Luminal cells have secretory properties. In the mouse mammary gland, luminal cells have been shown to express heat stable antigen and intermediate levels of Integrin b1 and cytokeratin 19, but not CK14. Within the luminal population, luminal progenitor cells have been described to express Integrin b3. Basal cells include mature myoepithelial cells and have contractile PI-103 clinical trial muscle as well as epithelial properties. In the mouse mammary gland, these cells are typically identified by the expression of CD24, high levels of CD29, CK14, smooth muscle actin but not CK19. Although a unique molecular marker for the MaSC has not been identified, single mammary epithelial cells capable of repopulating a mammary-free fat pad have been shown to be enriched in a CD24+CD29hi population of cells expressing high levels of Integrin a6, and lack expression of stem cell antigen 1. In various transgenic mouse models, a role for aberrant mammary epithelial cell differentiation in mammary carcinogenesis was recognized. For example, in preneoplastic mammary glands of transgenic mice expressing the wnt-1 oncogene under control of the Mouse Mammary Tumor Virus promoter, the percentage of mammary epithelial cells highly expressing CD29 is increased. Earlier, it was shown that ablation of Integrin b1 abolished mouse mammary tumor development. Integrin b1 has been shown to affect proliferation and differentiation in the luminal lineage and to be essential for MaSC repopulation ability. Similarly, targeted ablation in the mammary epithelium of focal adhesion kinase, a cytoplasmic tyrosine kinase and important mediator of Integrin signaling, significantly suppresses mammary carcinoma incidence in the mouse MMTV-PyVT model by affecting the pool of MaSC in the untransformed mammary gland and mammary cancer stem cells in the primary tumors. FAK is known to affect many cellular processes, including survival, proliferation, and differentiation. In this study, we used multicolor flow cytometry to annotate the luminal and basal/myoepithelial populations of RMECs. We quantified the protein expression phenotypes underlying these populations in mammary glands isolated at 1, 2, and 4 weeks after DMBA or MNU exposure as well as in carcinomas and mammary glands from untreated age-matched control animals of a highly susceptible congenic recombinant inbred rat line. Following exposure of the rats to the mammary carcinogens DMBA or MNU, the RMECs showed a distinct cellular differentiation etiology, while the carcinomas resulting from DMBA- or MNUinduced carcinogenesis have a very similar cellular differentiation profile. Rat chemical carcinogenesis models for breast cancer have been used extensively in preclinical research. The human breast and rat mammary gland have a similar ductal-lobular organization and mammary cancers induced in the rat are predominantly hormonedependent and of ductal origin, similar to the majority of human breast cancers. The two most widely used mammary carcinogens are the polycyclic hydrocarbon 7,12-dimethylbenzanthracene and the directly alkylating agent Nmethyl-N-nitrosourea. DMBA, unlike MNU, requires metabolic activation to become mutagenic.