k-FGF protoncogene expression is associated with murine testicular teratogenesis, but is not involved during mouse testicular development

dc.contributor.author
Anta i Vinyals, Josep Maria de
dc.contributor.author
Monzó Planella, Mariano
dc.contributor.author
Peris, B.
dc.contributor.author
Ruano Gil, Domingo
dc.date.issued
2016-12-02T09:07:16Z
dc.date.issued
2016-12-02T09:07:16Z
dc.date.issued
1997-01
dc.date.issued
2016-12-02T09:07:21Z
dc.identifier
0213-3911
dc.identifier
https://hdl.handle.net/2445/104402
dc.identifier
110526
dc.identifier
9046041
dc.description.abstract
A l'article en PDF consta com a vol.11 (1996)
dc.description.abstract
The k-FGF gene, which belongs to the family of the fibroblast growth factor genes, is implicated in tumoral and developmental processes. It is expressed in embryonal carcinoma cells, in embryonic stem cells, during limb and tooth formation and in some germ cell tumors. However, the expression of this protooncogene during testicular development as well its relationship to spontaneous teratogenesis have not been determined. Here we investigate k-FGF xpression during testicular development in mice, as well as in a spontaneous testicular teratoma (STT) and in the OTT6050 teratocarcinoma (TC) by Northern blotting, RT-PCR and in situ hybridization. Severa1 data indicate that k-FGF gene contains downstream regulatory sequences which bind octamer factors. One of these transcription factors which binds to k-FGF enhancer is Oct-4. Although the k-FGF gene is activated by Oct-4 in embryonal carcinoma and embryonic stem cells and Oct-4 is expressed in the germ cells of the embryo, our results indicate that there is no detectable k-FGF expression in mouse testicular germ cells at any stage of development. This indicates that Oct-4 does not activate transcription of the k-FGF gene in mouse germ cells, and that k-FGF is not implicated during testicular development. We also show that there is a high k-FGF expression in the experimental OTT6050 TC, but only very low levels in a murine differentiated STT, suggesting that k-FGF activation may be responsible for the genesis and development of STT, behaving as a marker of malignancy in these neoplasms.
dc.format
10 p.
dc.format
application/pdf
dc.language
eng
dc.publisher
Universidad de Murcia
dc.relation
Reproducció del document publicat a: https://digitum.um.es/xmlui/bitstream/10201/18914/1/kFGF%20protoncogene%20expression%20is%20associated%20with%20murine%20testicular%20teratogenesis%20but%20is%20not%20involved%20during%20mouse%20testicular%20development.pdf
dc.relation
Histology and Histopathology, 1997, vol. 12, num. 1, p. 32-41
dc.rights
cc-by-nc-nd (c) Universidad de Murcia, 1997
dc.rights
http://creativecommons.org/licenses/by-nc-nd/3.0/es
dc.rights
info:eu-repo/semantics/openAccess
dc.source
Articles publicats en revistes (Patologia i Terapèutica Experimental)
dc.subject
Teratoma
dc.subject
Rates (Animals de laboratori)
dc.subject
Múrids
dc.subject
Malalties del testicle
dc.subject
Gens
dc.subject
Oncogens
dc.subject
Tumors
dc.subject
RNA
dc.subject
Càncer
dc.subject
Teratoma
dc.subject
Rats as laboratory animals
dc.subject
Muridae
dc.subject
Testis diseases
dc.subject
Genes
dc.subject
Oncogenes
dc.subject
Tumors
dc.subject
RNA
dc.subject
Cancer
dc.title
k-FGF protoncogene expression is associated with murine testicular teratogenesis, but is not involved during mouse testicular development
dc.type
info:eu-repo/semantics/article
dc.type
info:eu-repo/semantics/publishedVersion


Ficheros en el ítem

FicherosTamañoFormatoVer

No hay ficheros asociados a este ítem.