Adding PPARc agonists, such as troglitazone or rosiglitazone to the induction medium or extending induction time to 3 or 4 days to compensate for the loss of adipogenic potential in the ageing cells were quite common in the literature. These measures and the adipogenic induction cocktail only accelerated but were otherwise not essential in 3T3-L1 differentiation. The AbMole Nitroprusside disodium dihydrate practice to boost the adipogenicity of ageing 3T3-L1 cells by inducing them for more than 3 days suggested that some adipogenic cells AbMole Hexyl Chloroformate required longer induction time to show their adipogenic potential. We suspected that some cells that could not form adipocytes when induced like 3T3-L1 cells might have formed adipocytes if given longer induction time. This work tried to find new models of adipocytes by screening and characterizing cell lines that could not form adipocytes when induced like 3T3-L1 cells but could do so when given longer induction time. In this work, we tested the hypothesis that increasing the length of induction time during adipogenesis could increase the degree of differentiation to the extent that qualitatively different conclusions would be reached. Our results supported this hypothesis. First we showed that non-confluent 3T3-L1 cells were induced into adipocytes by doubling the induction time or with the help of rosiglitazone. This effect was not limited to 3T3-L1 cells. Multipotential NIH/3T3 is one such cell line that showed increased adipogenicity after prolonged induction. Figure 1 showed that the NIH/3T3 fibroblasts can consistently form insulin responsive adipocytes without exogenous genes when induced with double concentration of FBS for extended period. When testing the adipogenic potential of cell lines or the roles of genes in adipogenesis, the length of induction period above which the cell lines will be judged as non-adipogenic has not been clearly defined. Our results showed that slow rate of adipocytes conversion could be interpreted as inability to form adipocytes in some cases. Cancer stem cells are believed to have the capacity to proliferate and self-renew and to be responsible for tumorigenesis, metastasis and recurrence. The presence of cancer stem cells has been demonstrated in a variety of tumors. In particular, glioblastoma stem cells have been extensively studied as they can be maintained in serum-free media that favor the growth of neural stem cells. However, it is still difficult to maintain and expand cancer stem cells derived from other tissues in vitro. In the present study, we succeeded in establishing a cancer stem cell line from clear cell carcinoma of the ovary, which has the worst prognosis among epithelial ovarian cancers and show that CD133 interacts with plakoglobin, controls desmoglein-2 protein levels and is required for cell-cell adhesion and tumorigenicity of CCC stem cells. We cultured CCC stem cells isolated from a patient diagnosed with CCC under serum-free conditions. Similar to glioblastoma stem cells, CCC stem cells grew exponentially on laminincoated dishes under serum-free conditions. As reported previously for other cancers, CCC stem cells underwent differentiation when cultured in serum-containing medium : they exhibited a slight morphological change, and the expression levels of stem cell markers, such as CD133, SOX2 and Lgr5, were significantly reduced. When CCC stem cells were subcutaneously injected into immunocompromised mice, all mice developed tumors that were histopathologically similar to their original tumor.