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Stacking the DEK: From chromatin topology to cancer stem cells

, , &
Pages 51-66 | Published online: 19 Dec 2012
 

Abstract

Stem cells are essential for development and tissue maintenance and display molecular markers and functions distinct from those of differentiated cell types in a given tissue. Malignant cells that exhibit stem cell-like activities have been detected in many types of cancers and have been implicated in cancer recurrence and drug resistance. Normal stem cells and cancer stem cells have striking commonalities, including shared cell surface markers and signal transduction pathways responsible for regulating quiescence vs. proliferation, self-renewal, pluripotency and differentiation. As the search continues for markers that distinguish between stem cells, progenitor cells and cancer stem cells, growing evidence suggests that a unique chromatin-associated protein called DEK may confer stem cell-like qualities. Here, we briefly describe current knowledge regarding stem and progenitor cells. We then focus on new findings that implicate DEK as a regulator of stem and progenitor cell qualities, potentially through its unusual functions in the regulation of local or global chromatin organization.

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Acknowledgments

L.M.P.V. was supported by Kirschstein National Research Service Award (NRSA) F32CA139931 from the National Cancer Institute of the National Institutes of Health. Additional funding for L.M.P.V. was provided by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health under award number K12HD051953, the Building Interdisciplinary Research Careers in Women’s Health (BIRCWH) Research Scholars mentored career development award sponsored by The Center for Clinical and Translational Science and Training at the University of Cincinnati. Research in the laboratory of F.K. is supported by the START Program of the Faculty of Medicine, RWTH Aachen and by the German Research Foundation (DFG). N.N. is supported by Public Health Service Grant CA115611–01. Research in the laboratory of S.I.W. is funded by Public Health Service grant R01 CA116316 and Department of Defense award W81XWH-12–1-0194. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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