Importance of preheating temperature and time for the induction of thermotolerance in a solid tumour in vivo

Nielsen, Ole Steen; Overgaard, Jens

doi:10.1038/bjc.1982.299

“…A similar study was done by Nielson and Overgaard, using a mouse tumor model. The temperature of the test heating was also 43.5°C (35). In this case, the endpoint was tumor growth delay time.…”

Section: Thermotolerancementioning

confidence: 99%

Thermal dose requirement for tissue effect: experimental and clinical findings

Dewhirst

¹

,

Viglianti

²

,

Lora-Michiels

³

et al. 2003

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In this review we have summarized the basic principles that govern the relationships between thermal exposure (Temperature and time of exposure) and thermal damage, with an emphasis on normal tissue effects. We have also attempted to identify specific thermal dose information (for safety and injury) for a variety of tissues in a variety of species. We address the use, accuracy and difficulty of conversion of an individual time and temperature (thermal doses) to a standardized value (eg equivalent minutes at 43 degrees C) for comparison of thermal treatments. Although, the conversion algorithm appears to work well within a range of moderately elevated temperatures (2-15 deg C) above normal physiologic baseline (37-39 deg C) there is concern that conversion accuracy does not hold up for temperatures which are minimally or significantly above baseline. An extensive review of the literature suggests a comprehensive assessment of the "thermal doesto-tissue effect" has not previously been assembled for most individual tissues and never been viewed in a semi-comprehensive (tissues and species) manner.Finally, we have addressed the relationship of thermal does-to-effect vs. baseline temperature. This issues is important since much of the thermal dose-to-effect information has been accrued in animal models with baseline temperatures 1-2 deg higher than that of humans. INTRODUCTIONThe purpose of this review is to present basic concepts relating thermal dose (time at temperature) to cell killing and tissue damage. © 2003 SPIE HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptThis review summarizes the basic principles that govern the relationships between thermal exposure (temperature and time of exposure) and thermal damage, with an emphasis on normal tissue effects. Methods for converting one time-temperature combination to a time at a standardized temperature (cumulative minutes at 43° / CEM) are provided as well as some discussion about the underlying assumptions that go into these calculations. There are few in vivo papers, examining the type and extent of damage that occurs in the lower temperature range for hypothermic exposures (e.g. 39-42°C). Although not specifically calculated, the authors believe the CEM analysis for estimating an equivalent thermal does not retain a high degree of accuracy when temperatures above 55°C or so. Therefore it is appears that estimation of thermal dose to effect at low (temperatures a few degree above baseline body temperature) and high temperatures are more difficult to assesses and quantify. It is also apparent from this review that an extremely large variation in the type and the quality of tissue damage endpoint assessment significantly affects the ability to accurately compared study results.The authors have assembled a detailed review of thermal thresholds for tissue damage in the majority of organs (based on what is detectable in vivo). The data are normalized using thermal dosimeter concepts. This database is available by reques...

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“…There is considerable evidence in animal systems showing that thermotolerance can be induced in tumours [9,10,[12][13][14][15]19]. If valid extrapolation can be made to human tumours the induction of thermotolerance may influence the treatment outcome of fractionated hyperthermia.…”

Section: Introductionmentioning

confidence: 99%

“…An initial non-lethal heat treatment can induce in cells a temporary state of heat resistance, termed thermotolerance [1][2][3]. The induction, development, and subsequent decay of thermotolerance have been studied extensively, both in vitro and in vivo [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]. Even though many different endpoints were used the results from the in vivo and in vitro studies were qualitatively similar.…”

