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dc.contributor.authorKnappskog, Stian
dc.contributor.authorGansmo, Liv Beathe
dc.contributor.authorRomundstad, Pål Richard
dc.contributor.authorBjørnslett, Merete Pauline
dc.contributor.authorTrovik, Jone
dc.contributor.authorSommerfelt-Pettersen, Jan
dc.contributor.authorLøkkevik, Erik
dc.contributor.authorTollenaar, Rob A.E.M.
dc.contributor.authorSeynaeve, Caroline
dc.contributor.authorDevilee, Peter
dc.contributor.authorSalvesen, Helga Birgitte
dc.contributor.authorDørum, Anne
dc.contributor.authorHveem, Kristian
dc.contributor.authorVatten, Lars Johan
dc.contributor.authorLønning, Per Eystein
dc.date.accessioned2015-10-30T12:03:36Z
dc.date.accessioned2015-11-25T12:18:23Z
dc.date.available2015-10-30T12:03:36Z
dc.date.available2015-11-25T12:18:23Z
dc.date.issued2012
dc.identifier.citationPLoS ONE 2012, 7(4)nb_NO
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/11250/2365723
dc.description.abstractThe MDM2 proto-oncogene plays a key role in central cellular processes like growth control and apoptosis, and the gene locus is frequently amplified in sarcomas. Two polymorphisms located in the MDM2 promoter P2 have been shown to affect cancer risk. One of these polymorphisms (SNP309T>G; rs2279744) facilitates Sp1 transcription factor binding to the promoter and is associated with increased cancer risk. In contrast, SNP285G>C (rs117039649), located 24 bp upstream of rs2279744, and in complete linkage disequilibrium with the SNP309G allele, reduces Sp1 recruitment and lowers cancer risk. Thus, fine tuning of MDM2 expression has proven to be of significant importance with respect to tumorigenesis. We assessed the potential functional effects of a third MDM2 promoter P2 polymorphism (SNP344T>A; rs1196333) located on the SNP309T allele. While in silico analyses indicated SNP344A to modulate TFAP2A, SPIB and AP1 transcription factor binding, we found no effect of SNP344 status on MDM2 expression levels. Assessing the frequency of SNP344A in healthy Caucasians (n = 2,954) and patients suffering from ovarian (n = 1,927), breast (n = 1,271), endometrial (n = 895) or prostatic cancer (n = 641), we detected no significant difference in the distribution of this polymorphism between any of these cancer forms and healthy controls (6.1% in healthy controls, and 4.9%, 5.0%, 5.4% and 7.2% in the cancer groups, respectively). In conclusion, our findings provide no evidence indicating that SNP344A may affect MDM2 transcription or cancer risk.nb_NO
dc.language.isoengnb_NO
dc.publisherPublic Library of Sciencenb_NO
dc.titleMDM2 Promoter SNP344T>A (rs1196333) Status Does Not Affect Cancer Risknb_NO
dc.typeJournal articlenb_NO
dc.typePeer revieweden_GB
dc.date.updated2015-10-30T12:03:36Z
dc.source.volume7nb_NO
dc.source.journalPLoS ONEnb_NO
dc.source.issue4nb_NO
dc.identifier.doi10.1371/journal.pone.0036263
dc.identifier.cristin946589
dc.description.localcode© 2012 Knappskog et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.nb_NO


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