Abstract

Abstract The cancer cell attractors theory provides a novel understanding of carcinogenesis. The mechanisms that the ectopic expression of some germline genes result in somatic tumors such as melanoma and brain tumors are emerging but not well understood. From mammals to model organisms like Caenorhabditis elegans and Drosophila melanogaster, the versatile Mi-2/Nucleosome remodeling and histone deacetylation (NuRD) complexes alongside their functionally related chromatin remodeling complexes (CRCs), i.e. the dREAM/Myb-MuvB(MMB)complex and polycomb group (PcG) complex are typical bottle-necked regulators of cell attractors. The trajectory that benign cells switch to cancerous could be the reverse (or close) of navigation of embryonic cells converging from a series of intermediate transcriptional states to a final adult state, which is supported by Gene Expression Dynamics Inspector (GEDI) assays and some cross-species genetic evidences. Hence Cancer could be triggered by cells undergoing abnormal cell attractor transitions, and may be reversible with “cyto-education”. In additon, we identified multidrug resistence genes and extracellular matrix (ECM) genes as conserved hub molecule fro Mi-2/NuRD. A complementary study will go to tumorigenicity and immunogenicity of induced pluripotent stem celles and the strategies of supppression. The understanding of involvement of CRCs in locking cancer attractors may forecast cancer “weather” and help find the recipes of perturbing genes to achieve successful reprogramming such that the reprogrammed cancer cell function in the same way as the normal cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr C26.

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