Olig2, a basic helix–loop–helix transcription factor, is involved in oligodendroglial specification. Olig2 expression has been reported in most glial tumors, such as oligodendrogliomas and astrocytomas.1-2 More than half of glioblastomas are weakly positive for Olig2. No Olig2 expression has been found in the non-glial tumors including neuroepithelial tumors, ependymomas, subependymomas, medulloblastomas, and nonneuroepithelial tumors, such as CNS lymphomas, meningiomas, schwannomas, atypical teratoid/rhabdoid tumor, and haemangioblastomas.1-2 In order to characterize cellular subtypes that constitute astrocytomas, oligoastrocytomas and oligodendrogliomas, double labeling of Olig2 and GFAP has been performed which identified two phenotypically distinct tumor populations. The first is Olig2+/GFAP– which has an oligodendroglial morphology, corresponding to pure oligodendrogliomas that contain only oligodendroglial cells; the second is Olig2–/GFAP+ which has an astrocytic phenotype, including not only oligoastrocytomas, but also WHO astrocytomas1-2
1. Mokhtari K, et al. Olig2 expression, GFAP, p53 and 1p loss analysis contribute to glioma subclassification. Neuropathol Appl Neurobiol. 2005; 31:62-9.
2. Otero JJ, et al. OLIG2 is differentially expressed in pediatric astrocytic and in ependymal neoplasms. J Neurooncol. 2011; 104:423-438.
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Olig2 (EP112)
Rabbit Monoclonal
Olig2, a basic helix–loop–helix transcription factor, is involved in oligodendroglial specification. Olig2 expression has been reported in most glial tumors, such as oligodendrogliomas and astrocytomas.1-2 More than half of glioblastomas are weakly positive for Olig2. No Olig2 expression has been found in the non-glial tumors including neuroepithelial tumors, ependymomas, subependymomas, medulloblastomas, and nonneuroepithelial tumors, such as CNS lymphomas, meningiomas, schwannomas, atypical teratoid/rhabdoid tumor, and haemangioblastomas.1-2 In order to characterize cellular subtypes that constitute astrocytomas, oligoastrocytomas and oligodendrogliomas, double labeling of Olig2 and GFAP has been performed which identified two phenotypically distinct tumor populations. The first is Olig2+/GFAP– which has an oligodendroglial morphology, corresponding to pure oligodendrogliomas that contain only oligodendroglial cells; the second is Olig2–/GFAP+ which has an astrocytic phenotype, including not only oligoastrocytomas, but also WHO astrocytomas1-2
1. Mokhtari K, et al. Olig2 expression, GFAP, p53 and 1p loss analysis contribute to glioma subclassification. Neuropathol Appl Neurobiol. 2005; 31:62-9.
2. Otero JJ, et al. OLIG2 is differentially expressed in pediatric astrocytic and in ependymal neoplasms. J Neurooncol. 2011; 104:423-438.
Rabbit Monoclonal
Olig2, a basic helix–loop–helix transcription factor, is involved in oligodendroglial specification. Olig2 expression has been reported in most glial tumors, such as oligodendrogliomas and astrocytomas.1-2 More than half of glioblastomas are weakly positive for Olig2. No Olig2 expression has been found in the non-glial tumors including neuroepithelial tumors, ependymomas, subependymomas, medulloblastomas, and nonneuroepithelial tumors, such as CNS lymphomas, meningiomas, schwannomas, atypical teratoid/rhabdoid tumor, and haemangioblastomas.1-2 In order to characterize cellular subtypes that constitute astrocytomas, oligoastrocytomas and oligodendrogliomas, double labeling of Olig2 and GFAP has been performed which identified two phenotypically distinct tumor populations. The first is Olig2+/GFAP– which has an oligodendroglial morphology, corresponding to pure oligodendrogliomas that contain only oligodendroglial cells; the second is Olig2–/GFAP+ which has an astrocytic phenotype, including not only oligoastrocytomas, but also WHO astrocytomas1-2
1. Mokhtari K, et al. Olig2 expression, GFAP, p53 and 1p loss analysis contribute to glioma subclassification. Neuropathol Appl Neurobiol. 2005; 31:62-9.
2. Otero JJ, et al. OLIG2 is differentially expressed in pediatric astrocytic and in ependymal neoplasms. J Neurooncol. 2011; 104:423-438.
