scholarly journals Radiation-induced upregulation of telomerase activity escapes PI3-kinase inhibition in two malignant glioma cell lines

2013 ◽  
Vol 43 (2) ◽  
pp. 375-382 ◽  
Author(s):  
P. MILLET ◽  
C. GRANOTIER ◽  
O. ETIENNE ◽  
F.D. BOUSSIN
Keyword(s):  
Malignant Glioma ◽  
Cell Lines ◽  
Glioma Cell ◽  
Telomerase Activity ◽  
Pi3 Kinase ◽  
Kinase Inhibition ◽  
Glioma Cell Lines ◽  
Radiation Induced

Human Malignant Glioma Cell Lines are Refractory to Retinoic Acid-Mediated Differentiation and Sensitization to Apoptosis1

2000 ◽  
Vol 10 (3) ◽  
pp. 159-168 ◽  
Author(s):  
Friederike Schmidt ◽  
Peter Groscurth ◽  
Johannes Dichgans ◽  
Michael Weller
Keyword(s):  
Retinoic Acid ◽  
Malignant Glioma ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cell Lines ◽  
Human Malignant Glioma

scholarly journals Temozolomide sensitivity of malignant glioma cell lines – a systematic review assessing consistencies between in vitro studies

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Michael T. C. Poon ◽  
Morgan Bruce ◽  
Joanne E. Simpson ◽  
Cathal J. Hannan ◽  
Paul M. Brennan
Keyword(s):  
Cell Viability ◽  
Malignant Glioma ◽  
Cell Line ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
In Vitro Studies ◽  
Experimental Conditions ◽  
Glioma Cell Lines

Abstract Background Malignant glioma cell line models are integral to pre-clinical testing of novel potential therapies. Accurate prediction of likely efficacy in the clinic requires that these models are reliable and consistent. We assessed this by examining the reporting of experimental conditions and sensitivity to temozolomide in glioma cells lines. Methods We searched Medline and Embase (Jan 1994-Jan 2021) for studies evaluating the effect of temozolomide monotherapy on cell viability of at least one malignant glioma cell line. Key data items included type of cell lines, temozolomide exposure duration in hours (hr), and cell viability measure (IC50). Results We included 212 studies from 2789 non-duplicate records that reported 248 distinct cell lines. The commonest cell line was U87 (60.4%). Only 10.4% studies used a patient-derived cell line. The proportion of studies not reporting each experimental condition ranged from 8.0–27.4%, including base medium (8.0%), serum supplementation (9.9%) and number of replicates (27.4%). In studies reporting IC50, the median value for U87 at 24 h, 48 h and 72 h was 123.9 μM (IQR 75.3–277.7 μM), 223.1 μM (IQR 92.0–590.1 μM) and 230.0 μM (IQR 34.1–650.0 μM), respectively. The median IC50 at 72 h for patient-derived cell lines was 220 μM (IQR 81.1–800.0 μM). Conclusion Temozolomide sensitivity reported in comparable studies was not consistent between or within malignant glioma cell lines. Drug discovery science performed on these models cannot reliably inform clinical translation. A consensus model of reporting can maximise reproducibility and consistency among in vitro studies.

Resistance to growth inhibition by transforming growth factor—β in malignant glioma cells with functional receptors

1998 ◽  
Vol 88 (3) ◽  
pp. 529-534 ◽  
Author(s):  
Shiro Isoe ◽  
Hirofumi Naganuma ◽  
Shin Nakano ◽  
Atsushi Sasaki ◽  
Eiji Satoh ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Malignant Glioma ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Content Type ◽  
Glioma Cell Lines ◽  
Malignant Glioma Cells ◽  
Tgf Β1 ◽  
Fine Print

Object. The aim of this study was to investigate the mechanism by which malignant glioma cells escape from growth inhibition mediated by transforming growth factor-β (TGF-β), a ubiquitous cytokine that inhibits cell proliferation by causing growth arrest in the G1 phase of the cell cycle. Methods. The authors measured the response of eight malignant glioma cell lines to the growth-inhibiting activity of TGF-β in vitro and the expression of TGF-β Types I and II receptors in malignant glioma cells. The effect of TGF-β on the expression of a p27Kip1 cyclin-dependent kinase inhibitor was also investigated to assess the downstream signal transmission from TGF-β receptors. All malignant glioma cell lines were insensitive to growth inhibition by TGF-β1 and TGF-β2. Analyses of TGF-β receptors by means of affinity labeling in which 125I-TGF-β1 was used showed that six glioma lines had both TGF-β Types I and II receptors on their cell surfaces, whereas two lines had very small amounts of TGF-β Type I and/or Type II receptors. Northern blot analysis showed that all tumor lines expressed variable levels of messenger RNAs for both TGF-β Types I and II receptors. Flow cytometric analyses revealed that treatment of malignant glioma cells with TGF-β1 significantly downregulated the expression of p27Kip1 protein in all malignant glioma cell lines except one. Conclusions. The authors suggest that most malignant glioma cells express TGF-β Types I and II receptors, which can transmit some signals downstream and that the loss of response to TGF-β growth inhibition may not be caused by an abnormality of the TGF-β receptors.

scholarly journals Antiproliferative Effect of Multiple Autocrine Loop Blockade in Human Malignant Glioma Cell Lines

1995 ◽  
Vol 35 (10) ◽  
pp. 723-727 ◽  
Author(s):  
Masanori KURIMOTO ◽  
Kanehito NOGAMI ◽  
Tsuneaki OGIICHI ◽  
Michiharu NISHIJIMA ◽  
Akira TAKAKU
Keyword(s):  
Malignant Glioma ◽  
Cell Lines ◽  
Glioma Cell ◽  
Antiproliferative Effect ◽  
Autocrine Loop ◽  
Glioma Cell Lines ◽  
Human Malignant Glioma

scholarly journals Calcineurin Regulates Nuclear Factor I Dephosphorylation and Activity in Malignant Glioma Cell Lines

2013 ◽  
Vol 288 (33) ◽  
pp. 24104-24115 ◽  
Author(s):  
Miranda Brun ◽  
Darryl D. Glubrecht ◽  
Shairaz Baksh ◽  
Roseline Godbout
Keyword(s):  
Malignant Glioma ◽  
Cell Lines ◽  
Glioma Cell ◽  
Nuclear Factor ◽  
Factor I ◽  
Glioma Cell Lines ◽  
Nuclear Factor I
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