Publications by authors named "Giselle Pinto de Faria"

Laryngeal squamous cell carcinoma (LSCC) is the most common among several types of head and neck cancers. Current treatments have a poor effect on early and advanced cases, and further investigations for novel agents against LSCCs are desirable. In this study, we elucidate the cytotoxic enhancing effect of arsenic trioxide (As2O3) combined with L-buthionine sulfoximine (BSO) in LSCC.

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Multidrug resistance in gliomas is the major challenges in the clinical setting. We investigated the expression of P-glycoprotein (Pgp) and multidrug resistance-related protein 1 (MRP1) in 50 gliomas using immunohistochemistry. Compared to Pgp, MRP1 positivity was observed in highest percentage of gliomas grade IV samples (p = 0.

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The search for new drugs and treatment approaches is of particular importance for glioblastomas (GBMs), as with other types of malignant gliomas, as they are lethal without the available medical care. Current anticancer cocktails have failed to prolong survival beyond 1 year, in part owing to the natural resistance of GBM cells and to the toxic side effects of the available drugs. In many organisms, cell death can be induced by cytolysins, which are proteins that can form pores in biological membranes.

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The harmonious development of the central nervous system depends on the interactions of the neuronal and glial cells. Extracellular matrix elements play important roles in these interactions, especially laminin produced by astrocytes, which has been shown to be a good substrate for neuron growth and axonal guidance. Glioblastomas are the most common subtypes of primary brain tumors and may be astrocytes in origin.

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Background: One of the best characterized resistance mechanisms of leukemias is multidrug resistance (MDR) mediated by P-glycoprotein (Pgp) and multidrug-resistant related protein (MRP). In addition to Pgp and MRP, p53 mutation or inactivation might play a relevant role in therapeutic failure. Some studies have demonstrated that Pgp and MRP may be activated in association with overexpression of mutant or inactivated p53 protein.

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