摘要: Solid tumors are comprised of a surprisingly heterogeneous collection cells. As discussed in an introductory talk by Dr. Rudin, recent studies focused on wide diversity malignancies have begun to define phenotypically distinct subsets cancer cells that differ terms both clonogenic potential vitro and tumorigenic vivo. These been interpreted many as supporting the stem cell hypothesis.1 In brief, this hypothesis holds small subpopulation within tumor retain unique proliferative differentiative capacity regenerate tumors. contrast, majority has limited replicative may represent terminally differentiated progeny An increasingly broad consistent body evidence, from hematologic solid tumors, supports separable populations radically different regenerative capacities. Even very numbers purified high-tumorigenic can be successfully transplanted, resulting consistently recapitulating full heterogeneity morphologies present origin.1 Several articles sought characteristics putative for human lung cancer. Ho et al.2 demonstrated bulk sorting non-small (NSCLC) lines flow cytometry used isolate subset markedly enriched Eramo al.3 demonstrated, across all major histologies, expressing elevated CD133 (a known marker progenitor glioblastoma) is highly recapitulates CD133-high low recipient animals. Most recently, Jiang al.4 series primary xenograft demonstrate transcription factor ASCL1, implicated multiple embryonic developmental pathways, upregulated CD133+ compartment. ASCL1 was found transcriptional regulator suppression shRNA inhibited potential. Taken together, these strongly support existence cancers characterized capacity.