ArticleNeoplasia (New York, N.Y.)
A unique model system for tumor progression in GBM comprising two developed human neuro-epithelial cell lines with differential transforming potential and coexpressing neuronal and glial markers.
Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- Immunophenotypic characterization of canine oligodendroglioma cells cultured in an oligodendrocyte precursor cell-tailored medium.The Journal of veterinary medical science · 2026Article
- Characterization of adherent primary cell lines from fresh human glioblastoma tissue, defining glial fibrillary acidic protein as a reliable marker in establishment of glioblastoma cell culture.Cancer reports (Hoboken, N.J.) · 2021Article
- Astrocytes Decreased the Sensitivity of Glioblastoma Cells to Temozolomide and Bay 11-7082.International journal of molecular sciences · 2020Article
- Chlorogenic acid effectively treats cancers through induction of cancer cell differentiation.Theranostics · 2019Article
- Attenuation of Tumor Suppressive Function of FBXO16 Ubiquitin Ligase Activates Wnt Signaling In Glioblastoma.Neoplasia (New York, N.Y.) · 2019Article
- Differential expression of p42.3 in low- and high-grade gliomas.World journal of surgical oncology · 2014Article
- Expression and regulation of prostate apoptosis response-4 (Par-4) in human glioma stem cells in drug-induced apoptosis.PloS one · 2014Article
- Tumor suppressive miRNA-34a suppresses cell proliferation and tumor growth of glioma stem cells by targeting Akt and Wnt signaling pathways.FEBS open bio · 2014Article
- MiR-145 functions as a tumor-suppressive RNA by targeting Sox9 and adducin 3 in human glioma cells.Neuro-oncology · 2013Article
- Epigenetic regulation of DNA methyltransferases: DNMT1 and DNMT3B in gliomas.Journal of neuro-oncology · 2011Article
- Dlxin-1, a member of MAGE family, inhibits cell proliferation, invasion and tumorigenicity of glioma stem cells.Cancer gene therapy · 2011Article
- Sumoylation of vimentin354 is associated with PIAS3 inhibition of glioma cell migration.Oncotarget · 2010Article
- Stimulation of glioma cell motility by expression, proteolysis, and release of the L1 neural cell recognition molecule.Cancer cell international · 2009Article
- Article
- A review of the past, present, and future directions of neoplasia.Neoplasia (New York, N.Y.) · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms involved in tumor progression from a low-grade astrocytoma to the most malignant glioblastoma multiforme (GBM) have been hampered due to lack of suitable experimental models. We have established a model of tumor progression comprising of two cell lines derived from the same astrocytoma tumor with a set of features corresponding to low-grade glioma (as in HNGC-1) and high-grade GBM (as in HNGC-2). The HNGC-1 cell line is slow-growing, contact-inhibited, nontumorigenic, and noninvasive, whereas HNGC-2 is a rapidly proliferating, anchorage-independent, highly tumorigenic, and invasive cell line. The proliferation of cell lines is independent of the addition of exogenous growth factors. Interestingly, the HNGC-2 cell line displays a near-haploid karyotype except for a disomy of chromosome 2. The two cell lines express the neuronal precursor and progenitor markers vimentin, nestin, MAP-2, and NFP160, as well as glial differentiation protein S100beta. The HNGC-1 cell line also expresses markers of mature neurons like Tuj1 and GFAP, an astrocytic differentiation marker, hence contributing toward a more morphologically differentiated phenotype with a propensity for neural differentiation in vitro. Additionally, overexpression of epidermal growth factor receptor and c-erbB2, and loss of fibronectin were observed only in the HNGC-2 cell line, implicating the significance of these pathways in tumor progression. This in vitro model system assumes importance in unraveling the cellular and molecular mechanisms in differentiation, transformation, and gliomagenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.