Embryonic stem cells (ESCs) can self-renew indefinitely and undergo multi-lineage differentiation with proper cues, which provides unlimited material for cell-based therapies. However, understanding how cell identity is established and maintained remains a challenge for regenerative medicine. Cell fate decisions involve coordinated regulation on a genome-wide scale; unfortunately, the precise mechanisms underlying these complex processes are largely uncharacterized. Recently, the process known as cellular reprogramming has provided new opportunities to advance in our understanding of the fundamental basis of cell identity for scientific and therapeutic purposes. Reprogramming of somatic cells to a pluripotent state can be achieved by ectopic expression of four transcription factors (Oct4, Sox2, Klf4, and c-Myc) (Takahashi and Yamanaka, 2006). This induced pluripotent stem cell technology facilitates the generation of immortal pluripotent stem cell (iPSC) lines avoiding ethical obstacles that arise from employing human embryonic stem cells (hESCs), and offers great hope for personalized medicine using patient-specific iPSCs. In addition, the iPSC technology represents a promising tool for cell therapies and offers unique opportunities in human disease modelling, drug testing and drug discovery, toxicity screening, and novel therapeutic approaches for both general and personalized medicine. Although much additional work is still required to solve safety issues related to using iPSCs for clinical practices (i.e. avoid epigenetic aberrations linked to potential tumor formation), recent advances and important results have confirmed the value of using iPSCs for better understanding of etiology, modeling and treatment of numerous diseases.
Our lab is interested in understanding epigenetic regulation of transcription in the mammalian genome that governs cell fate decisions during embryonic development and human diseases. We aim to develop novel therapeutic strategies for age-related disorders (i.e. cancer) as well as rare diseases (i.e. multiple familial cerebral cavernomatosis). For this purpose we use a variety of methods in molecular biology, genomic and proteomic approaches, genome editing and bioinformatics.
Funding and Support
|
|
|
|
|
|
|
|
