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P M Corry

Publications and source records attributed to P M Corry.

At least 73 records · Page 4Linked to original sources
PubMed1990

Heat-induced preferential synthesis and redistribution of HSP 70 and 28 families in Chinese hamster ovary cells.

We observed that members of two HSP families (70 and 28 kDa) preferentially redistributed into the nucleus after heating at 45.5 degrees C for 10 min. The rates of synthesis and redistribution of these proteins were different for each member of HSP families during incubation period at 37 degrees C after heat shock. The maximum rates of synthesis of HSP 70 and HSP 28 families, except HSP 28c, were 6-9 hr after heat shock, whereas the maximum rates of redistribution were 3-6 hr after heat shock. These results suggest that the rates of redistribution of these proteins may be dependent on the amount of intracellular proteins as well as the alteration of binding affinity of nucleoproteins following heat shock.

Animals↗
PubMed1990

Effect of histidine on histidinol-induced heat protection in Chinese hamster ovary cells.

The possible mechanism for heat protection by the protein synthesis inhibitor histidinol was investigated in CHO cells. Histidinol (HST, 5 mM), an analogue of the essential amino acid L-histidine, added for 2 hr before and during heating at 43 degrees C, protected cells from killing at 43 degrees C. Treatment with HST produced a 600-fold increase in survival from 3 x 10(-4) to 1.8 x 10(-1) after 2.5 hr at 43 degrees C. Although the cells were washed after HST treatment, substantial protective effect was still observed during heating at 43 degrees C. This protective effect gradually decreased with increased incubation time after the drug treatment. However, the protective effect was immediately reduced by treatment with histidine (HIS, 0.25-5 mM) during heating. The amount of reduction was dependent upon HIS concentration: five millimolar HIS completely inhibited HST-induced heat protection. Furthermore, protein synthesis which was inhibited by 95% by 5 mM HST, resumed immediately with 5 mM HIS treatment. In addition, when cells were labeled during or after HST treatment, neither preferential accumulation of heat shock protein families nor phosphorylation of 28 kDa protein was observed. Therefore, these results suggest that the cessation of protein synthesis itself is one of the events involved in protection.

Animals↗
PubMed1990

Correlation between redistribution of a 26 kDa protein and development of chronic thermotolerance in various mammalian cell lines.

Previous studies suggested that a 26 kDa protein might play an important role in protein synthesis-independent thermotolerance development in CHO cells. To determine if this phenomenon was universal, four mammalian cell lines, viz., CHO, HA-1, murine Swiss 3T3, and human HeLa, were studied. Cells were heated at 42 degrees C, and the level of 26 kDa protein in the nucleus was measured, together with clonogenic survival and protein synthesis. The results demonstrated that 1) the 26-kDa protein was present in the four different cell lines, and 2) the level of the 26 kDa protein in their nuclei was decreased by 30-70% after heating at 42 degrees C for 1 hr. However, restoration of this protein occurred along with development of chronic thermotolerance. The protein synthesis inhibitor cycloheximide (10 micrograms/ml) neither inhibited the development of chronic thermotolerance nor affected the restoration of the 26 kDa protein in the nucleus. In fact, this drug protected cells from hyperthermic killing and heat-induced reduction of 26 kDa protein in the nucleus. Heat sensitizers, quercetin (0.1 mM), 3,3'-dipentyloxacarbocyanine iodide (DiOC5[3]: 5 micrograms/ml), and stepdown heating (45 degrees C-10 min----42 degrees C), potentiated hyperthermic killing and inhibited or delayed the restoration of the 26 kDa protein to the nucleus. These results support a correlated, perhaps causal relationship between the restoration of the 26 kDa protein and chronic thermotolerance development in four different mammalian cell lines.

Animals↗
PubMed1990

Differences in thermotolerance induced by heat or sodium arsenite: cell killing and inhibition of protein synthesis.

