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Biomedical subjects

R J Yaes

Publications and source records attributed to R J Yaes.

At least 19 recordsLinked to original sources
PubMed1992

Megavoltage grid total body irradiation of C3Hf/SED mice.

The effect of a grid on whole-body megavoltage radiation tolerance in C3Hf/SED mice was studied. Adult mice were irradiated beneath a 50% megavoltage grid. LD50 (50% lethality) values were measured at ten and 30 days. LD50/30 day increased by a factor of 1.5 for mice receiving both single and two fraction irradiation beneath the grid. LD50/ten day increased by factors of 1.1 to 1.2 for single, two, and five fraction irradiation beneath the grid.

Animals↗
PubMed1991

On using the linear-quadratic model in daily clinical practice.

To facilitate its use in the clinic, Barendsen's formulation of the Linear-Quadratic (LQ) model is modified by expressing isoeffect doses in terms of the "Standard Effective Dose," Ds, the isoeffective dose for the "standard" fractionation schedule of 2 Gy fractions given once per day, 5 days per week. For any arbitrary fractionation schedule, where total dose D is given in N fractions of size d in a total time T, the corresponding "Standard Effective Dose," Ds, will be proportional to the total dose D and the proportionality constant will be called the "Standard Relative Effectiveness," SRE, to distinguish it from Barendsen's "Relative Effectiveness," RE. Thus, Ds = SRE.D. The constant SRE depends on the parameters of the fractionation schedule, and on the tumor or normal tissue being irradiated. For the "simple" LQ model with no time dependence, which is applicable to late reacting tissue, SRE = [(d + delta)/(2 + delta)], where d is the fraction size and delta = alpha/beta is the alpha/beta ratio for the tissue of interest, with both d and delta expressed in units of Gy. Application of this method to the Linear Quadratic model with a time dependence, the "LQ + time" model, and to low dose rate brachytherapy will be discussed. To clarify the method of calculation, and to demonstrate its simplicity, examples from the clinical literature will be used.

Brachytherapy↗
PubMed1990

The biological effect of inhomogeneous dose distributions in fractionated radiotherapy.

The linear quadratic (LQ) model is applied to an organ receiving a fractionated course of radiotherapy with an inhomogeneous dose distribution. It is shown that the gradient in the extrapolated response dose (ERD) will be steeper than the gradient in the physical dose. This effect will be greatest for an organ with a small alpha/beta ratio treated with large dose fractions. Clinical implications are discussed with an emphasis on radiation myelitis.

Dose-Response Relationship, Radiation↗
PubMed1990

Volume effects.

Explore the source record for details and available documents.

Animals↗
PubMed1989

Linear-quadratic model isoeffect relations for proliferating tumor cells for treatment with multiple fractions per day.

A modified linear-quadratic model isoeffect relation that includes the effect of proliferation is proposed. As for a planned course of therapy, the treatment time T and the number of fractions N are not independent variables; the new isoeffect relation involves only the fraction size d and the total dose D, but differs from the unmodified linear-quadratic model isoeffect relation and predicts higher isoeffect doses for small dose fractions. Using the new isoeffect relation it is explicitly shown, for a simple model, that decreasing the fraction size will improve the therapeutic ratio only if multiple fractions per day are given.

Cell Division↗
PubMed1989

Tumor heterogeneity, tumor size, and radioresistance.

Mutant clonogenic cells, resistant to individual chemotherapeutic agents, are known to play a central role in clinical chemotherapy failure. The possibility that mutant cells, resistant to conventionally fractionated megavoltage photon radiotherapy, exist in human tumors is considered. Applying the mutation theory of Luria and Delbruck to describe the appearance of resistant cells, several conclusions follow: (a) the mean number of resistant cells in a tumor will be determined by the tumor size and the mutation rate; (b) a wide variation in radiosensitivity in tumors of the same histology is expected, because of a large variation in the number of resistant cells that they contain; (c) the presence of a resistant clone will not reduce the tumor-control probability until the tumor becomes sufficiently large; (d) initial response will not be a reliable predictor of long-term control; (e) clonogenic assays may not accurately predict treatment outcomes; (f) the mutation rate may be the most accurate predictor of tumor aggressiveness and resistance to various treatment modalities; (g) tumors with a low mutation rate, which may include seminoma, Hodgkin's disease and many pediatric tumors would be curable by either chemotherapy or radiation; (h) pleomorphic tumors with a high mutation rate, which may include glioblastoma multiforme, would be difficult to cure by any means. Clinical and experimental evidence is reviewed for the existence of radioresistant cell lines in human and animal tumors, and further experiments are proposed to test this hypothesis. Treatment strategies for targeting radioresistant clones are discussed.

Animals↗
PubMed1988

Some implications of the Linear Quadratic model for tumor control probability.

To define an optimal radiation therapy strategy, the dependence of the probability of cure and of significant complications, on the parameters controlled by the radiotherapist must be determined. The recent success of the Linear Quadratic (LQ) model in constructing isoeffect relations for normal tissue damage and in describing in vitro cell survival curves, indicate that this model could be used to determine this dependence. The problem of tumor control is addressed. Using LQ model parameters obtained from human tumor cell lines, the sigmoid dose-response curves for controlling tumors of fixed size but of several histologies, with a fractionated course of radiotherapy is obtained. Except for squamous cell carcinoma, the calculated average tumor control doses (TCD37 or TCD50) are unrealistically low, but the model can be made more realistic by including inhomogeneities in the spatial dose distribution and heterogeneous tumor cell populations. The slope of the dose response curves are determined and the significance of the "relative slope" parameter rho as a measure of the number of cells in a tumor's most radioresistant clone is noted. The relation of the model's predictions to qualitative features of the experimental animal data for both tumor control and for normal tissue damage is discussed. Experiments to test the validity of this type of model are suggested.

Cell Line↗