RESUMEN
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.