rdf:type |
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0023907,
umls-concept:C0026336,
umls-concept:C0033414,
umls-concept:C0126033,
umls-concept:C0162508,
umls-concept:C0185117,
umls-concept:C0227525,
umls-concept:C0332325,
umls-concept:C0449258,
umls-concept:C1512409,
umls-concept:C1882726,
umls-concept:C2911684
|
pubmed:issue |
1-2
|
pubmed:dateCreated |
1996-6-14
|
pubmed:abstractText |
During promotion in the RH-model, the mRNA expression of c-jun and LRF-1 was 2- to 8-fold elevated in both initiated and uninitiated rats receiving 2-AAF. The increase was more pronounced in male than in female rats, and GH treatment of male rats down-regulated the expression towards the level in females. The level in uninitiated 2-AAF-treated livers was as high as in isolated early nodules. jun-B also showed 3- to 8-fold increased expression, but without sex differences. An increased nuclear transcription of the LRF-1 and jun-B genes but not of c-jun was observed. During progression, LRF-1 and ets-2 showed a 2- to 3-fold higher expression in persistent nodules and hepatocellular carcinomas than in the corresponding surrounding liver tissues, whereas the expression of the jun genes was 3- to 4-fold increased both in lesions and in surrounding livers when compared to age-matched control rats. In conclusion, while the changes during promotion might not be connected with control of early focal growth, the increased levels of LRF-1 and ets-2 in advanced lesions might indicate that these genes could contribute to the growth advantage for persistent nodules during progression.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-Acetylaminofluorene,
http://linkedlifedata.com/resource/pubmed/chemical/Activating Transcription Factor 3,
http://linkedlifedata.com/resource/pubmed/chemical/Carcinogens,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/ERF protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ets2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Protein c-ets-2,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/liver regeneration factor 1
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
0304-3835
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
27
|
pubmed:volume |
100
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
215-21
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:8620444-2-Acetylaminofluorene,
pubmed-meshheading:8620444-Activating Transcription Factor 3,
pubmed-meshheading:8620444-Animals,
pubmed-meshheading:8620444-Carcinogens,
pubmed-meshheading:8620444-DNA-Binding Proteins,
pubmed-meshheading:8620444-Disease Models, Animal,
pubmed-meshheading:8620444-Disease Progression,
pubmed-meshheading:8620444-Female,
pubmed-meshheading:8620444-Gene Expression,
pubmed-meshheading:8620444-Genes, jun,
pubmed-meshheading:8620444-Liver,
pubmed-meshheading:8620444-Liver Neoplasms, Experimental,
pubmed-meshheading:8620444-Male,
pubmed-meshheading:8620444-Proto-Oncogene Protein c-ets-2,
pubmed-meshheading:8620444-Proto-Oncogene Proteins,
pubmed-meshheading:8620444-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:8620444-Rats,
pubmed-meshheading:8620444-Rats, Wistar,
pubmed-meshheading:8620444-Repressor Proteins,
pubmed-meshheading:8620444-Trans-Activators,
pubmed-meshheading:8620444-Transcription Factors
|
pubmed:year |
1996
|
pubmed:articleTitle |
Expression of the c-jun, jun-B, ets-2 and liver regeneration factor-1 (LRF-1) genes during promotion and progression of rat liver carcinogenesis in the resistant hepatocyte model.
|
pubmed:affiliation |
Department of Medical Nutrition, Karolinska Institute, Huddinge University Hospital, Sweden.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|