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Iso-effect tables for normal tissue tolerance
1847
ASTR Poster Abstracts B9 "Iso-effect Lionel Michael
Tables
Cohen
for Normal
and Margaret
Reese
Hospital
Tissue
Tolerance"
Creditor
& Medical
Center,
Chicago,
Illinois
parameters were derived from Best fitting cell lethality, repair and repopulation clinical data on radiation reactions in specific tissues (spinal cord, brain, lung and Probit analysis provided estimates of the cellular surviving fractions assogut). ciated with a moderate (5%) risk of radiation injury in each of the tissues studied. a computer program was designed to generate tables of tolerance With this information, The doses for specific tissues treated with a wide variety of fractionation schemes. Since these tables are tissue-specific and not conrelevant tables are presented. they provide a more reliable strained to log-linear plots or NSD-type formulations, guide to tolerance limits in clinical radiation oncology.
BlO THF:RllA[. DISTRIRUTIONS Mich
D. Ford
O’Hare,
Fred
IN A ?lICROWAVE FIELD W.
Hetzel,
Stanley
Frinak
Hospital
Thermal distributions have been examined in CjH/Sed mice, in both normal tissue and malignant transplantable mammary carcinoma. An array of nine microthermocouples, each A 2450 with a diameter of 150 microns was used to determine the thermal distributions. MHz microwave generator constructed in our lab and an applicator with an irradiating surface of 3 cm x 3 cm was used to heat the tissues. The diameter of the tumors varied between 8 to 10 mm. At the time of temperature measurement the mice were anesthesized with Thorazine (50 mg/kg) and Ketamine (40 mg/kg). Preliminary results have been obtained in normal and malignant tissue. The temperature is found to increase with movement of the thermal probe in the tumor from the region proximal to the body to that most distal on the limb. In some instances, temperature gradients of up to 2 degrees are observed across the tumor while in normal tissue the gradient is significantly lower. A general observation made is that, significantly lower power levels are required to achieve the same level of heating in the tumor as compared to normal muscle. These data and the implications of temperature distributions produced by microwave heating will be discussed.
Bll PHASE I STUDY TO DETERMINE MACROPHAGE ACTIVATION ELEVATION OF WHOLE BODY TEMPERATURE TO 39-40°C. Richard Johnson, Katherine Story
James Humbert*,
Roswell Park Memorial *Children's Hospital,
Ben Park*,
AND INCREASED
Ronald
Institute, Buffalo, NY 14263 Buffalo, NY 14222 USA
Scott,
POLYMORPHOUS
Adolph
Gunnarrson,
PHAGOCYTOSIS
INDUCED WITH THE
John Pearce, Peter Reese and
USA
Body temperatures of 39-40°C are produced by infection, febrile reactions resulting immunostimulation such as C-Parvum and BCG and as a result of regional hyperthermia.
from nonspecific
The literature suggests a synergism between temperature elevation and immune responses in tumor cells. Mondovi et al (Cancer 1972:30 885) reported that Ehrlich ascites tumor cells pretreated with hyperthermia to to a temperature of 42.5'C for three hours were more immunogenic than untreated cells. Szmigielski et al (Cancer Therapy by Hyperthermia and Radiation 1978, 80) demonstrated that local hyperthermia at 43.0°C far one hour in viva stimulated in-vitro cytocidal reactivity of T-lymphocytes and macrophages against murine sarcoma cells. Steblin et al (Sura Gvncol Obstet 1975:140. 339) reoorted that in-vitro cvtotoxicitv of patients lymphocytes toward their-own melanoma cells was enhanced following 39-40°C limb-hyperthermia. Increased T-lymphocyte activity in patients melanoma cells after hyperthermia therapy of 42'C for two hours has been reported by Delloratius et al (J Nat1 Cancer Inst 1977: 58, 905). Shah and Dickson (Cancer Res 1976:67, 508) showed regression of the VX metastases in rabbits after local radiofrequency treatment of the primary tumors. Regression was corre ? ated with increased skin reactivity together with production of antibodies in tumor cell antigens. Van Oss et al (J Retie endo Sot 1980:27. 561) have conducted invitro determinations of chemotaxis, phagocytic engulfment, phagocytic digestion and oxygen consumption of
ASTR Poster Abstracts B9 "Iso-effect Lionel Michael
Tables
Cohen
for Normal
and Margaret
Reese
Hospital
Tissue
Tolerance"
Creditor
& Medical
Center,
Chicago,
Illinois
parameters were derived from Best fitting cell lethality, repair and repopulation clinical data on radiation reactions in specific tissues (spinal cord, brain, lung and Probit analysis provided estimates of the cellular surviving fractions assogut). ciated with a moderate (5%) risk of radiation injury in each of the tissues studied. a computer program was designed to generate tables of tolerance With this information, The doses for specific tissues treated with a wide variety of fractionation schemes. Since these tables are tissue-specific and not conrelevant tables are presented. they provide a more reliable strained to log-linear plots or NSD-type formulations, guide to tolerance limits in clinical radiation oncology.
