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They underwent an experimental design of multistage model of hepatocarcinogenesis: hepatic cells were initiated with the complete carcinogen Aflatoxin B1 (0.5 mg/Kg b.w).
Here, we investigated the hierarchical architecture of control modules in autism using an experimental paradigm based upon a multistage model of executive functions.
To selectively address stromal gene expression changes during cancer progression, we performed cDNA microarray analysis of laser-microdissected stromal cells derived from prostate intraepithelial neoplasia (PIN) and invasive cancer in a multistage model of prostate carcinogenesis.
These results have obvious implications for the large number of other quasi-biological cancer models that are special cases of these models, in particular those of Armitage and Doll [13], the two-mutation model [10], the generalized multistage model of Little [14], and a recently developed cancer model of Nowak et al. [15] that incorporates genomic instability.
It should be noted that the results given here are for the fully stochastic solution of the model, and would not be applicable, for example, to the deterministic approximation of the multistage model of Armitage and Doll [13] that is often employed in applications.
These models generalize a large number of other quasi-biological cancer models, in particular those of Armitage and Doll [13], the two-mutation model [10], the generalized multistage model of Little [14], and a recently developed cancer model of Nowak et al. [15] that incorporates genomic instability.
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I interpret these patterns in light of a multistage theory of aging, developed by analogy with multistage models of cancer progression [ 8- 11].
Multistage models of carcinogenesis, of which the best known is the Armitage Doll model, involve the mathematic expression of hypotheses about the process of carcinogenesis (Armitage and Doll 1954).
However, as noted above, the generalized multistage models of Little [ 4], Little and Wright [ 5] and Little et al. [ 6] allow for modelling of a final stochastic-growth or stochastic birth-death process of tumour growth from the first malignant cell; in particular this last process could be used to model the "angiogenic switch".
The objective of these analyses was to use exposure time windows and a multistage model to evaluate temporal modifiers of the impact of benzene on leukemia rates.
Quantitative estimates of human carcinogenic risk from chemical exposure are currently derived primarily from linearized multistage model analyses of the tumor response as observed in chronic laboratory animal bioassays versus administered dose.
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