Theory of dose-effect relations

Kellerer, Albrecht M.; Hug, O.

doi:10.1007/978-3-642-80710-7_1

Cited by 20 publications

(15 citation statements)

References 25 publications

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“…For high doses, the exponent in the LQ model becomes quadratic, which disagrees with both equation (3.2) and most experimental data (Kellerer and Hug, 1972). A model that describes clonogenic survival both at low, intermediate and high doses, including low-dose hypersensitivity (Marples et al, 2004), is the recent RCR model (Lind et al, 2003):…”

Section: Basic Cell Survivalmentioning

confidence: 76%

Accurate description of heterogeneous tumors for biologically optimized radiation therapy

Nilsson

2005

Medical Physics

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In this thesis, a model of tissue oxygenation is presented, that takes into account the heterogeneous nature of tumor vasculature. Even though the model is rather simple, the resulting oxygen distributions agree very well with clinically observed oxygen distributions for most tumors and healthy normal tissues. The model shows that the vascular density may not describe the oxygenation of a tissue sufficiently well, unless the heterogeneity of the vascular system is taken into account. Based on the oxygen distributions from the tissue model, the associated radiation response at low and high doses can be determined.The radiation response of heterogeneous tumors should preferably be described by two clonogen compartments, one resistant and one sensitive, dominating the response at high and low radiation doses, respectively. Furthermore, each compartment should be characterized by the effective radiation resistance and the effective clonogen number. The resistant-sensitive model of radiation response has been analyzed in great detail. It accurately describes the response of severely heterogeneous tumors, both at low and high doses and LET values. The effective response parameters are given as integrals, averaged over the whole spectrum of radiation resistance. The parameters can also be determined from clinically established dose-response relations.The main properties of the dose-response relation for a generally heterogeneous tumor is described in some detail. The normalized dose-response gradient has been generalized to take heterogeneities in both dose delivery and radiation response into account. This quantity is important for accurate treatment plan optimization using intensity modulated radiation therapy for individual patients.

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Section: Basic Cell Survivalmentioning

confidence: 76%

Accurate description of heterogeneous tumors for biologically optimized radiation therapy

Nilsson

2005

Medical Physics

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“…7): Finally, we mention without demonstration another limiting equation [Kellerer and Hug (1972), Eq(7.l1)]: 7): Finally, we mention without demonstration another limiting equation [Kellerer and Hug (1972), Eq(7.l1)]:…”

Section: Applications Of Microdosimetry In Biologymentioning

confidence: 97%

“…d) The Kellerer-Hug theorem A relation first stated by Kellerer and Hug (1972) sets up a lower limit for the mean number of inactivating events, and thus for the number of microdosimetric events at the mean inactivation dose (see below). This theorem expresses a global condition, that is it relates to the overall dose response curve.…”

Section: Applications Of Microdosimetry In Biologymentioning

confidence: 99%

Microdosimetry and Its Applications

1996

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PrefaceMicrodosimetry originated more than 35 years ago when the senior author studied energy deposition in small irradiated masses and formulated what is now termed Regional Microdosimetry. A.M. Kellerer developed the further concepts of Structural Microdosimetry. Microdosimetry and its applications have been the subject of an extensive literature. This includes several hundred papers which have appeared in the Proceedings of what to date have been eleven Symposia on Microdosimetry. General reviews are contained in chapters of books and in a journal dealing with a broader range of subjects. The International Commission on Radiation Units and Measurements has produced Report 36 on Microdosimetry. The form of these publications limited their scope and in this work it is our aim to provide a more comprehensive account.Dealing extensively with interdisciplinary matters (from atomic and solid state physics to integral geometry and molecular biology) we were confronted with the standard problem of presenting material in a manner that makes it comprehensible to readers with diverse backgrounds, without providing a superficial treatise. Although some readers may find it too difficult to absorb the entire contents of some chapters, they should be able to gain substantial information from introductory sections and from data presented. Occasional repetitions, including identical formulae, have reduced the need for cross-references between chapters.With the exception of chapter III it is recommended to read the book sequentially; this appeared to us to be the logical way of learning microdosimetry. The conceptual framework of microdosimetry is introduced in the first two chapters. At this stage of the presentation the details of energy deposition in matter are unimportant. The fourth and fifth chapter are the twin workhorses of microdosimetry. The fourth chapter is about the art of measuring microdosirnetric spectra. It gives details on the construction and operation of microdosimetric detectors. It also makes aware both the experimentalist and the theorist that what one measures may sometimes be different from the actual pattern of energy deposition. The material in Chapter V, the theoretical companion of the preceding chapter, comes as a result of the tremendous progress made during the past 20 years or so in obtaining cross sections for the interaction of charged particles with matter, and of the subsequent effort made to integrate these into sophisticated Monte Carlo transport codes that simulate the passage of particles through structured or unstructured matter. This chapter also brings forth the two VI Preface complementary descriptions of microdosimetric events: regional microdosimetry and structural microdosimetry. The applications of microdosimetry are described in the last two chapters. The selection of topics here reflects the research interests of the authors and also the need to provide this information within the limitations of a single volume. As a result the list of topics here should be seen as illustrative...

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“…For cell killing and mutation induction we found linear-quadratic dependences on the dose while linear relationships were obtained for ssb and dsb . Table 1 gives the parameters of the best fits and the doses required to achieve various levels of effect : these were chosen at 10% survival for cell killing and, for mutation induction, at 10 mutants per 10 -5 survivors above the background (D +10 ) and at twice the (Kellerer and Hug 1972) has been also reported in the same table according to a calculation method derived from that reported by Fertil et al (1984) . Clearly a single parameter cannot uniquely describe nonlinear dose-response curves, and its use results in a loss of information .…”

Section: M=m + a MD + Pmd2mentioning

confidence: 99%

Relationships Between Cell Killing, Mutation Induction and DNA Damage in X-irradiated V79 Cells: The Influence of Oxygen and DMSO

Sapora

Barone

Belli

et al. 1991

International Journal of Radiation Biology

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The relationships between cell killing, mutation induction and DNA double (dsb) and single (ssb) strand breaks have been studied in V79 cells irradiated with X-rays under oxic and anoxic conditions in the presence and in the absence of dimethylsulphoxide (DMSO). Curvilinear relationships were found between all pairs of endpoints, except for dsb versus ssb. Statistical analysis of experimental data has shown that in the absence of DMSO there is evidence of good correlations between cell killing, mutation induction and dsb in oxic and anoxic conditions. However, when DMSO was present, no significant correlation was found. In the presence of oxygen DMSO always exerts a protective effect while in anoxia it is generally much less protective and induces a strong sensitization with respect to mutation induction. Possibly DMSO acts not only as a radical scavenger but also as an agent inducing chromatin relaxation and/or under anoxia, forming highly mutagenic short-term radicals. The present data suggest that lethal and mutational events are at least partially independent and not proportional to the initial number of DNA breaks. This may imply that either other kinds of lesions are involved in cell lethality and mutability, or dose-dependent repair mechanisms of dsb have to be considered.

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Theory of dose-effect relations

Cited by 20 publications

References 25 publications

Accurate description of heterogeneous tumors for biologically optimized radiation therapy

Accurate description of heterogeneous tumors for biologically optimized radiation therapy

Microdosimetry and Its Applications

Relationships Between Cell Killing, Mutation Induction and DNA Damage in X-irradiated V79 Cells: The Influence of Oxygen and DMSO

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