HROG33 T0 M1 Cells

HROG33 T0 M1 is a primary human glioblastoma multiforme (GBM) cell line established from freshly resected tumor tissue of an adult female patient with WHO grade IV glioblastoma located in the left occipitotemporal region. The designation “T0” refers to the primary tumor at initial diagnosis, and “M1” denotes the corresponding in vitro model derived from this specimen. The cell line was generated as part of a systematic effort to establish ultra-low passage GBM cultures from both fresh and vitally cryopreserved tumor material, with the aim of preserving patient-specific molecular and functional characteristics.

HROG33 T0 M1 exhibits adherent growth with a fibroblast-like morphology typical of primary GBM cultures. Cells form a monolayer and display consistent proliferative capacity in vitro. In the comparative establishment study, paired cultures derived from fresh and cryopreserved tumor tissue showed no significant differences in morphology, growth kinetics, or drug responsiveness. Immunophenotypic characterization of representative HROG cell lines demonstrated expression of neural lineage-associated markers including glial fibrillary acidic protein (GFAP), nestin, and vimentin, consistent with a glioma-derived phenotype. Molecular analyses performed across the HROG series included assessment of MGMT promoter methylation, EGFR amplification, and mutational status of TP53, IDH1/2, KRAS, and BRAF, supporting the retention of tumor-specific genomic features in established cultures.

Functionally, HROG-derived cell lines have been evaluated for sensitivity to standard-of-care and investigational agents used in GBM therapy, including temozolomide, BCNU (carmustine), vincristine, and imatinib. Drug response profiles of matched cell line pairs indicated stable and reproducible pharmacologic behavior following tissue cryopreservation. As an ultra-low passage primary GBM model, HROG33 T0 M1 provides a clinically relevant in vitro system for investigating glioblastoma biology, therapeutic response prediction, and patient-specific tumor heterogeneity while minimizing artifacts associated with long-term continuous cell line adaptation.