Embryonic stem cell-specific signatures in cancer: insights into genomic regulatory networks and implications for medicine
1 Molecular Cell and Developmental Biology, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712, USA
2 Department of Pediatric Oncology, Children's Hospital and Dana Farber Cancer Institute, Harvard Stem Cell Institute, Harvard Medical School, Howard Hughes Medical Institute, Boston, MA 02115, USA
Genome Medicine 2011, 3:75 doi:10.1186/gm291Published: 29 November 2011
Embryonic stem (ES) cells are of great interest as a model system for studying early developmental processes and because of their potential therapeutic applications in regenerative medicine. Obtaining a systematic understanding of the mechanisms that control the 'stemness' - self-renewal and pluripotency - of ES cells relies on high-throughput tools to define gene expression and regulatory networks at the genome level. Such recently developed systems biology approaches have revealed highly interconnected networks in which multiple regulatory factors act in combination. Interestingly, stem cells and cancer cells share some properties, notably self-renewal and a block in differentiation. Recently, several groups reported that expression signatures that are specific to ES cells are also found in many human cancers and in mouse cancer models, suggesting that these shared features might inform new approaches for cancer therapy. Here, we briefly summarize the key transcriptional regulators that contribute to the pluripotency of ES cells, the factors that account for the common gene expression patterns of ES and cancer cells, and the implications of these observations for future clinical applications.