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Anticancer Res ; 31(5): 1653-8, 2011 May.
Article in English | MEDLINE | ID: mdl-21617223

ABSTRACT

BACKGROUND: Deletions or mutations of the phosphatase and tensin homolog (PTEN) are frequently observed in malignant glioma and are responsible for progression of the disease. Since the molecule is a promising target for gene therapy, the effects of PTEN on glioma proliferation in combination with the anti-neoplastic agent, temozolomide, and ionizing radiation were investigated. MATERIALS AND METHODS: An adenoviral vector encoding PTEN was used. After infection, changes in proliferation, the cell cycle, as well as drug- and radiosensitivity were investigated. RESULTS: Expression of PTEN led to a 1.21-fold prolongation of the doubling time of the cells. It reduced G(1) and increased G(2)/M populations. Forced PTEN expression conferred sensitivity to temozolomide and/or ionizing radiation. CONCLUSION: In addition to counteracting cell proliferation, expression of PTEN presented advantages in the chemo- and radiosensitivity of glioma cells. Methods for up-regulation of PTEN may have a role in increasing the efficacy of current adjuvant therapies.


Subject(s)
Brain Neoplasms/therapy , Dacarbazine/analogs & derivatives , Glioma/therapy , PTEN Phosphohydrolase/metabolism , Radiation Tolerance , Radiation, Ionizing , Adenoviridae/genetics , Antineoplastic Agents, Alkylating/pharmacology , Apoptosis/drug effects , Apoptosis/radiation effects , Blotting, Western , Brain Neoplasms/pathology , Cell Cycle/drug effects , Cell Cycle/radiation effects , Cell Proliferation/drug effects , Cell Proliferation/radiation effects , Combined Modality Therapy , Dacarbazine/pharmacology , Genetic Therapy , Glioma/pathology , Humans , PTEN Phosphohydrolase/genetics , Temozolomide , Tumor Cells, Cultured
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