The immunological response of Wistar rats to the intracranially implanted C-6 glioma cell line

1983 ◽  
Vol 1 (4) ◽  
pp. 365-372 ◽  
Author(s):  
Kang M. Chiu ◽  
Jules E. Harris ◽  
Jeffrey S. Kroin ◽  
William Slayton ◽  
Donald P. Braun
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Wistar Rats ◽  
Immunological Response ◽  
Glioma Cell Line

scholarly journals P01.17 * ROLE OF PHOSPHATYDILCHOLINE-SPECIFIC PHOSPHOLIPASE C IN MODULATION OF CXCL12/CXCR4 AXIS IN A HUMAN GLIOMA CELL LINE

2014 ◽  
Vol 16 (suppl 2) ◽  
pp. ii30-ii30 ◽  
Author(s):  
L. Mercurio ◽  
A. Ricci ◽  
S. Cecchetti ◽  
A. Pacella ◽  
F. Podo ◽  
...  
Keyword(s):  
Phospholipase C ◽  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
Human Glioma ◽  
Human Glioma Cell Line ◽  
Human Glioma Cell ◽  
Cxcr4 Axis

Antiproliferative effect of quercetin in the human U138MG glioma cell line

2006 ◽  
Vol 17 (6) ◽  
pp. 663-671 ◽  
Author(s):  
Elizandra Braganhol ◽  
Lauren L. Zamin ◽  
Andr??s Delgado Canedo ◽  
Fabiana Horn ◽  
Alessandra S.K. Tamajusuku ◽  
...  
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
Antiproliferative Effect

Inability of translation of mRNA for HVJ (Sendai virus) M protein in a rat glioma cell line at nonpermissive temperatures

1988 ◽  
Vol 102 (3-4) ◽  
pp. 263-268
Author(s):  
H. Ogura ◽  
H. Sato ◽  
T. Ogura ◽  
J. Tanaka ◽  
S. Kamiya ◽  
...  
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Sendai Virus ◽  
Glioma Cell Line ◽  
M Protein ◽  
Rat Glioma

Three new nor-dammarane triterpenoids from Dysoxylum hainanense with particular cytotoxicity against glioma cell line

2013 ◽  
Vol 36 (3) ◽  
pp. 322-326 ◽  
Author(s):  
Peng Cao ◽  
Guobiao Liang ◽  
Xu Gao ◽  
Xiaogang Wang ◽  
Zhiqing Li
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line

scholarly journals Characterization of cells recovered from the xenotransplanted NG97 human-derived glioma cell line subcultured in a long-term in vitro

BMC Cancer ◽  
2008 ◽  
Vol 8 (1) ◽  
Author(s):  
Camila ML Machado ◽  
Rafael Y Ikemori ◽  
Tatiana Q Zorzeto ◽  
Ana CMA Nogueira ◽  
Suse DS Barbosa ◽  
...  
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line

Enhancement of radiosensitivity of wild-type p53 human glioma cells by adenovirus-mediated delivery of the p53 gene

1998 ◽  
Vol 89 (1) ◽  
pp. 125-132 ◽  
Author(s):  
Frederick F. Lang ◽  
W. K. Alfred Yung ◽  
Uma Raju ◽  
Floralyn Libunao ◽  
Nicholas H. A. Terry ◽  
...  
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Radiation Treatment ◽  
P53 Protein ◽  
Glioma Cells ◽  
Glioma Cell Line ◽  
Wild Type ◽  
Content Type ◽  
Infected Cells ◽  
Fine Print