Section: Introductionmentioning

confidence: 99%

Re-induction of hsp70 synthesis: An assay for thermotolerance

Li

¹

,

Mak

²

2009

International Journal of Hyperthermia

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Of the many heat shock proteins (HSPs), hsp70 appears to correlate best with heat resistance, either permanent or transient. We have investigated various approaches to quantify the concentration of hsp70, and examined the relationship between hsp70 and cells' thermal sensitivity during the development and decay of thermotolerance in model systems. Here, experiments were performed to determine the possibility of using the rate of synthesis of hsp70 after a second test heat shock to predict the kinetics of thermotolerance. Specifically, we studied the relationship between the retained thermotolerance in a murine tumor cell line SQ-1 and a human tumor cell line, HCT-8, after fractionated heat doses and the cells' ability to re-initiate synthesis of hsp70 in response to an additional test heat dose in vitro. Monolayers of cells were exposed to a first heat treatment (e.g., 41 C, 4 h) and then incubated at 37 C for 0-72 h. At various times after the first heat treatment, cells were either challenged with a 45 C, 45 min heat shock to assess the residual thermotolerance by colony formation, or labelled with [ 35 S]methionine before or after an additional test heat dose (e.g. 43.5 C, 15 min). We found that the cells' ability to re-initiate hsp70 synthesis in response to the test heat shock inversely correlated with retained thermotolerance. Our data suggest the level of hsp70 in thermotolerant cells regulates the rate of synthesis of additional hsp70 in response to the subsequent heat challenge. Furthermore, the results showed that the rate of re-induction of hsp70 synthesis after a test shock can be used as a rapid measure of retained thermotolerance. This study suggests an approach for quantifying the level of retained thermotolerance during a course of fractionated hyperthermia.

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“…However, the optimum periodicity of hyperthermia treatments was uncertain because of the potential influence of thermotolerance. Studies examining the kinetics of thermotolerance have been performed in rodent model systems, both in vitro and in vivo, and using both normal and tumor tissues [3,8,13,15,17,[27][28][29]. These studies have shown that thermotolerance is a transient, non-inheritable phenomenon, but that its magnitude and induction kinetics depends on the initial heat dose, and that its decay kinetics is variable and depends on the tissue type.…”

mentioning

confidence: 99%

“…Mammalian cells, when exposed to a non-lethal heat shock, have the ability to acquire a transient resistance to subsequent exposures at elevated temperature, a phenomenon termed thermotolerance [1,2]. Thermotolerance has been observed in a variety of organisms and cells, including mammalian cell lines, tumors and normal tissues [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Initially, the mechanism for the development of thermotolerance was not well understood, but emerging experimental evidence suggested that protein synthesis may play a role in its manifestation [21].…”

mentioning

confidence: 99%

Hyperthermia classic article commentary: ‘Re-induction of hsp70 synthesis: An assay for thermotolerance’ by Gloria C. Li and Johnson Y. Mak,International Journal of Hyperthermia1989;5:389-403

Li

¹

,

Calderwood

²

2009

International Journal of Hyperthermia

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Of the many heat shock proteins (HSPs), hsp70 appears to correlate best with heat resistance, either permanent or transient. We have investigated various approaches to quantify the concentration of hsp70, and examined the relationship between hsp70 and cells' thermal sensitivity during the development and decay of thermotolerance in model systems. Specifically, experiments were performed to determine the possibility of using the rate of synthesis of hsp70 after a second test heat shock to predict the kinetics of thermotolerance in tumor cells in vitro and in animal tumor models. We found that the cells' ability to re-initiate hsp70 synthesis in response to the test heat shock inversely correlated with retained thermotolerance. These data suggest the level of hsp70 in thermotolerant cells regulates the rate of synthesis of additional hsp70 in response to the subsequent heat challenge. Furthermore, the results showed that the rate of re-induction of hsp70 synthesis after a test heat shock can be used as a rapid measure of retained thermotolerance. This study suggests an approach for quantifying the level of retained thermotolerance during fractionated hyperthermia.

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Importance of preheating temperature and time for the induction of thermotolerance in a solid tumour in vivo

Cited by 50 publications

References 15 publications

Thermal dose requirement for tissue effect: experimental and clinical findings

Thermal dose requirement for tissue effect: experimental and clinical findings

Re-induction of hsp70 synthesis: An assay for thermotolerance

Hyperthermia classic article commentary: ‘Re-induction of hsp70 synthesis: An assay for thermotolerance’ by Gloria C. Li and Johnson Y. Mak,International Journal of Hyperthermia1989;5:389-403

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