Chinese hamster ovary (CHO) cells became thermotolerant after treatment with either heat for 10 min at 45.5 degrees C or incubation in 100 microM sodium arsenite for 1 h at 37 degrees C. Thermotolerance was tested using heat treatment at 45 degrees C or 43 degrees C administered 6-12 h after the inducing agent. At 45 degrees C thermotolerance ratios at 10(-2) isosurvival levels were 4.2 and 3.8 for heat and sodium arsenite, respectively. Recovery from heat damage as measured by resumption of protein synthesis was more rapid in heat-induced thermotolerant cells than in either sodium arsenite-induced thermotolerant cells or nonthermotolerant cells. Differences in inhibition of protein synthesis between heat-induced thermotolerant cells and sodium arsenite-induced thermotolerant cells were also evident after test heating at 43 degrees C for 5 h. At this temperature heat-induced thermotolerant cells were protected immediately from inhibition of protein synthesis, whereas sodium arsenite-induced thermotolerant cells, while initially suppressed, gradually recovered within 24 h. Furthermore, adding cycloheximide during the thermotolerance development period greatly inhibited sodium arsenite-induced thermotolerance (SF less than 10(-6] but not heat-induced thermotolerance (SF = 1.7 X 10(-1] when tested with 43 degrees C for 5 h. Our results suggest that both the development of thermotolerance and the thermotolerant state for the two agents, while similar in terms of survival, differed significantly for several parameters associated with protein synthesis.

Animals↗
PubMed1989

Heat protectors and heat-induced preferential redistribution of 26 and 70 kDa proteins in Chinese hamster ovary cells.

An overall increase of 40% in nuclear-associated protein has been shown to be one of the sequellae of exposure of eukaryotic cells to elevated temperatures. Several investigators have shown that the increased protein/DNA ratios correlated well with the degree of cytotoxicity. In previous investigations, we have shown that cycloheximide, which protects the cell from the killing effects of heat, produces a dramatic reduction of the bulk nuclear-associated proteins after heating. In this investigation, we studied a previously unobserved efflux of a 26 kDa protein after heat shock and the preferential accumulation of the 70 kDa protein. The 26 kDa protein was shown not to be a member of previously described heat shock protein families. Preferential reduction of a 26 kDa protein and accumulation of a 70 kDa protein was observed in nuclei isolated from Chinese hamster ovary cells after heating at 43 degrees C. After heat treatment, the 26 kDa protein in the nucleus was decreased to a level 0.1-0.3 times the original amount in unheated cells, and the 70 kDa protein in the nucleus increased by a factor of 1.6-1.8. The normal levels of these two proteins were restored when cells were incubated at 37 degrees C following heat shock. Cells treated with heat protectors, cycloheximide and histidinol, demonstrated approximately the same redistribution in nuclear 26 and 70 kDa proteins immediately after heating as those not exposed to these drugs. On the other hand, restoration to control levels was much faster in the protector-treated cells, suggesting that "repair" of heat-induced damage is an important factor in the cells ability to survive this insult. Return to normal protein levels did not require new protein synthesis.

Animals↗
PubMed1989

A proposed standard data file format for hyperthermia treatments.

One of the most critical areas of research essential to improve the clinical use of hyperthermia in cancer therapy is the determination and evaluation of temperature during therapy. In order to improve the dissemination of newly developed thermometry measurement and analysis programs and facilitate the transport of hyperthermia data files between computers for both intra- and inter- institutional use, we propose a standard file format, the Hyperthermia Data Standard (HDS), which can be used for all hyperthermia data. This data file consists of segments of which nine have been defined. The first is an initial /VERSION segment which identifies the file standard. This is followed by eight major segments: 2) a /IDENT segment which contains file and patient identification information; 3) a /TEXT segment containing additional miscellaneous documentation; 4) a /TUMOR segment which provides tumor and treatment site information; 5) a /HSETUP segment which contains treatment setup information; 6) a /FORMAT segment which defines the data segment structure; 7) a /DATA segment containing the actual thermometry data; 8) a /FOLLOWUP segment for documenting patient response; and 9) an /ANALYSIS segment containing summary information. All segments begin and end with a specified delimiter and, except for the first two (/VERSION and /IDENT), may be repeated more than once. For ease in debugging and verifying adherence to the standard, all information in the file is encoded in printable ASCII characters. All segments consist solely of records containing KEYWORDS and KEYWORD VALUES which identify specified information. Certain KEYWORDS are standard, i.e., having specified names and information formats as defined in this document. The /DATA segment consists of ASCII encoded chronological treatment thermometry and other data whose format and structure is identified in the /FORMAT segment. The /ANALYSIS segment provides the flexibility to store the results of any analysis program along with the actual data file for ease of data management. This thermometry data file standard is designed to provide both flexibility and extendability for all possible forms of hyperthermia treatment data. Furthermore, it is designed to provide a simple format which may be easily read by higher level languages. This document is intended for commercial manufacturers and others who are writing programs to document clinical hyperthermia treatments with the intention that they either use this format for their data storage or provide a means to convert their data into this format.(ABSTRACT TRUNCATED AT 400 WORDS)

Body Temperature↗
PubMed1988

Protection from heat-induced protein migration and DNA repair inhibition by cycloheximide.

