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It exerts its influence through three clinical/epidemiological "mediators" (clonal multiplicity, the threat of infection, level of human immunity) which ultimately determine the dynamics of resistance via five "effector" variables: sexual recombination, intrahost dynamics, community drug use, proportion of malaria infections treated, and the number of parasites per host.
Critical assumptions in these models relate to the number of genes encoding resistance [10], [11], [52], [53], the existence of intra host dynamics [12] and a direct tie between transmission intensity and recombination rate via the level of clonal multiplicity [13].
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Our data suggest that TP53 mutations develop in NNEDV and are intrinsic to the clonal evolution that leads to SCC, as the multiplicity of TP53 mutational events indicate that identical mutations are unlikely to occur independently (Greenblatt et al, 1994).
Technological advances in genetically engineered permanent cell labeling, together with a multiplicity of fluorescent markers and sophisticated imaging, open new possibilities for prospective and retrospective clonal analysis.
The idea that altered DNA methylation plays a variety of roles in carcinogenesis is compatible with three key features of this multistage process: clonal selection of abnormal cells in a progressive fashion, the reversibility of tumor promotion, and the multiplicity of tumor phenotypes.
Clonal distributions.
Multiplicity of activity predominates.
Clonal Evolution of Autoreactive Germinal Centers.
Duchene, G. & Kraus, A. Stellar multiplicity.
Boundless multiplicity is the rule.
The third advantage is multiplicity.
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