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dc.contributor.authorPaige, Adam J.W.en_GB
dc.contributor.authorBrown, Roberten_GB
dc.date.accessioned2012-06-14T11:37:51Z
dc.date.available2012-06-14T11:37:51Z
dc.date.issued2008-12
dc.identifier.citationPaige, A.J.W., Brown, R. (2008) 'Pharmaco(epi)genomics in ovarian cancer' Pharmacogenomics 9 (12):1825-1834en_GB
dc.identifier.issn1744-8042
dc.identifier.pmid19072641
dc.identifier.doi10.2217/14622416.9.12.1825
dc.identifier.urihttp://hdl.handle.net/10547/228927
dc.description.abstractOvarian cancer shows considerable variability in its chemoresponse, however, the prospect of individualized medicine holds high hopes for improving patient survival. The influence of interindividual genomic polymorphisms on drug response (pharmacogenomics) is well established, and a variety of candidate loci in ovarian tumors have been identified, including ERCC1, ABCB1 and p53 variants. Recently pharmacoepigenomic modulators of key genes and pathways, such as promoter methylation (MLH1 and BRCA1 genes) and microRNA regulation (PTEN/AKT and NF-kappaB pathways) have been implicated in ovarian cancer chemoresponse. Epigenomic studies have until now mainly focused on tumor-specific changes, although germ-line epigenetic change may also be of importance. However, assessing the relevance of these potential pharmaco(epi)genomic biomarkers in clinical trials requires well powered studies in homogeneous populations, with independent validation sets, to distinguish real associations from false-positives. In addition, the selection of one gene or locus as having sufficient phenotypic effect to impact on clinical outcome may be an oversimplification. Integrated approaches that identify stable pharmacogenomic and epigenomic patterns and their relationship with expression patterns and gene function will be increasingly necessary.
dc.language.isoenen
dc.publisherFuture Medicineen_GB
dc.relation.urlhttps://www.futuremedicine.com/doi/abs/10.2217/14622416.9.12.1825?rfr_dat=cr_pub%3Dpubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&journalCode=pgsen_GB
dc.subject.meshAntineoplastic Combined Chemotherapy Protocols
dc.subject.meshDrug Resistance, Neoplasm
dc.subject.meshEpigenesis, Genetic
dc.subject.meshFemale
dc.subject.meshGenetic Markers
dc.subject.meshHumans
dc.subject.meshOvarian Neoplasms
dc.subject.meshPharmacogenetics
dc.titlePharmaco(epi)genomics in ovarian cancer.en
dc.typeArticleen
dc.contributor.departmentImperial Collegeen_GB
dc.identifier.journalPharmacogenomicsen_GB
html.description.abstractOvarian cancer shows considerable variability in its chemoresponse, however, the prospect of individualized medicine holds high hopes for improving patient survival. The influence of interindividual genomic polymorphisms on drug response (pharmacogenomics) is well established, and a variety of candidate loci in ovarian tumors have been identified, including ERCC1, ABCB1 and p53 variants. Recently pharmacoepigenomic modulators of key genes and pathways, such as promoter methylation (MLH1 and BRCA1 genes) and microRNA regulation (PTEN/AKT and NF-kappaB pathways) have been implicated in ovarian cancer chemoresponse. Epigenomic studies have until now mainly focused on tumor-specific changes, although germ-line epigenetic change may also be of importance. However, assessing the relevance of these potential pharmaco(epi)genomic biomarkers in clinical trials requires well powered studies in homogeneous populations, with independent validation sets, to distinguish real associations from false-positives. In addition, the selection of one gene or locus as having sufficient phenotypic effect to impact on clinical outcome may be an oversimplification. Integrated approaches that identify stable pharmacogenomic and epigenomic patterns and their relationship with expression patterns and gene function will be increasingly necessary.


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