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Tumors caused by overexpression and forced activation of Stat5 in mammary epithelial cells of transgenic mice are parity-dependent and developed in aged, postestropausal females
Year:
2007
Source of publication :
International Journal of Cancer
Authors :
Barash, Itamar
;
.
Eilon, Tali
;
.
Volume :
121
Co-Authors:
Eilon, T., Institute of Animal Science, ARO, Volcani Center, Bet-Dagan, Israel
Groner, B., Georg Speyer Haus, Institute for Biomedical Research, Frankfurt/M, Germany
Barash, I., Institute of Animal Science, ARO, Volcani Center, Bet-Dagan, Israel, Institute of Animal Science, ARO, Volcani Center, P.O. Box 6, Bet-Dagan 50250, Israel
Facilitators :
From page:
1892
To page:
1902
(
Total pages:
11
)
Abstract:
In transgenic mice overexpressing Stat5 or a constitutively activated Stat5 variant (STAT5ca), we show for the first time that parity is required for the development of tumors in postestropausal females. Tumors were detected in glands of multiparous transgenic female mice after latency period of 14 months, but rarely in their age-matched virgin (AMV) counterparts. This period was not affected by distinguishable tumor pathologies and was not dependent upon transgenic Stat5 variant. To associate Stat5 deregulation, parity and the postestropausal tumor occurrence with mammary cancer formation, the activities of endogenous and transgenic Stat5 were measured in the glands of aged multiparous and AMV females. No differences in phosphorylated Stat5 (pStat5) levels were found between the 2 cohorts. However, promoter sequences comprising the Stat5 binding sites from the cyclin D1 or the bcl-x genes associate differentially with acetylated histone H4 in aged multiparous and AMV STAT5ca transgenic females. Individual epithelial cells varied greatly with respect to the presence of nuclear pStat5. A small subset of epithelial cells, in which pStat5 and cyclin D1 were co-expressed, was exclusively present in the multiparous glands. Changes in chromatin structure might persist past the reproductive life time of the multiparous mice and contribute to the transcription of the cyclin D1 gene by activated Stat5. This may cause the detectable expression of cyclin D1 and add to the process of tumorigenesis. © 2007 Wiley-Liss, Inc.
Note:
Related Files :
aging
animal experiment
animal model
Animals
breast tumor
Cancer
Female
mice
phenotype
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Related Content
More details
DOI :
10.1002/ijc.22954
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
21443
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:44
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Scientific Publication
Tumors caused by overexpression and forced activation of Stat5 in mammary epithelial cells of transgenic mice are parity-dependent and developed in aged, postestropausal females
121
Eilon, T., Institute of Animal Science, ARO, Volcani Center, Bet-Dagan, Israel
Groner, B., Georg Speyer Haus, Institute for Biomedical Research, Frankfurt/M, Germany
Barash, I., Institute of Animal Science, ARO, Volcani Center, Bet-Dagan, Israel, Institute of Animal Science, ARO, Volcani Center, P.O. Box 6, Bet-Dagan 50250, Israel
Tumors caused by overexpression and forced activation of Stat5 in mammary epithelial cells of transgenic mice are parity-dependent and developed in aged, postestropausal females
In transgenic mice overexpressing Stat5 or a constitutively activated Stat5 variant (STAT5ca), we show for the first time that parity is required for the development of tumors in postestropausal females. Tumors were detected in glands of multiparous transgenic female mice after latency period of 14 months, but rarely in their age-matched virgin (AMV) counterparts. This period was not affected by distinguishable tumor pathologies and was not dependent upon transgenic Stat5 variant. To associate Stat5 deregulation, parity and the postestropausal tumor occurrence with mammary cancer formation, the activities of endogenous and transgenic Stat5 were measured in the glands of aged multiparous and AMV females. No differences in phosphorylated Stat5 (pStat5) levels were found between the 2 cohorts. However, promoter sequences comprising the Stat5 binding sites from the cyclin D1 or the bcl-x genes associate differentially with acetylated histone H4 in aged multiparous and AMV STAT5ca transgenic females. Individual epithelial cells varied greatly with respect to the presence of nuclear pStat5. A small subset of epithelial cells, in which pStat5 and cyclin D1 were co-expressed, was exclusively present in the multiparous glands. Changes in chromatin structure might persist past the reproductive life time of the multiparous mice and contribute to the transcription of the cyclin D1 gene by activated Stat5. This may cause the detectable expression of cyclin D1 and add to the process of tumorigenesis. © 2007 Wiley-Liss, Inc.
Scientific Publication
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