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Cancers evolve by a reiterative process of clonal expansion, genetic diversification and clonal selection within the adaptive landscapes of tissue ecosystems. The dynamics are complex, with highly variable patterns of genetic diversity and resulting clonal architecture. Therapeutic intervention may destroy cancer clones and erode their habitats, but it can also inadvertently provide a potent selective pressure for the expansion of resistant variants. The inherently Darwinian character of cancer is the primary reason for this therapeutic failure, but it may also hold the key to more effective control. 相似文献
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朱士群 《苏州大学学报(医学版)》1990,6(2):195-199
Effects of multiplicatioe noise in transient laser intensity are investigated theoretically. Analytic solutions are calculated through a reduced Fokker-Planck equation and the results with different pump parameters are discussed. 相似文献
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A C3Cl-type(bcc)-semi-infinite ferrimagnet with a single-ion uniaxial anisotropy and a magnetic impurity layer is considered through combining Green‘s function theory with the transfer-mairx method.The effect of the anisotropy term and the impurity layer on surface spin wave specirum is discussed.The influence of the impurity layer‘s distance from the surface or surface spin woves is also concerned. 相似文献
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Maley CC Galipeau PC Finley JC Wongsurawat VJ Li X Sanchez CA Paulson TG Blount PL Risques RA Rabinovitch PS Reid BJ 《Nature genetics》2006,38(4):468-473
Neoplasms are thought to progress to cancer through genetic instability generating cellular diversity and clonal expansions driven by selection for mutations in cancer genes. Despite advances in the study of molecular biology of cancer genes, relatively little is known about evolutionary mechanisms that drive neoplastic progression. It is unknown, for example, which may be more predictive of future progression of a neoplasm: genetic homogenization of the neoplasm, possibly caused by a clonal expansion, or the accumulation of clonal diversity. Here, in a prospective study, we show that clonal diversity measures adapted from ecology and evolution can predict progression to adenocarcinoma in the premalignant condition known as Barrett's esophagus, even when controlling for established genetic risk factors, including lesions in TP53 (p53; ref. 6) and ploidy abnormalities. Progression to cancer through accumulation of clonal diversity, on which natural selection acts, may be a fundamental principle of neoplasia with important clinical implications. 相似文献
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