Irradiation of human mammary tumor cells led to late cell death, during 2 to 3 weeks, associated to mitotic catastrophe. From irradiated cells, we observe the emergence of persistent genetic instability, together with a radioresistant CD24- subpopulation (cancer stem-like cells (CSC)). We have observed that CD24- cells present a low genetic instability but may transmit (epigenetic mechanisms) to their progeny, CD24+ essentially, a long term genetic instability. Furthermore, data from literature show that the epithelial-mesenchymal transition (EMT) permit the appearance and the maintenance of CSC. The EMT plays an important role in the metastatic process, allowing the acquisition of an invasive potential. Preliminary results indicate that alteration of CD24 expression lead to the modification of the position of the cells in EMT. In the same way, if we modulate the TGF-beta pathway (strongly implicated in the EMT), we observe a modification of ?stem? cell characteristics. The aim of our work is to study the role of CD24 as an ?actor? of radiation response, and the mechanisms of regulation of CD24 by the EMT. This work will be done in relationship with the generation of chromosomal instability. Main techniques used will be: cell culture, Q RT-PCR, Western Blot, FACS, transfections, etc?