Abstract
Enhanced expression of the nucleotide excision repair gene XPA is associated with resistance to cisplatin treatment in human ovarian cancer. Understanding the cause of enhanced XPA expression will provide new molecular targets for therapy directed at overcoming chemoresistance. Enhanced gene expression in cancer cells is often caused by mutations or gene amplification. Molecular analyses of the XPA genes in human ovarian cancers indicate that gene mutation and amplification are not the cause of enhanced XPA mRNA levels in ovarian cancers overexpressing XPA. Altered nucleotide excision repair (NER) gene regulation in chemoresistant tumors is discussed.
MeSH terms
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Antineoplastic Agents / pharmacology
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Cisplatin / pharmacology
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / metabolism
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Drug Resistance, Neoplasm / genetics
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Female
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Gene Amplification*
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Humans
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Mutation / genetics*
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Neoplasm Proteins / genetics*
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Neoplasm Proteins / metabolism
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Ovarian Neoplasms / genetics*
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Ovarian Neoplasms / metabolism
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Polymorphism, Single-Stranded Conformational
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RNA, Messenger / genetics
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RNA, Messenger / metabolism*
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Tumor Suppressor Protein p53 / metabolism
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Xeroderma Pigmentosum Group A Protein
Substances
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Antineoplastic Agents
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DNA-Binding Proteins
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Neoplasm Proteins
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RNA, Messenger
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Tumor Suppressor Protein p53
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XPA protein, human
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Xeroderma Pigmentosum Group A Protein
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Cisplatin