In 1976, Peter Nowell proposed a model of cancer as an evolutionary process in which a population of cells descended from a single cell of origin, or 'clone', acquires successive somatic mutations that allow sequential selection of fitter subclones—an evolution that underlies tumor progression, metastasis and resistance to therapy1 (Fig. 1). Nearly 36 years later, this model has been analyzed at the single-
nucleotide level in studies published in Cell2,3 and in the New England Journal of Medicine4. Hou et al.2 and Xu et al.3 carried out exome sequencing on single cells from an essential thrombocythemia tumor and a kidney tumor, respectively, whereas Gerlinger et al.4 analyzed exome-sequencing data, in combination with chromosome-aberration and ploidy data, from multiple samples of renal carcinomas and associated metastases4. The three studies have confirmed the clonal heterogeneity of primary tumors and metastases at the sequence level. in combination with chromosome-aberration and ploidy data, from multiple samples of renal carcinomas and associated metastases4. The three studies have confirmed the clonal heterogeneity of primary tumors and metastases at the sequence level.
正在翻譯中..