his.sePublikasjoner
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Genetic analysis of susceptibility to endometrial adenocarcinoma in the BDII rat model
CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
Department of Animal Science, Medical School of Hannover, Hannover 30625, Germany.
CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
Department of Animal Science, Medical School of Hannover, Hannover 30625, Germany.
Vise andre og tillknytning
2005 (engelsk)Inngår i: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 158, nr 2, s. 137-141Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Most cancers are genetically complex and heterogeneous, a serious obstacle to identifying specific genes underlying the disease. If inbred animal models are used, then both the genetic constitution and environmental influences can be carefully controlled. Females of the BDII inbred rat strain are genetically predisposed to endometrial cancer; more than 90% of virgin BDII females will develop endometrial adenocarcinoma (EAC) during their life span. BDII females were crossed to males from inbred strains with low EAC incidence (SPRD or BN). When F1 males were backcrossed to BDII females to generate N1 populations of offspring, about one fourth of the female progeny developed EAC. With transmission disequilibrium test analysis, significant association was detected in three chromosomal regions (on RNO1, RNO11, and RNO17) in the SPRD crosses and in the short arm of RNO20 in the BN crosses. It appears that several susceptibility genes with minor but cooperating effects are responsible for the susceptibility. Furthermore, it seems clear from the interstrain crosses not only that the onset of tumors depends on the presence of susceptibility alleles from the EAC-prone BDII strain, but also that tumor development is affected by the contribution of a genetic component derived from the nonsusceptible strains.

sted, utgiver, år, opplag, sider
Elsevier, 2005. Vol. 158, nr 2, s. 137-141
HSV kategori
Forskningsprogram
Medicin
Identifikatorer
URN: urn:nbn:se:his:diva-1667DOI: 10.1016/j.cancergencyto.2004.08.034ISI: 000228500200005PubMedID: 15796960Scopus ID: 2-s2.0-15744370918OAI: oai:DiVA.org:his-1667DiVA, id: diva2:31943
Tilgjengelig fra: 2007-08-08 Laget: 2007-08-08 Sist oppdatert: 2017-12-12bibliografisk kontrollert

Open Access i DiVA

Fulltekst mangler i DiVA

Andre lenker

Forlagets fulltekstPubMedScopus

Personposter BETA

Klinga-Levan, Karin

Søk i DiVA

Av forfatter/redaktør
Klinga-Levan, Karin
Av organisasjonen
I samme tidsskrift
Cancer Genetics and Cytogenetics

Søk utenfor DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric

doi
pubmed
urn-nbn
Totalt: 395 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf