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Anticancer Res ; 31(5): 1653-8, 2011 May.
Artículo en Inglés | MEDLINE | ID: mdl-21617223

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.


Asunto(s)
Neoplasias Encefálicas/terapia , Dacarbazina/análogos & derivados , Glioma/terapia , Fosfohidrolasa PTEN/metabolismo , Tolerancia a Radiación , Radiación Ionizante , Adenoviridae/genética , Antineoplásicos Alquilantes/farmacología , Apoptosis/efectos de los fármacos , Apoptosis/efectos de la radiación , Western Blotting , Neoplasias Encefálicas/patología , Ciclo Celular/efectos de los fármacos , Ciclo Celular/efectos de la radiación , Proliferación Celular/efectos de los fármacos , Proliferación Celular/efectos de la radiación , Terapia Combinada , Dacarbazina/farmacología , Terapia Genética , Glioma/patología , Humanos , Fosfohidrolasa PTEN/genética , Temozolomida , Células Tumorales Cultivadas
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