Object. The authors sought to determine whether combining p53 gene transfer with radiation therapy would enhance the therapeutic killing of p53 wild-type glioma cells. It has been shown in several reports that adenovirus-mediated delivery of the p53 gene into p53 mutant gliomas results in dramatic apoptosis, but has little effect on gliomas containing wild-type p53 alleles. Therefore, p53 gene therapy alone may not be a clinically effective treatment for gliomas because most gliomas are composed of both p53 mutant and wild-type cell populations. One potential approach to overcome this problem is to exploit the role p53 plays as an important determinant in the cellular response to ionizing radiation. Methods. In vitro experiments were performed using the glioma cell line U87MG, which contains wild-type p53. Comparisons were made to the glioma cell line U251MG, which contains a mutant p53 allele. Monolayer cultures were infected with an adenovirus containing wild-type p53 (Ad5CMV-p53), a control vector (dl312), or Dulbecco's modified Eagle's medium (DMEM). Two days later, cultures were irradiated and colony-forming efficiency was determined. Transfection with p53 had only a minor effect on the plating efficiency of nonirradiated U87MG cells, reducing the plating efficiency from 0.23 ± 0.01 in DMEM to 0.22 ± 0.04 after addition of Ad5CMV-p53. However, p53 transfection significantly enhanced the radiosensitivity of these cells. The dose enhancement factor at a surviving fraction of 0.10 was 1.5, and the surviving fraction at 2 Gy was reduced from 0.61 in untransfected controls to 0.38 in p53-transfected cells. Transfection of the viral vector control (dl312) had no effect on U87MG radiosensitivity. In comparison, transfection of Ad5CMV-p53 into the p53 mutant cell line U251MG resulted in a significant decrease in the surviving fraction of these cells compared with controls, and no radiosensitization was detected. To determine whether Ad5CMV-p53—mediated radiosensitization of U87MG cells involved an increase in the propensity of these cells to undergo apoptosis, flow cytometric analysis of terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridinetriphosphate nick-end labeling—stained cells was performed. Whereas the amount of radiation-induced apoptosis in uninfected and dl312-infected control cells was relatively small (2.1 ± 0.05% and 3.7 ± 0.5%, respectively), the combination of Ad5CMV-p53 infection and radiation treatment significantly increased the apoptotic frequency (18.6 ± 1.4%). To determine whether infection with Ad5CMV-p53 resulted in increased expression of functional exogenous p53 protein, Western blot analysis of p53 was performed on U87MG cells that were exposed to 9 Gy of radiation 2 days after exposure to Ad5CMV-p53, dl312, or DMEM. Infection with Ad5CMV-p53 alone increased p53 levels compared with DMEM- or dl312-treated cells. Irradiation of Ad5CMV-p53—infected cells resulted in a further increase in p53 that reached a maximum at 2 hours postirradiation. To determine whether exogenous p53 provided by Ad5CMV-p53 had transactivating activity, U87MG cells were treated as described earlier and p21 messenger RNA levels were determined. Infection of U87MG cells with Ad5CMV-p53 only resulted in an increase in p21 compared with DMEM- and dl312-treated cells. Irradiation of Ad5CMV-p53—infected cells resulted in an additional time-dependent increase in p21 expression. Conclusions. These data indicate that adenovirus-mediated delivery of p53 may enhance the radioresponse of brain tumor cells containing wild-type p53 and that this radiosensitization may involve converting from a clonogenic to the more sensitive apoptotic form of cell death. Although the mechanism underlying this enhanced apoptotic susceptibility is unknown, the Ad5CMV-p53—infected cells have a higher level of p53 protein, which increases further after irradiation, and this exogenous p53 is transcriptionally active. Thus, it is possible that the combination of Ad5CMV-p53 infection and radiation treatment increases p53 protein to a level that is sufficient to overcome at least partially the block in apoptosis existing in U87MG cells.

Radiobiological Effects of Boronated Porphyrin (STA-BX909) Compared to BSH in Cultured Glioma Cell Line

2001 ◽  
pp. 1311-1316
Author(s):  
Akira Matsumura ◽  
Yasushi Shibata ◽  
Tetsuya Yamamoto ◽  
Fumiyo Yoshida ◽  
Yoshinori Hayakawa ◽  
...  
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
Radiobiological Effects

LACK OF NEURON-ASSOCIATED MICROTUBULE PROTEINS IN THE C6 GLIOMA CELL LINE

1989 ◽  
Vol 48 (3) ◽  
pp. 359
Author(s):  
G. M. Zientek ◽  
A. Frankfurter ◽  
C. D. Katsetos ◽  
M. M. Herman
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
C6 Glioma ◽  
C6 Glioma Cell

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.

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