An imprinted signature helps isolate ESC-equivalent iPSCs

Department of Pathology Medicine, Institute for Stem Cell Biology and Regenerative Medicine, Standford University School of Medicine,Palo Alto, California 94304, USA.
Cell Research (Impact Factor: 12.41). 09/2010; 20(9):974-6. DOI: 10.1038/cr.2010.117
Source: PubMed


Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. It provides a single accessible source of information for both scientists and clinicians, keeping them up-to-date with advances in the field. It encompasses programmed cell death, cell death induced by toxic agents, differentiation and the interrelation of these with cell proliferation.

9 Reads
  • [Show abstract] [Hide abstract]
    ABSTRACT: Epigenetic dysregulation comprising DNA hypermethylation and hypomethylation, enhancer of zeste homologue 2 (EZH2) overexpression and altered patterns of histone modifications is associated with the progression of prostate cancer. DNA methylation, EZH2 and histone modifications also ensure the parental-specific monoallelic expression of at least 62 imprinted genes. Although it is therefore tempting to speculate that epigenetic dysregulation may extend to imprinted genes, expression changes in cancerous prostates are only well documented for insulin-like growth factor 2 (IGF2). A literature and database survey on imprinted genes in prostate cancer suggests that the expression of most imprinted genes remains unchanged despite global disturbances in epigenetic mechanisms. Instead, selective genetic and epigenetic changes appear to lead to the inactivation of a sub-network of imprinted genes, which might function in the prostate to limit cell growth induced via the PI3K/Akt pathway, modulate androgen responses and regulate differentiation. Whereas dysregulation of IGF2 may constitute an early change in prostate carcinogenesis, inactivation of this imprinted gene network is rather associated with cancer progression.
    Asian Journal of Andrology 02/2012; 14(3):436-50. DOI:10.1038/aja.2011.160 · 2.60 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The eye is an ideal target for exploiting the potential of human induced pluripotent stem cell (hiPSC) technology in order to understand disease pathways and explore novel therapeutic strategies for inherited retinal disease. The aim of this article is to map the pathway from state-of-the art laboratory-based discoveries to realising the translational potential of this emerging technique. We describe the relevance and routes to establishing hiPSCs in selected models of human retinal disease. Additionally, we define pathways for applying hiPSC technology in treating currently incurable, progressive and blinding retinal disease.
    Progress in Retinal and Eye Research 10/2013; 37(100). DOI:10.1016/j.preteyeres.2013.09.002 · 8.73 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: DLK1-DIO3 represents an imprinted cluster which genes are involved in physiological cell biology as early as the stem cell level and in the pathogenesis of several diseases. Transcription factor-mediated induced pluripotent cells (iPSCs) are considered an unlimited source of patient-specific hematopoietic stem cells for clinical application in patient-tailored regenerative medicine. However, to date there is no marker established able to distinguish embryonic stem cell-equivalent iPSCs or safe human iPSCs. Recent findings suggest that the DLK1-DIO3 locus possesses the potential to represent such a marker but there are also contradictory data. This review aims to report the current data on the topic describing both sides of the coin.
    Cellular and Molecular Life Sciences CMLS 08/2014; 71(22). DOI:10.1007/s00018-014-1698-9 · 5.81 Impact Factor

Similar Publications


9 Reads
Available from