The mechanism by which Cycloheximide (CHM) protects cells from heat induced killing has been investigated. Cycloheximide (10 micrograms/ml) added for 2 hr before and during a 3 hour heating at 43 degrees C prevented a 40% increase of heat-induced protein accumulation in the nucleus and protected cells (0.0001 vs. 0.15 surviving fraction) from heat-induced killing. Heat-induced DNA repair inhibition was also suppressed when cells were treated with CHM in the above manner. This combination of results suggests that protein accumulation in the nucleus and inhibition of DNA repair are related and these events are associated with CHM protection from heat induced cell killing.

Animals↗
PubMed1984

Induction of hyperthermia using implanted electrodes.

Initial experience with interstitial heating at M. D. Anderson Hospital dates from September 1978 and includes cases in which exploration was done for primary resections or metastatic lesions without evidence of distant metastasis, in which local control was indicated and was of clinical importance. Eleven such cases have been encountered and treated with hyperthermia durations of 1 hr, with 5 to 25 treatment episodes per patient. It is the most reliable and least toxic of the current methods used to induce local hyperthermia. Tumor temperatures of 50 degrees are easily achievable, and average temperatures over 43 degrees have always been obtained. The major limitation of interstitial hyperthermia is the surgical exploration required for implantation of the electrodes. We, therefore, currently limit use of this technique to patients who would undergo exploration with the goal of surgical extirpation of the tumor.

Body Temperature↗
PubMed1983

Hyperthermia by magnetic induction: experimental and theoretical results for coaxial coil pairs.

High-frequency magnetic induction for producing elevated temperatures in human tumors can be accomplished with several electrode arrangements. We describe the physical characteristics of a coaxial pair of electrodes or current loops placed on either side of the body. This electrode arrangement can improve the depth of power deposition within the body relative to that obtained with an electrode circumferentially encircling the body or a single surface applicator ("pancake coil"). We report results of measured and calculated magnetic field distributions and power density distributions obtained with a coaxial pair. The effect of varying load geometry upon the power density distribution was shown to be significant in several static phantom experiments. Electrode geometry was also important, as shown by calculations of power deposition as a function of electrode diameter in a simple model of body tissue conductivities. The power density was found to diminish at given depths as the electrode diameter decreased. Finally, values of magnetic fields were measured during treatment of human subjects with a coaxial electrode pair and were found to vary significantly from subject to subject. This resulted from variation in the geometry and electrical characteristics of tissues among subjects, and indicates the difficulty of formulating a standard accurate model for use with this magnetic induction technique.

Diathermy↗
PubMed1982

Sister-chromatid exchanges in mouse embryos after exposure to ultrasound in utero.

Mouse embryos at 2 stages of development were exposed to ultrasound. The bone-marrow cells of the mother, the whole embryo, and the embryonic liver cells were analyzed. There was no consistent increase of sister-chromatid exchanges. Furthermore, the thermal effect of ultrasound did not appear to influence the frequency. Thus, ultrasound doses much higher than those used in clinical diagnosis do not induce cytogenetic damage as assayed by sister-chromatid exchanges.

Animals↗
PubMed1982

Ultrasound-induced hyperthermia for the treatment of human superficial tumors.

Ultrasonic systems were developed for the treatment of superficial human tumors, generating local tumor hyperthermia at tumor center temperatures ranging from 43 degrees to 50 degrees. Twenty-eight patients with disease of varying histology were evaluable for response, and demonstrated an overall response rate of 57% with a complete response rate of 18%. In 11 patients who had received definitive radiation therapy to the heat treated area, the response rate was 81%; there were no toxicities other than those noted for the overall study. As temperature was escalated a marked increase was observed both in response rates (from 53% (43-44 degrees C) to 83% (48-50 degrees C) and in duration of response (from 29 to 250 days for the same temperatures). Toxicities were minimal, consisting of superficial blistering in four patients and pain in six patients. Pain was usually associated with tumor involvement in the periostium.

Adult↗
PubMed1982

Combined ultrasound and radiation therapy treatment of human superficial tumors.

