The cancer stem cell (CSC) hypothesis postulates that a rare population of tumor cells possessing increased capacities for self-renewal and tumor initiation is responsible for maintaining the growth of neoplastic tissue. absent despite the presence of CD133 protein. In addition, CD133 manifestation has recently been demonstrated to be modulated by oxygen levels. These factors, in combination with the uncertain biological role of CD133, suggest that the use of CD133 expression like a marker for CSCs should be critically evaluated in each fresh experimental system and highlight the need for more CSC surface markers that are directly involved in keeping CSC properties. in the diagram indicate transmembrane areas. b Potential for false bad data with AC133 and AC141 mAbs. If CD22 nonglycosylated CD133 is present, it will not become recognized from the AC133 and AC141 mAbs. c Potential for false positive data with AC133 and AC141 mAbs. Given that the nature of the glycosylated AC133 and AC141 epitopes are poorly defined, it is formally possible that glycosylated epitopes on extracellular molecules other than CD133 could cross-react with the AC133 or AC141 mAbs Although they are known to be glycosylated structures, the locations of the CD133 epitopes bound from the AC133 and AC141 monoclonal antibodies (mAbs; commercially available as CD133/1 and CD133/2 mAbs, respectively) have not been identified. Henceforth, we will refer to the epitopes bound from the AC133 and AC141 mAbs as the AC133 and AC141 epitopes, respectively. A summary of CD133-related nomenclature used in this review can be found in Table 1. Table 1 Explanation of CD133-related nomenclature used in this review European, ELISA, immunoprecipitation, immunohistochemistry, circulation cytometry Oxygen levels modulate CD133 expression It has been reported recently that CD133 expression is definitely modulated by oxygen levels in vitro in glioma cultures. Decreasing the oxygen pressure (from 20% to 2C3%) during the tradition of medulloblastoma and glioblastoma cells improved the expression of the AC133 and AC141 epitopes as well as CD133 mRNA levels [22, 48]. Because the oxygen tension in the brain is estimated to be 1C5% [49, 50] and is probably reduced most tumor cells [51], these conditions may be more physiologically relevant than normal cells tradition conditions. Prolonged tradition of tumor cell lines in the presence of 20% oxygen may therefore lead to a reduction in CD133 expression and could impact the tumor initiation potential of in vitro cultured cells reintroduced to a low oxygen pressure in vivo environment. Therefore, further studies will be needed to determine if oxygen tension is an important experimental variable in cis-Pralsetinib CSC experiments. CD133-epitope-negative glioblastoma stem cells Given the potential complex environmental factors influencing cis-Pralsetinib CD133 epitope manifestation in vitro, it is perhaps not amazing that there cis-Pralsetinib cis-Pralsetinib are conflicting reports in the literature regarding the living of CD133 epitope-negative glioblastoma-derived malignancy stem cells. In two related studies, cell lines generated from glioblastomas fell into two unique groups: neurosphere-like, nonadherent, AC133/AC141 epitope-positive cell lines, and adherent or semiadherent AC133/AC141 epitope-negative cell lines [52, 53]. Beier et al. reported that while tumor cells from your AC133/AC141 epitope-negative glioblastoma-derived cell lines have tumorigenicity much like AC133/AC141 epitope-positive cell lines, AC133CAC141-epitope-negative cells purified from your AC133/AC141 epitope-positive cell lines were nontumorigenic [52]. The manifestation of CD133 mRNA was confirmed to be very low in the AC133/AC141 epitope-negative cell lines, indicating that manifestation of CD133 is.