oru.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Deletion polymorphism of the UGT2B17 gene is associated with increased risk for prostate cancer and correlated to gene expression in the prostate
Örebro University, School of Health and Medical Sciences.
Show others and affiliations
2008 (English)In: The Pharmacogenomics Journal, ISSN 1470-269X, E-ISSN 1473-1150, Vol. 8, no 2, p. 147-151Article in journal (Refereed) Published
Abstract [en]

Metabolism of androgens includes glucuronidation, the major pathway of steroid elimination in several steroid target tissues. Glucuronidation is catalysed by UDP-glucuronosyltransferases (UGTs). UGT2B17 has been shown to be particularly active against androgens and is highly abundant in the prostate. Recently, we discovered that deletion of the UGT2B17 gene is associated with low or undetectable urinary testosterone levels. Here, we determined the phenotypic outcome of the deletion by quantifying the UGT2B17 mRNA expression in normal prostate tissues in individuals with different genotypes. Additionally, the frequency of UGT2B17 deletion polymorphism was studied in a Swedish population-based case–control study including 176 patients diagnosed with prostate cancer and 161 controls. We found that the individuals homozygous for the insertion allele expressed 30 times more UGT2B17 mRNA in prostate tissue than the heterozygotes. Carriers of the deletion allele had a significantly increased risk of prostate cancer (OR=2.07; 95% CI=1.32–3.25). In conclusion, these results show the UGT2B17 deletion polymorphism is associated with prostate cancer risk. 

Place, publisher, year, edition, pages
Avenet, NJ: Nature Pub. Group , 2008. Vol. 8, no 2, p. 147-151
Keywords [en]
Aged, Androgens/metabolism, Case-Control Studies, Gene Deletion, Gene Expression Regulation; Enzymologic, Gene Expression Regulation; Neoplastic, Gene Frequency, Genetic Predisposition to Disease, Glucuronosyltransferase/analysis/*genetics, Homozygote, Humans, Male, Middle Aged, Odds Ratio, Phenotype, Polymerase Chain Reaction, Prostate/*enzymology, Prostatic Neoplasms/enzymology/*genetics, RNA; Messenger/analysis, Risk Assessment, Risk Factors, Sweden, Up-Regulation
National Category
Pharmaceutical Sciences Medical and Health Sciences Cancer and Oncology Medical Genetics
Research subject
Medical Genetics
Identifiers
URN: urn:nbn:se:oru:diva-3672DOI: 10.1038/sj.tpj.6500449PubMedID: 17387331OAI: oai:DiVA.org:oru-3672DiVA, id: diva2:137970
Available from: 2008-12-17 Created: 2008-12-17 Last updated: 2018-01-13Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=17387331&dopt=Citation

Authority records BETA

Andersson, Swen-Olof

Search in DiVA

By author/editor
Andersson, Swen-Olof
By organisation
School of Health and Medical Sciences
In the same journal
The Pharmacogenomics Journal
Pharmaceutical SciencesMedical and Health SciencesCancer and OncologyMedical Genetics

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 45 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf