Apoptosis in Irradiated Murine Tumors

Early radiation responses of transplantable murine ovarian (OCaI) and hepatocellular (HCaI) carcinomas were examined at 6, 24, 48, 96, and 144 h after single photon doses of 25, 35, or 45 Gy. Previous studies using tumor growth delay and tumor radiocurability assays had shown OCaI tumors to be relat...

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Bibliographic Details
Published in:Radiation research 1991-09, Vol.127 (3), p.308-316
Main Authors: Stephens, L. Clifton, Ang, K. Kian, Schultheiss, Timothy E., Milas, Luka, Meyn, Raymond E.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biological and medical sciences
Cell death
Cell nucleus
Cell Survival - radiation effects
Cesium Radioisotopes - therapeutic use
Epithelial cells
Female
Gamma Rays
Giant cells
Irradiation
Liver Neoplasms, Experimental - pathology
Liver Neoplasms, Experimental - radiotherapy
Lymphocytes
Male
Medical sciences
Mice
Mice, Inbred C3H
Necrosis
Neoplasm Transplantation
Neutrophils
Ovarian Neoplasms - pathology
Ovarian Neoplasms - radiotherapy
Radiation therapy and radiosensitizing agent
Radiation Tolerance - physiology
Space life sciences
Treatment with physical agents
Treatment. General aspects
Tumors
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Summary:Early radiation responses of transplantable murine ovarian (OCaI) and hepatocellular (HCaI) carcinomas were examined at 6, 24, 48, 96, and 144 h after single photon doses of 25, 35, or 45 Gy. Previous studies using tumor growth delay and tumor radiocurability assays had shown OCaI tumors to be relatively radiosensitive and HCaI tumors to be radioresistant. At 6 h, approximately 20% of nuclei in OCaI tumors showed aberrations characteristic of cell death by apoptosis. This contrasted to an incidence of 3% in HCaI tumors. Mitotic activity was eliminated in OCaI tumors but was only transiently suppressed in HCaI tumors. At 24-96 h, OCaI tumors continued to display apoptosis and progressive necrosis, whereas HCaI tumors responded by exhibiting marked pleomorphism. Factors other than mitotic activity may influence tumor radiosensitivity, and one of these may be susceptibility to induction of apoptosis (programmed cell death), because this was a prominent early radiation response by the radiosensitive OCaI tumors.
ISSN:0033-7587
1938-5404
DOI:10.2307/3577946