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We have demonstrated recently that the binding of furosemide (FSM) to urinary proteins causes a decrease in the diuretic response that is proportional to the degree of proteinuria. Further studies were conducted to determine whether urinary drug-protein interactions also altered the renal excretion of FSM. Rats were treated with puromycin aminonucleoside to(More)
The inhibition of apoptosis is generally believed to be a major determinant of resistance to chemotherapy. However, recent findings have shown that caspase inhibitors do not protect cancer cells from death by cytotoxic agents, but may switch drug-induced apoptosis to an alternative 'default death'. The primary goals of this study were to determine the major(More)
MDR1 hypermethylation plays an important role in pathogenesis and progression of neuroblastoma tumors. This hypothesis was tested by studying the methylation status of MDR1 gene promoter in neureoblastoma biopsy specimens during the progression of tumor from stage-1 to stage-4. Results of our findings demonstrate an inverse correlation between the(More)
Irreversible growth arrest (also called senescence) has emerged recently as a tumor suppressor mechanism and a key determinant of cancer chemotherapy outcome. Previous work from our laboratory suggested that the cellular ability to undergo or to escape senescence dictates its fate to become drug-sensitive or drug-resistant, respectively. In the present(More)
The present study was undertaken to determine the significance of histone acetylation versus DNA damage in drug-induced irreversible growth arrest (senescence) and apoptosis. Cellular treatment with the DNA-damaging drugs doxorubicin and cisplatin or with the histone deacetylase inhibitor trichostatin A, led to the finding that all the three drugs induced(More)
Resistance to cytotoxic agents is a major limitation for their clinical use to treat human cancers. Tumors become resistant to chemotherapy when a subset of cells undergoes molecular changes leading to overexpression of drug transport proteins, alterations in drug-target interactions or reduced ability to commit apoptosis. However, such changes may not be(More)