Ultrasound, used to generate local tumor hyperthermia, was combined with radiation therapy in a pilot study to determine efficacy and toxicity of this combined-modality therapy. Twenty-one lesions in eighteen patients were treated at graded doses from 2400-4000 rads (24-40 Gy) with ultrasonic hyperthermia administered immediately prior to irradiation at 43.5 degrees C +/- 0.5 degrees C for one hour. The overall response rate was 100%, with a 62% complete response rate. Of those lesions that responded completely and were followed for periods of three to twenty-two months, there have been no recurrences of the lesions treated with the combined modalities. The response rate for control unheated lesions in the same patient in the same radiation field was markedly lower (30% overall and no complete responses). Heat treatment alone in the same patients also showed lower response rates (50% overall and 10% complete) with a short response duration. Toxicities were minimal, consisting of one case with long-term treatment-associated sequelae. It is concluded that this combined modality of therapy is safe and effective where applied in human superficial tumors and that further development is warranted.

Hot Temperature↗
PubMed1981

Technical note. Use of CT in the placement of heat monitoring thermocouples for hyperthermia therapy.

In 12 cancer patients undergoing hyperthermia therapy, computed tomography (CT) was used for placement of thermocouples within the tumoral tissue. Tumors were located in the thorax, abdomen, and pelvis. Computed tomography provided accurate angulation of the introduction angiocatheter as well as the ability to choose the shortest and safest path. The cross-sectional display was especially helpful in placing the heat monitoring thermocouple within the active part of the tumor rather than a necrotic portion. It is our opinion that CT is superior to fluoroscopy in this regard.

Abdominal Neoplasms↗
PubMed1980

Persistence of EEG activity with prolonged induced hyperthermic fever.

Ten instances of deliberate systemic temperature elevation in the 41.5 degrees C to 42.2 degrees C range have been evaluated electroencephalographically, demonstrating decrease in predominant frequency and voltage. Persistence of electro-cerebral activity suggests that previous reports of electro-cerebral inactivity with elevated temperatures reflect indirect serious effects due to cardiovascular compromise with cerebral ischemia, rather than to a direct temperature-related loss of CNS electrical activity.

Anesthesia, General↗
PubMed1980

Thermal enhancement of DNA damage in mammalian cells treated with cis-diamminedichloroplatinum(II).

The cytotoxic effects of cis-diamminedichloroplatinum(II) (cis-DDP) were shown to be strongly potentiated by hyperthermia. The molecular mechanisms responsible for this potentiation were investigated by assaying the degree of DNA cross-linking produced under the different drug treatment conditions by the technique of alkaline elution. The results showed that the cells treated with the drug at 43 degrees had a greater amount of DNA cross-linking immediately after treatment than did cells treated with the drug at 37 degrees, indicating a possible thermal enhancement of drug uptake by the cells. Whereas the hyperthermia potentiated the cytotoxicity of cis-DDP by a factor of nearly 10, the degree of DNA cross-linking was only enhanced by a factor of 6.5, suggesting that while a large portion of the enhanced cytotoxicity may be attributed to the increased cross-linking other factors may also play some role. The possible influence of hyperthermia on the repair of the DNA damage induced by cis-DDP was investigated; however, no significant differnence in the rate of disappearance of cross-links between cells treated at 37 or 43 degrees was observed. Advantageous combination of chemotherapy with cis-DDP and hyperthemia for the treatment of cancer is implied by these results.

Animals↗
PubMed1980

In vitro thermochemotherapy of human colon cancer cells with cis-dichlorodiammineplatinum(II) and mitomycin C.

The thermosensitivity of human colon adenocarcinoma (LoVo) cells was investigated as a function of temperature and duration of heating in exponentially growing cultures. At 39-43 degrees, time-dependent survival followed a simple exponential function. Do values decreased progressively with a rise in temperature, from Do at 40 degrees = 38 hr to Do at 42 degrees = 17 hr to Do at 43 degrees = 1.5 hr. thus indicating relative thermoresistance of LoVo cells compared to Chinese hamster ovary cells. Dose-dependent 1-hr survival of LoVo cells treated with cis-dichlorodiammineplatinum(II) and mitomycin C was effectively modified when treatment was conducted under hyperthermic conditions. For both agents and cultures in exponential and stationary growth phases, hyperthermia abolished the initial shoulder portion and steepened the subsequent exponential part of the survival curves for dose-modifying factors at the 10% survival level of 1.5 to 2.0 at 41 degrees and 2.6 to 2.8 at 42 degrees. This significant enhancement of drug-induced cell kill by moderate hyperthermia suggests that thermochemotherapy with mitomycin C and cis-dichlorodiammineplatinum(II) should be tested clinically with both regional and total-body hyperthermia.

Adenocarcinoma↗