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Start Over Author "G Tallen" Journal anticancer research
4 results on '"G Tallen"'

1. Expression of p33ING1 mRNA and chemosensitivity in brain tumor cells

Author

G, Tallen, K, Riabowol, and J E, Wolff

Subjects
Paclitaxel, Cell Cycle Proteins, Nerve Tissue Proteins, Microtubules, Predictive Value of Tests, Humans, Genes, Tumor Suppressor, RNA, Messenger, RNA, Neoplasm, Enzyme Inhibitors, Etoposide, Brain Neoplasms, Tumor Suppressor Proteins, Intracellular Signaling Peptides and Proteins, Nuclear Proteins, Proteins, Glioma, Fibroblasts, Neoplasm Proteins, DNA-Binding Proteins, Doxorubicin, Drug Resistance, Neoplasm, Vincristine, Protein Biosynthesis, Cisplatin, Topoisomerase I Inhibitors, Biomarkers, Inhibitor of Growth Protein 1, DNA Damage, Medulloblastoma
Abstract

Mutations and down-regulation of tumor suppressor genes can contribute to both tumorigenesis and chemotherapy resistance. The tumor suppressor p33ING1 has growth-inhibitory and pro-apoptotic effects recruiting p53 and it plays a role in DNA repair through interaction with PCNA. We questioned whether p33ING1 mRNA expression correlates with the chemosensitivity of brain tumor cells.Various malignant brain tumor cell lines were examined for their sensitivity to cisplatin, doxorubicin, etoposide and the antimitotic agents vincristine and paclitaxel by MTT-cytotoxicity assays. p33ING1 mRNA expression was determined by RT-PCR.We found that, unlike other tumor types, ING1 levels were higher in glioma cell lines than in normal control cells. Medulloblastoma cells revealed the lowest ING1 expression of the lines tested. Comparing all cell lines, p33ING1 gene expression significantly (p = 0.028) correlated with resistance to vincristine (r2 = 0.87).Our results suggest that p33ING1 mRNA levels may be used to predict the chemosensitivity of brain tumor cells to vincristine.

Published
2003

2. Overcoming cisplatin resistance: design of novel hydrophobic platinum compounds

Author

G, Tallen, C, Mock, S B, Gangopadhyay, B, Kangarloo, B, Krebs, and J E, Wolff

Subjects
Chemical Phenomena, DNA Repair, Molecular Structure, Organoplatinum Compounds, Brain Neoplasms, Chemistry, Physical, Antineoplastic Agents, Glioma, Fibroblasts, Structure-Activity Relationship, Cross-Linking Reagents, Drug Resistance, Neoplasm, Drug Design, Tumor Cells, Cultured, Humans, Benzimidazoles, Cisplatin, Drug Screening Assays, Antitumor, Medulloblastoma
Abstract

The anticancer activity of cisplatin derives from its ability to crosslink DNA. Cisplatin-resistance is partially caused by enhanced nucleotide excision repair (NER). Major 1,2-intrastrand crosslinks can create a hydrophobic notch at the damage site, which can be specifically bound by damage-recognition proteins, thus shielded from NER-activity. We aimed at preventing resistance by enhancing this mechanism using more hydrophobic platinum compounds.We synthesized three platinum analogs with increased hydrophobic characteristics. Performing MTT-assays, the efficacy of cisplatin and the novel agents was compared in a fibroblast and eight brain tumour cell lines.Among the novel compounds, the most hydrophobic molecule, methylpyridineplatinum, was most cytotoxic (LC50 = 5.84 x 10(-5) M), followed by methylpyrazineplatinum, the second most hydrophobic (LC50 = 1.79 x 10(-4) M), and pyridineplatinum (LC50 = 2.76 x 10(-4) M). Overall, cisplatin revealed highest cytotoxicity (LC50 = 8.77 x 10(-6) M).Comparison of the novel compounds supports the hypothesis that increased hydrophobicity contributes to higher antitumour-activity. Other advantageous characteristics of cisplatin might relate to its remaining highest efficacy.

