in tumour oxygen levels rendered a significantly greater, synergistic, tumour growth inhibition. In vitro clonogenic survival responses of the individual cell types associated (endothelial cells, fibroblasts, pericytes and tumour cells) indicated only a direct cellular thermotolerance in endothelial cells. Overall, this suggests that tumour thermotolerance is a physiological phenomenon mediated through improvement of functional vasculature.

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Section: Discussionmentioning

confidence: 99%

Tumour thermotolerance, a physiological phenomenon involving vessel normalisation

Dings

Loren

Zhang

et al. 2011

International Journal of Hyperthermia

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“…Nicotinamide, a vitamin B 3 analogue, is known to prevent these transient fluctuations in tumor blood flow that lead to the development of acute hypoxia [14]. MTH was clarified to increase the tumor response to radiation by improving tumor oxygenation through an increase in tumor blood flow [15], thereby overcoming chronic hypoxia at least based on our previous report employing SCC VII mouse squamous cell carcinoma tumors [6,16]. In this study, nicotinamide and MTH in combination remarkably reduced the size of the HF in total and Q cell populations of B16-BL6 mouse melanoma tumors, respectively (Fig.…”

Section: Discussionmentioning

confidence: 99%

Significance of manipulating intratumor hypoxia in the effect on lung metastases in radiotherapy, with reference to its effect on the sensitivity of intratumor quiescent cells

Masunaga

Matsumoto²,

Hirayama³

et al. 2009

Clin Exp Metastasis

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“…Tirapazamine (TPZ), a lead compound in the development of bioreductive hypoxic cytotoxins, in combination with radiation has been shown to be very useful for controlling solid tumors as a whole, especially for controlling Q tumor cell populations that are rich in hypoxic region [2,5]. Mild temperature hyperthermia (MTH) was reported to increase the response of tumors to radiation by improving oxygennation through an increase in tumour blood flow [6]. Further, MTH was also shown to enhance the tumor response, especially of the intratumor Q cell population, to TPZ [7].…”

Section: Introductionmentioning

confidence: 99%

Effect of Tirapazamine and Mild Temperature Hyperthermia on the Recovery from Radiation-Induced Damage in Pimonidazole-Unlabeled Quiescent Tumor Cell Population

Masunaga¹,

Sakurai²,

Tanaka³

et al. 2013

JCT

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The aim in this study is to examine the effect of tirapazamine (TPZ) and mild temperature hyperthermia (MTH) on the repair of radiation-induced damage in pimonidazole-unlabeled quiescent (Q) tumor cells. Labeling of proliferating (P) cells in C57BL/6J mice bearing EL4 tumors was achieved by continuous administration of 5-bromo-2-deoxyuridine (BrdU). Tumors were irradiated with γ-rays at 1 h after the administration of pimonidazole followed by TPZ treatment or MTH. Twenty-four hours later, assessment of the responses of Q and total (= P + Q) cells were based on the frequencies of micronucleation and apoptosis using immunofluorescence staining for BrdU. The response of the pimonidazole-unlabeled tumor cell fractions was assessed by means of apoptosis frequency using immunofluorescence staining for pimonidazole. With γ-rays only, the pimonidazole-unlabeled cell fraction showed significantly enhanced radio-sensitivity compared with the whole cell fraction more remarkably in Q cells than total cells. However, a significantly greater decrease in radio-sensitivity in the pimonidazole-unlabeled than the whole cell fraction, evaluated using a delayed assay, was more clearly observed in Q cells than total cells. Post-irradiation MTH more remarkably repressed the decrease in radio-sensitivity in the Q cell than the total cells. Post-irradiation TPZ administration produced a large radio-sensitizing effect on both total and Q cells, especially on Q cells. On the other hand, in pimonidazole-unlabeled cell fractions in both total and Q cells, TPZ suppressed the reduction in sensitivity due to delayed assay much more efficiently than MTH, whereas no radio-sensitizing effect was produced. Not only through suppressing the recovery from radiation-induced damage but also through radio-sensitizing effect, post-irradiation TPZ administration is very useful for repressing the increase in the difference in radio-sensitivity due to the delayed assay not only between total and Q tumor cells but also between the pimonidazole-unlabeled and the whole cell fractions within the total and Q tumor cells.

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Radiosensitization of two murine tumours with mild temperature hyperthermia and carbogen breathing

Abstract: MTH treatment alone and combined with carbogen breathing substantially increased the tumour radiation response probably through an increase in the tumour oxygenation status.

Cited by 34 publications

References 17 publications

Tumour thermotolerance, a physiological phenomenon involving vessel normalisation

Tumour thermotolerance, a physiological phenomenon involving vessel normalisation

Significance of manipulating intratumor hypoxia in the effect on lung metastases in radiotherapy, with reference to its effect on the sensitivity of intratumor quiescent cells

Effect of Tirapazamine and Mild Temperature Hyperthermia on the Recovery from Radiation-Induced Damage in Pimonidazole-Unlabeled Quiescent Tumor Cell Population

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