Columbia University PS-OC
Recent large-scale genomic projects have begun to reveal the complex landscape of genetic alterations that cause cancer, pointing toward a powerful new paradigm for precision medicine. Despite some early successes against blood cancers, however, currently available experimental and computational methods have made limited progress in the identification of targeted therapies for solid tumors. One reason is that cells in a solid tumor are not all the same, but form many genetically distinct subpopulations of cellular clones. Recent studies have shown, for example, that gene expression signatures vary across different regions in the same tumor and that the most abundant mutations in a tumor are not always the ones that drive its growth. In addition, very small subclonal populations are often immune to the therapies that target more abundant clones, evading the effects of treatment and initiating relapse and metastasis. Such findings suggest that genomic methods that do not account for clonal heterogeneity and the dynamics of tumor development will continue to be insufficient for identifying effective targeted therapies.
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