Cytogenetic analysis of tumor clonality.

摘要: All or almost all neoplasias subjected to systematic cytogenetic scrutiny have been found harbor acquired chromosomal aberrations. The paradigm stemming from the study of hematopoietic malignancies and sarcomas is that cancers are monoclonal origin (i.e., they developed a single transformed somatic progenitor) because neoplastic parenchyma cells share at least one primary abnormality, with subsequent clonal evolution along lines Darwinian selection occurring among various subclones carrying secondary When carcinomas began be studied more extensively by methods, however, sometimes many cytogenetically unrelated clones were found, in seeming contradiction hypothesis. Also studies multiple samples same patient led rethinking what evidence really revealed about tumor clonality, both its early stages during disease development. observed heterogeneity in, for example, tumors breast pancreas vastly surpasses leukemias, lymphomas, connective tissue tumors, even most epithelial, including uroepithelial, tumors. Theoretical reasoning as well available experimental data we here review show cell populations follows either four principal pathways: (1) initial monoclonality retained throughout entire course no additional, aberrations accrued judged karyotypic appearance; (2) tumorigenesis but additional develop time leading (clonal divergence); (3) polyclonal exists beginning followed an overall reduction genomic complexity convergence) due progression, resulting oligo- monoclonality; (4) convergence later divergence acquisition changes clone(s) survived middle phases progression. Further individual necessary elicit precise information cell-to-cell variability many, especially neoplasms which holds key profound understanding complex issue clonality cancer