BlO THF:RllA[. DISTRIRUTIONS Mich
D. Ford
O’Hare,
Fred
IN A ?lICROWAVE FIELD W.
Hetzel,
Stanley
Frinak
Hospital
Thermal distributions have been examined in CjH/Sed mice, in both normal tissue and malignant transplantable mammary carcinoma. An array of nine microthermocouples, each A 2450 with a diameter of 150 microns was used to determine the thermal distributions. MHz microwave generator constructed in our lab and an applicator with an irradiating surface of 3 cm x 3 cm was used to heat the tissues. The diameter of the tumors varied between 8 to 10 mm. At the time of temperature measurement the mice were anesthesized with Thorazine (50 mg/kg) and Ketamine (40 mg/kg). Preliminary results have been obtained in normal and malignant tissue. The temperature is found to increase with movement of the thermal probe in the tumor from the region proximal to the body to that most distal on the limb. In some instances, temperature gradients of up to 2 degrees are observed across the tumor while in normal tissue the gradient is significantly lower. A general observation made is that, significantly lower power levels are required to achieve the same level of heating in the tumor as compared to normal muscle. These data and the implications of temperature distributions produced by microwave heating will be discussed.
Bll PHASE I STUDY TO DETERMINE MACROPHAGE ACTIVATION ELEVATION OF WHOLE BODY TEMPERATURE TO 39-40°C. Richard Johnson, Katherine Story
James Humbert*,
Roswell Park Memorial *Children's Hospital,
Ben Park*,
AND INCREASED
Ronald
Institute, Buffalo, NY 14263 Buffalo, NY 14222 USA
Scott,
POLYMORPHOUS
Adolph
Gunnarrson,
PHAGOCYTOSIS
INDUCED WITH THE
John Pearce, Peter Reese and
USA
Body temperatures of 39-40°C are produced by infection, febrile reactions resulting immunostimulation such as C-Parvum and BCG and as a result of regional hyperthermia.
from nonspecific
The literature suggests a synergism between temperature elevation and immune responses in tumor cells. Mondovi et al (Cancer 1972:30 885) reported that Ehrlich ascites tumor cells pretreated with hyperthermia to to a temperature of 42.5'C for three hours were more immunogenic than untreated cells. Szmigielski et al (Cancer Therapy by Hyperthermia and Radiation 1978, 80) demonstrated that local hyperthermia at 43.0°C far one hour in viva stimulated in-vitro cytocidal reactivity of T-lymphocytes and macrophages against murine sarcoma cells. Steblin et al (Sura Gvncol Obstet 1975:140. 339) reoorted that in-vitro cvtotoxicitv of patients lymphocytes toward their-own melanoma cells was enhanced following 39-40°C limb-hyperthermia. Increased T-lymphocyte activity in patients melanoma cells after hyperthermia therapy of 42'C for two hours has been reported by Delloratius et al (J Nat1 Cancer Inst 1977: 58, 905). Shah and Dickson (Cancer Res 1976:67, 508) showed regression of the VX metastases in rabbits after local radiofrequency treatment of the primary tumors. Regression was corre ? ated with increased skin reactivity together with production of antibodies in tumor cell antigens. Van Oss et al (J Retie endo Sot 1980:27. 561) have conducted invitro determinations of chemotaxis, phagocytic engulfment, phagocytic digestion and oxygen consumption of