In 1997 Bonnet and Dick first isolated the CSCs in leukemic cells expressing SC marker CD34 and afterwards, also, in other solid tumors [55–64]. Classically, SCs are defined by their two main characteristics: self-renewal and pluripotency [63]. Experiments performed on human acute myeloid leukemia and solid tumors show that CSC have three functional characteristics: transplantability, CH5424802 order tumorigenic potential to form tumors when injected into nude mice; distinct surface markers; ability to recreate the full phenotypic

heterogeneity of the parent tumor [64–66]. In characterizing normal and CSC s the problem is that these cellular populations are rare and the absence of specific cell surface markers represents a challenge to isolate and identify pure SC populations [67–72]. Cancer stem cell BIRB 796 molecular weight markers The limitation of using cell surface marker expression to characterize CSCs is that this approach requires prior knowledge of cell surface markers that are expressed by the putative CSCs in the tissue of interest, and often the choice of markers is inferred from known expression of markers in normal adult SCs. Several studies have prospectively isolated CSCs by looking for the presence of extracellular markers that are thought to be SC specific. The markers most commonly used are CD133 and CD44 [73]. These markers have been used

successfully to isolate SCs in normal and tumor tissue [74, 75]. Whilst CD133 and CD44 are thought

to be indicative of a CSC phenotype, it is not clear if they are universal markers for characterizing CUDC-907 chemical structure CSCs derived from all types of tumors. Furthermore, expression of CD133 and CD44 may not be restricted to the CSC population and may be present in early progenitor cells. The pentaspan transmembrane glycoprotein CD133, also known as Prominin-1, was originally described as a hematopoietic stem cell marker [73] and was subsequently shown to be expressed by a number of progenitor cells including those of the epithelium, where it is expressed on the apical surface [76]. Regarding EOC, Ferrandina G et al. demonstrated Nitroxoline that CD133(+) cells gave rise to a larger number of colonies than those documented in a CD133(−) population. Moreover, CD133(+) cells showed an enhanced proliferative potential compared to CD133(−) cells. The percentages of CD133-1 and CD133-2 epitopes expressing cells were significantly lower in normal ovaries/benign tumors with respect to those in ovarian carcinoma. Both the percentages of CD133-1- and CD133-2-expressing cells were significantly lower in metastases than in primary ovarian cancer. They didn’t detect any difference in the distribution of the percentage of CD133-1- and CD133-2-expressing cells according to clinicopathologic parameters and response to primary chemotherapy. Using flow cytometry, Ferrandina et al.