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U-87 MG (Uppsala 87 Malignant Glioma) is a widely utilized human glioblastoma cell line frequently employed in neuro-oncology research to study tumor biology and evaluate therapeutic candidates [1]. Originally derived from a grade IV glioma in 1966, it is characterized by specific genetic alterations, including the loss of the PTEN tumor suppressor and CDKN2A, which drive hyperactive PI3K/AKT signaling [2, 3]. While it is a cornerstone of in vitro and in vivo (xenograft) glioblastoma models, it is not a therapeutic target but rather a biological system used to identify molecular targets like EGFR or VEGF [4]. Research has highlighted significant genomic drift and identity discrepancies between the ATCC-distributed version and the original Uppsala line, necessitating careful validation in drug development studies [5]. Its high proliferative capacity and ability to form tumors in immunocompromised mice make it a standard for testing the efficacy of chemotherapeutics like temozolomide [1, 4].
Not applicable. U-87 MG is a cell line used as a model system to study drug effects on glioblastoma, rather than being a specific molecular target itself [1, 4]. Drugs tested against this cell line typically target its underlying pathways, such as the PI3K/AKT/mTOR pathway (due to PTEN loss) or the VEGF pathway for angiogenesis [3, 4].
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