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Title: Model for the induction of bone cancer by /sup 224/Ra. [In man]

Abstract

A mathematical model for the transformation of normal endosteal cells into malignant tumor cells by ..cap alpha.. irradiation is applied to /sup 224/Ra. The model postulates that a normal endosteal cell near the bone surface is transformed into a malignant cell by three consecutive events. The first two events are the initiation events. The probability of their occurrence is proportional to the absorbed endosteal dose and they generate dormant tumor cells. These dormant tumor cells are promoted by the third event, the promotion event. The probability of this last event is proportional to the rate of bone remodeling but independent of the radiation dose. In competition with these transforming events is the killing of any endosteal cell by ..cap alpha.. irradiation. Killing is balanced by replacement of killed endosteal cells by normal stem cells. This model provides the following interesting predictions for the human /sup 224/Ra cases: after the decay of /sup 224/Ra the tumor rate decreases exponentially at a rate proportional to the bone turnover rate; for exposure to the same dose the model predicts an increased number of tumors for protracted exposure (i.e., exposure at a lower dose rate). Implications of this model for the therapy of ankylosingmore » spondylitis are discussed. Statistical procedures are suggested for comparison of this theoretical model with the existing data on the induction of osteosarcomas by /sup 224/Ra in man.« less

Authors:
;
Publication Date:
Research Org.:
Argonne National Lab., IL (USA)
OSTI Identifier:
7319458
Report Number(s):
CONF-760992-17
TRN: 77-014744
DOE Contract Number:  
W-31-109-ENG-38
Resource Type:
Conference
Resource Relation:
Conference: 2. international symposium on biological effects of Ra-224, Neuherberg/Muenchen, F.R. Germany, 20 Sep 1976
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; BONE TISSUES; PATHOLOGICAL CHANGES; MAN; BIOLOGICAL RADIATION EFFECTS; OSTEOSARCOMAS; RADIOINDUCTION; RADIUM 224; BIOLOGICAL MODELS; CARCINOGENESIS; DOSE-RESPONSE RELATIONSHIPS; INTERNAL IRRADIATION; MATHEMATICAL MODELS; NEOPLASMS; TIME DEPENDENCE; ALKALINE EARTH ISOTOPES; ALPHA DECAY RADIOISOTOPES; ANIMALS; BIOLOGICAL EFFECTS; BODY; CONNECTIVE TISSUE; DAYS LIVING RADIOISOTOPES; DISEASES; EVEN-EVEN NUCLEI; HEAVY NUCLEI; IRRADIATION; ISOTOPES; MAMMALS; NUCLEI; PATHOGENESIS; PRIMATES; RADIATION EFFECTS; RADIOISOTOPES; RADIUM ISOTOPES; SARCOMAS; SKELETAL DISEASES; TISSUES; VERTEBRATES; 560161* - Radionuclide Effects, Kinetics, & Toxicology- Man

Citation Formats

Groer, P G, and Marshall, J H. Model for the induction of bone cancer by /sup 224/Ra. [In man]. United States: N. p., 1976. Web.
Groer, P G, & Marshall, J H. Model for the induction of bone cancer by /sup 224/Ra. [In man]. United States.
Groer, P G, and Marshall, J H. 1976. "Model for the induction of bone cancer by /sup 224/Ra. [In man]". United States. https://www.osti.gov/servlets/purl/7319458.
@article{osti_7319458,
title = {Model for the induction of bone cancer by /sup 224/Ra. [In man]},
author = {Groer, P G and Marshall, J H},
abstractNote = {A mathematical model for the transformation of normal endosteal cells into malignant tumor cells by ..cap alpha.. irradiation is applied to /sup 224/Ra. The model postulates that a normal endosteal cell near the bone surface is transformed into a malignant cell by three consecutive events. The first two events are the initiation events. The probability of their occurrence is proportional to the absorbed endosteal dose and they generate dormant tumor cells. These dormant tumor cells are promoted by the third event, the promotion event. The probability of this last event is proportional to the rate of bone remodeling but independent of the radiation dose. In competition with these transforming events is the killing of any endosteal cell by ..cap alpha.. irradiation. Killing is balanced by replacement of killed endosteal cells by normal stem cells. This model provides the following interesting predictions for the human /sup 224/Ra cases: after the decay of /sup 224/Ra the tumor rate decreases exponentially at a rate proportional to the bone turnover rate; for exposure to the same dose the model predicts an increased number of tumors for protracted exposure (i.e., exposure at a lower dose rate). Implications of this model for the therapy of ankylosing spondylitis are discussed. Statistical procedures are suggested for comparison of this theoretical model with the existing data on the induction of osteosarcomas by /sup 224/Ra in man.},
doi = {},
url = {https://www.osti.gov/biblio/7319458}, journal = {},
number = ,
volume = ,
place = {United States},
year = {Thu Jan 01 00:00:00 EST 1976},
month = {Thu Jan 01 00:00:00 EST 1976}
}

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