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• W2234454054 abstract "Renal cell carcinoma represents about 3% of malignant neoplasms in adults, but is among the most treatment-refractory human malignancies. Neither surgery, nor radiation therapy or chemotherapy have a significant impact on the outcome of this disease. Thus, these poor results indicate a need to evaluate alternative forms of treatment for this malignancy. The epipodophyllotoxin etoposide has a broad activity spectrum that includes various hematological and solid tumors in both children and adults. These agent act by inhibiting the nuclear enzyme topoisomerase II. Recent in vitro studies demonstrated that the antitumor activity of epipodophyllotoxins are highly schedule-dependent, improving with more frequent and extended administration schedules instead of as one high dose at once. Employing this concept in the clinic, encouraging response rates have been noted in (etoposide-) pretreated patients that received daily repeated doses. Unfortunately, early experimental studies with this agent against advanced renal cell carcinoma showed no significant antitumor activity. For this reason, its drug sister, teniposide, although having a comparable activity spectrum as etoposide, is still an investigational anticancer agent, since no studies have been performed to assess the impact of schedule alterations on teniposide’s efficacy in this disease. Available data with cultured tumor cells showed about a ten times greater potency of teniposide when compared to etoposide, which is possibly due to better cellular retention. Moreover, teniposide has been suggested to be selectively retained by tumor cells when compared to normal cells. These features, together with the greater efficacy of etoposide with more prolonged administration schedules, led us to assess teniposide in this study at diverse schedules for its potential antitumor efficacy in an in vitro model of advanced renal cell carcinoma, a characteristically drug-resistant tumor. We used three human kidney carcinoma cell lines, RXF-393, A498, and TK-10, that were incubated with IC50 concentrations of teniposide in the absence or presence of agents that inhibited the function of P-glycoprotein, an efflux pump that exports drugs from the interior of cells, rendering them so–called ‘multidrug resistance’. We also examined whether the growth-inhibitory effect of teniposide could be further improved by biochemical modulation, employing the DNA polymerase αinhibiting agent aphidicolin glycinate (0.2 μM); or the ribonucletide reductase-inhibiting agent hydroxyurea (200 μM), following a 24 h pre-treatment with the latter agents at these same lowly cytotoxic concentrations. Cellular responses were assessed with the SRB method. When compared to short-term exposure or fragmented exposure, continuous exposure improved teniposide cytotoxicity significantly, suggesting that the growth inhibitory effects of teniposide is highly schedule-dependent. Consequently, we showed a increasing amount of DNA damage in all three cell lines upon continuous exposure. Interestingly, no differences in topoisomerase II activity was observed in the various administration schedules of teniposide, neither in the number of DNA-topoisomerase II complexes. Indeed, our data show that the" @default.
• W2234454054 created "2016-06-24" @default.
• W2234454054 creator A5004756380 @default.
• W2234454054 date "2000-01-01" @default.
• W2234454054 modified "2023-09-27" @default.
• W2234454054 title "EFEITOS CITOTÓXICOS DO TENIPOSIDE, UM DERIVADO SEMI-SINTÉTICO DAS EPIPODOFILOTOXINAS, SOBRE LINHAGENS CELULARES DE CARCINOMA RENAL HUMANO" @default.
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