Use of multistage models to infer stage affected by carcinogenic exposure: Example of lung cancer and cigarette smoking
References (15)
Radiation damage to the genetic material
Sci Prog
(1951)A new theory of the cancer inducing mechanism
Br J Cancer
(1953)- et al.
Initiation and promotion at different ages and doses in 2200 mice. I. Methods, and the apparent persistence of initiated cells
Br J Cancer
(1981) - et al.
Initiation and promotion at different ages and doses in 2200 mice. II. Decrease in promotion by TPA with aging
Br J Cancer
(1981) - et al.
Initiation and promotion at different ages and doses. III. Linear extrapolation from high doses may underestimate low-dose tumour risks
Br J Cancer
(1981) The age distribution of human cancer for carcinogenic exposures of varying intensity
Am J Epidemiol
(1977)- et al.
Multistage models and primary prevention of cancer
J Natl Cancer Inst
(1980)
Cited by (58)
How rapidly does the excess risk of lung cancer decline following quitting smoking? A quantitative review using the negative exponential model
2013, Regulatory Toxicology and PharmacologyCitation Excerpt :Thus, if the RR is, for example, 15 for current smokers, so that the excess risk is 14, our interest is in estimating the time after quitting at which the excess risk is 7 (or the RR is 8), and in estimating the excess risk (and RR) at other time points since quitting. In Additional file 1: “Multistage” (downloadable from http://www.pnlee.co.uk/downloads/ieslc3/LC_Quitting_Paper_AdditionalFiles.htm), we demonstrate that the predictions of the decline in excess risk following quitting are quite similar to those of the multistage model, often used for detailed analysis of individual subject data on smoking and lung cancer (Brown and Chu, 1987; Doll and Peto, 1978; Freedman and Navidi, 1990; Lee, 1995; Whittemore, 1988), and that estimates of H depend little on the assumed magnitude of the excess risk in current smokers. Although, for a given current smoker RR, estimates of H tend to be somewhat greater for populations with a longer duration of smoking, the negative exponential model appears a useful simple method to summarize published epidemiological data.
Application of a two-stage Syrian hamster embryo cell transformation assay to cigarette smoke particulate matter
2005, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisA flexible modeling approach to estimating the component effects of smoking behavior on lung cancer
2004, Journal of Clinical EpidemiologyCitation Excerpt :The independent effect of early age at started smoking on lung cancer risk remains controversial. Previous studies [5,16,25,28,29,33–35] reported an effect of age started, although some found no effect [36–39]. Most of these studies failed to account for confounding by duration, which is naturally correlated with age started or by years since quitting.
Cigarette smoking and the risk of invasive epithelial ovarian cancer in a prospective cohort study
2003, European Journal of CancerCitation Excerpt :In contrast, we did not observe a clear trend for mucinous tumours, but the number of cases of these tumours in our data-set was low. If a carcinogen acts early in cancer development, its association with cancer risk will be characterised by a relatively long period of time between the causal action of cigarette smoking and diagnosis, or that smoking acts at different stages in the development of the respective tumour types [24,25]. In contrast, the association with risk of a carcinogen that acts late in cancer development would tend towards the null with increasing years since cessation of exposure to that carcinogen [24,25].
Life Course Tobacco Smoking and Risk of HPV-Negative Squamous Cell Carcinomas of Oral Cavity in Two Countries
2022, Frontiers in Oral HealthIntroduction to mathematical oncology
2016, Introduction to Mathematical Oncology