Predicting chemoresistance in human malignant glioma cells: The role of molecular genetic analyses

Weller, Michael; Rieger, Johannes; Grimmel, Cornelia; Meir, Erwin G. Van; Tribolet, Nicolas de; Krajewski, Stanisław; Reed, John C.; Deimling, Andreas von; Dichgans, J.

doi:10.1002/(sici)1097-0215(19981218)79:6<640::aid-ijc15>3.0.co;2-z

Cited by 159 publications

(95 citation statements)

References 17 publications

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“…6 A shift to acidotic conditions of pH 7.0 had little effect on the growth of T98G and LN-18 cells. In contrast, the growth of U87MG and LN-229 cells was inhibited significantly at pH 7.0.…”

Section: Modulation Of Glioma Cell Proliferation By Acidosismentioning

confidence: 91%

“…Glioma cell proliferation was assessed by crystal violet assay 6 and [ 3 H]methylthymidine incorporation. Briefly, [ 3 H]methylthymidine (1 Ci) was added to the cells at 56 hours after adaptation to the respective pH conditions.…”

Section: Viability Assaysmentioning

confidence: 99%

“…6 The following antibodies were used: anti-p21 (C19; SC397; Santa Cruz Biotechnology, Santa Cruz, CA); anti-p53 (polyclonal antibody [pAb] 240 and pAb 1801; Oncogene Research Products, Cambridge, MA); and antiactin (1-19; SC1616; Santa Cruz Biotechnology).…”

Section: Immunoblot Analysismentioning

confidence: 99%

“…6,8 Accordingly, next, we examined whether p53 mediates the growth inhibition imposed by mild acidosis in U87MG and LN-229 cells. To this end, we transfected U87MG cells (Fig.…”

Section: Inhibition Of Proliferation By Acidosis: the Role Of P53mentioning

confidence: 99%

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Modulation of growth and radiochemosensitivity of human malignant glioma cells by acidosis

Reichert

Steinbach

Supra

et al. 2002

Cancer

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BACKGROUNDGlioblastoma commonly is characterized by hypoxia and acidosis and the histologic features of tissue necrosis and neovascularization. Current approaches of adjuvant radiochemotherapy for patients with glioblastoma have only a modest impact on the natural course of this disease.METHODSThe authors examined the effects of acidosis on growth and response to irradiation and chemotherapy in cultured human malignant glioma cells.RESULTSThe authors found that mild acidosis (pH 7.0) inhibited the growth of cell lines that retained wild type p53 activity but did not inhibit the growth of cell lines that were devoid of p53 function. Transfer of a dominant‐negative p53 gene into p53 wild type cells failed to override the acidosis‐conferred growth arrest, suggesting that loss of p53 activity per se does not mediate escape from acidosis‐induced growth inhibition. Moderate acidosis (pH 6.6) inhibited the growth of all cell lines. Acidosis‐mediated growth arrest was not associated with a specific type of cell cycle arrest, e.g., in G0/G1 or G2/M phase. Acidosis did not result in consistent changes in radiosensitivity; however, it enhanced the cytotoxic effects of lomustine but conferred protection from topotecan, vincristine, teniposide, and cisplatin cytotoxicity. Lomustine exhibited enhanced stability at low pH, providing a putative mechanism for the enhanced cytotoxic effects of lomustine in acidotic conditions. Decreased sensitivity to the other drugs did not result from altered multidrug resistance drug transport activity.CONCLUSIONSTaken together, the current results suggest that tissue acidosis may be an important determinant of glioma cell responses to adjuvant radiochemotherapy. The superior activity of nitrosoureas, such as lomustine, compared with other agents in patients with glioblastoma may result in part from prolonged drug stability in an acidotic microenvironment. Cancer 2002;95:1113–9. © 2002 American Cancer Society.DOI 10.1002/cncr.10767

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Section: Modulation Of Glioma Cell Proliferation By Acidosismentioning

confidence: 91%

Section: Viability Assaysmentioning

confidence: 99%

Section: Immunoblot Analysismentioning

confidence: 99%

“…6,8 Accordingly, next, we examined whether p53 mediates the growth inhibition imposed by mild acidosis in U87MG and LN-229 cells. To this end, we transfected U87MG cells (Fig.…”

Section: Inhibition Of Proliferation By Acidosis: the Role Of P53mentioning

confidence: 99%

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Modulation of growth and radiochemosensitivity of human malignant glioma cells by acidosis

Reichert

Steinbach

Supra

et al. 2002

Cancer

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“…This panel of cell lines has been characterized before. 12,13 A comparison of APRIL mRNA expression and the expression of other members of the TNF family (CD95L, TRAIL/Apo2L), of the TNF receptor family (CD95, death receptors (DR) 4 and 5), or of the antiapoptotic proteins Bcl-2, Bcl-X L , FLIP or XIAP, did not reveal significant correlations as determined by Spearman rank order correlation analysis (data not shown). Similarly, there was no correlation of APRIL expression with the susceptibility of the glioma cells to CD95L or TRAIL/Apo2L, or to the cytotoxic drugs vincristine, lomustine, cytarabine, teniposide, doxorubicin, camptothecin, paclitaxel or gemcitabine, analyzed by ANOVA (data not shown).…”

Section: Expression Of April By Human Malignant Glioma Cell Linesmentioning

confidence: 96%

APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis

et al. 2001

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Antiapoptotic Bcl-2 family protein expression increases with progression of oligodendroglioma

Deininger

Weller

Streffer

et al. 1999

Cancer

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Predicting chemoresistance in human malignant glioma cells: The role of molecular genetic analyses

Cited by 159 publications

References 17 publications

Modulation of growth and radiochemosensitivity of human malignant glioma cells by acidosis

Modulation of growth and radiochemosensitivity of human malignant glioma cells by acidosis

APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis

Antiapoptotic Bcl-2 family protein expression increases with progression of oligodendroglioma

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