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									<identifier>oai:www.peertechzpublications.org:10.17352/gjct.000001</identifier>
									<datestamp>2015-01-07</datestamp>
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										<dc:title>
										Genetic Polymorphisms and Cisplatin- Related Nephrotoxicity
										</dc:title><dc:creator>Arundhati Bag</dc:creator><dc:creator> Lalit Mohan Jeena</dc:creator><dc:creator>Niladri Bag</dc:creator><dc:description>&lt;p&gt;Cis- diamminedichloroplatinum (cisplatin) is one of the most commonly used present day hemotherapeutic agents. It is used to treat a wide range of cancers including head and neck, lung, gastrointestinal tract, ovarian and genitourinary cancers. However, dose- limiting toxicity is often associated with cisplatin. It is known that cisplatin works more effectively with dose escalation, but significant risk for nephrotoxicity is often associated with higher doses [1]. &lt;br&gt;&lt;/p&gt;&lt;p&gt;Recovery of renal function occurs over a period of 2-4 weeks, although lack of recovery can also take place [2]. Kidney accumulates cisplatin in much higher concentration in comparison to other organs and is the major route of its excretion [3]. Five times higher cisplatin concentration was observed in proximal tubular epithelial cells in comparison to serum [4]. Highest accumulation of cisplatin occurs in S3 segment of proximal tubule followed by the distal collecting tubule and the S1 segment of proximal tubule [5]. Cisplatin nephrotoxicity may be presented in various ways of which the most serious presentation is acute kidney injury, which occurs in 20-30% of patients despite hyperhydration and forced Diuresis [6].&lt;/p&gt;</dc:description>
										<dc:publisher>Global Journal of Cancer Therapy - Peertechz Publications</dc:publisher>
										<dc:date>2015-01-07</dc:date>
										<dc:type>Review Article</dc:type>
										<dc:identifier>https://doi.org/10.17352/gjct.000001</dc:identifier>
										<dc:language>en</dc:language>
										<dc:rights>Copyright © Arundhati Bag et al.</dc:rights>
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