1 eration, we find no evidence to suggest that dedifferentiated cells acquire a ductal fate during this

2 , the proliferation and the migration of the dedifferentiated cells are dependent on Hh signaling.

3  transcription factors and that diseased and dedifferentiated cells can be returned to normal functio

4 transition, and exogenous PHD2 expression in dedifferentiated cells can restore an epithelial phenoty

5 lular matrix, and proliferation of partially dedifferentiated cells, evidence strongly supports the l

6  and three IR-resistant clones isolated from dedifferentiated cells have acquired the ability to prol

7           RNAi-mediated knockdown of Oct4 in dedifferentiated cells led to diminished CSC phenotypes.

8 could be detected in similar assays with the dedifferentiated cell line HepG2.1 or the nonhepatic cel

9 n organized structure of lineage restricted, dedifferentiated cells that cooperate to regenerate the

10                                              Dedifferentiated cells were morphologically indistinguis

11 val may be manifested by the production of a dedifferentiated cell with broader potential and that th