In addition, the RMECs from mammary carcinomas have a higher percentage of cells in S/G2+M phase of the cell cycle. As the RMECs from mammary carcinomas also express higher levels of Integrin a6, which is a marker previously associated with MaSCs, show increased proliferation, and show increased pFAK expression that was also found be associated with a stemprogenitor cell pool, we hypothesize that DMBA- and MNUinduced mammary carcinomas may have an increased pool of stem/progenitor-like cells driving tumorigenesis. In the future, the existance of such a population, as well as its tumorigenic potential would have to be verified in transplantation studies. Mammary specific ablation of FAK was earlier reported to ameliorate mammary tumor progression in mice by affecting the mammary cancer stem/progenitor cells. Early work has demonstrated that FAK autophosphorylation at Y397 is strongly increased upon interaction with activator proteins, such as Integrin bs, rendering pFAK in its active state. We found in the mammary gland of untreated control rats that about 60% of the RMECs stained positive for intracellular FAK and about 35% of RMECs stained positive for pFAK. DMBAand MNU-induced mammary carcinomas showed specific upregulation of FAK expression and FAK autophosphorylation in CD29hi cells. The upregulation of Integrin b1 and a6, as well as the activation of FAK in the mammary carcinomas may provide an important research tool for potential use of rat carcinogenesis models for preclinical evaluation FAK- and/or Integrin-signaling inhibitors as anticancer drugs. The results provide detailed insights into different populations of RMECs. Importantly, the methodology established in this study allowed us to quantify changes in RMEC differentiation in the process of chemical carcinogenesis with the two most commonly used mammary carcinogens, namely DMBA and MNU. We also noticed an effect of age on the RMEC differentiation profile, as rats of 22 weeks of age have a higher percentage of luminal cells as compared with rats of 12 weeks of age. In the future, the contribution of age to RMEC differentiation would have to be addressed in a separate study. Detailed knowledge of changes in RMEC differentiation after carcinogen exposure is important to understand the cellular differentiation states associated with genetic and/or environmentally-induced susceptibility to breast cancer for which the rat is a widely studied model organism. A thorough understanding of the underpinnings of the disease process is essential in searching new treatments for AD. Therefore, a combination of structural and functional information of the human brain could provide more detailed information of the influence of the neurodegenerative diseases on cortical brain areas. Bortezomib Transcranial magnetic stimulation of the motor cortex can evaluate different aspects of cortical excitability. In particular, the resting motor threshold has been shown to reliably reflect cortical excitability. Furthermore, rMT is altered in certain diseases such as vascular dementia, Parkinson’s disease, juvenile myoclonus epilepsy and progressive myoclonus epilepsy EPM1.