Published
2000

3. Expression of p33ING1 mRNA and chemosensitivity in brain tumor cells.

Author

Tallen G, Riabowol K, and Wolff JE

Subjects
Biomarkers, Brain Neoplasms genetics, Brain Neoplasms metabolism, Cell Cycle Proteins, Cisplatin pharmacology, DNA Damage, DNA-Binding Proteins, Doxorubicin pharmacology, Enzyme Inhibitors pharmacology, Etoposide pharmacology, Fibroblasts metabolism, Genes, Tumor Suppressor, Glioma genetics, Glioma metabolism, Humans, Inhibitor of Growth Protein 1, Intracellular Signaling Peptides and Proteins, Medulloblastoma genetics, Medulloblastoma metabolism, Microtubules drug effects, Neoplasm Proteins biosynthesis, Nerve Tissue Proteins biosynthesis, Nerve Tissue Proteins genetics, Nuclear Proteins, Paclitaxel pharmacology, Predictive Value of Tests, Protein Biosynthesis, RNA, Messenger genetics, RNA, Neoplasm genetics, Topoisomerase I Inhibitors, Tumor Suppressor Proteins, Vincristine pharmacology, Brain Neoplasms pathology, Drug Resistance, Neoplasm genetics, Glioma pathology, Medulloblastoma pathology, Neoplasm Proteins genetics, Proteins genetics, RNA, Messenger biosynthesis, RNA, Neoplasm biosynthesis
Abstract

Background: Mutations and down-regulation of tumor suppressor genes can contribute to both tumorigenesis and chemotherapy resistance. The tumor suppressor p33ING1 has growth-inhibitory and pro-apoptotic effects recruiting p53 and it plays a role in DNA repair through interaction with PCNA. We questioned whether p33ING1 mRNA expression correlates with the chemosensitivity of brain tumor cells., Materials and Methods: Various malignant brain tumor cell lines were examined for their sensitivity to cisplatin, doxorubicin, etoposide and the antimitotic agents vincristine and paclitaxel by MTT-cytotoxicity assays. p33ING1 mRNA expression was determined by RT-PCR., Results: We found that, unlike other tumor types, ING1 levels were higher in glioma cell lines than in normal control cells. Medulloblastoma cells revealed the lowest ING1 expression of the lines tested. Comparing all cell lines, p33ING1 gene expression significantly (p = 0.028) correlated with resistance to vincristine (r2 = 0.87)., Conclusion: Our results suggest that p33ING1 mRNA levels may be used to predict the chemosensitivity of brain tumor cells to vincristine.

Published
2003

4. Overcoming cisplatin resistance: design of novel hydrophobic platinum compounds.

Author

Tallen G, Mock C, Gangopadhyay SB, Kangarloo B, Krebs B, and Wolff JE

Subjects
Antineoplastic Agents chemical synthesis, Benzimidazoles chemistry, Benzimidazoles pharmacology, Brain Neoplasms pathology, Chemical Phenomena, Chemistry, Physical, Cisplatin chemistry, Cross-Linking Reagents chemical synthesis, DNA Repair genetics, Drug Design, Drug Resistance, Neoplasm genetics, Drug Screening Assays, Antitumor, Fibroblasts drug effects, Glioma pathology, Humans, Medulloblastoma pathology, Molecular Structure, Organoplatinum Compounds chemistry, Organoplatinum Compounds pharmacology, Structure-Activity Relationship, Tumor Cells, Cultured drug effects, Antineoplastic Agents pharmacology, Benzimidazoles chemical synthesis, Cisplatin pharmacology, Cross-Linking Reagents pharmacology, Organoplatinum Compounds chemical synthesis
Abstract

Background: The anticancer activity of cisplatin derives from its ability to crosslink DNA. Cisplatin-resistance is partially caused by enhanced nucleotide excision repair (NER). Major 1,2-intrastrand crosslinks can create a hydrophobic notch at the damage site, which can be specifically bound by damage-recognition proteins, thus shielded from NER-activity. We aimed at preventing resistance by enhancing this mechanism using more hydrophobic platinum compounds., Methods: We synthesized three platinum analogs with increased hydrophobic characteristics. Performing MTT-assays, the efficacy of cisplatin and the novel agents was compared in a fibroblast and eight brain tumour cell lines., Results: Among the novel compounds, the most hydrophobic molecule, methylpyridineplatinum, was most cytotoxic (LC50 = 5.84 x 10(-5) M), followed by methylpyrazineplatinum, the second most hydrophobic (LC50 = 1.79 x 10(-4) M), and pyridineplatinum (LC50 = 2.76 x 10(-4) M). Overall, cisplatin revealed highest cytotoxicity (LC50 = 8.77 x 10(-6) M)., Conclusions: Comparison of the novel compounds supports the hypothesis that increased hydrophobicity contributes to higher antitumour-activity. Other advantageous characteristics of cisplatin might relate to its remaining highest efficacy.

Published
2000

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