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Stat5 in breast cancer: Potential oncogenic activity coincides with positive prognosis for the disease
Year:
2012
Source of publication :
Carcinogenesis
Authors :
Barash, Itamar
;
.
Volume :
33
Co-Authors:
Barash, I., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Ireland
Facilitators :
From page:
2320
To page:
2325
(
Total pages:
6
)
Abstract:
Nuclear localization of signal transducer and activator of transcription (Stat) 5 marks good prognosis in estrogen receptor/progesterone receptor-positive breast tumors. This positive characteristic is counteracted by studies in laboratory animals demonstrating that deregulated Stat5 activity may convert proper mammary development into a latent oncogenic process. Tumorigenesis is initiated during the parity cycles, most probably during pregnancy, when the activated Stat5 antagonizes or manipulates parity's protective mechanisms. For example, it can alter the differentiation/proliferation balance, induce growth hormone signaling, cause specific alteration in chromatin structure, inhibit tumor-suppressor activity and induce DNA damage that counteracts the enhanced DNA-damage response exerted by parity. Palpable tumors develop after a latent period from individual cells. This happens in the estropausal period in transgenic mice maintaining deregulated Stat5 activity in the mammary gland, or during involution, months after transplantation of transfected cells with constitutively active Stat5. Candidate vulnerable cells are those which maintain high nuclear Stat5 activity. Due to the hazardous outcome of deregulated Stat5 activity in these cells, such as induced DNA damage or high cyclin D1 activity, the gland is prone to transformation. The developing tumors are mostly adenocarcinomas or their subtypes. They are estrogen receptor-positive and maintain a specific Stat5 gene signature that allows tracking their inducer. From a clinical point of view, deregulated Stat5 activity represents a genuine risk factor for breast cancer. Monitoring Stat5 activity during vulnerable periods and developing specific tools for its suppression in breast epithelial cells could potentially limit new incidence of the disease. © The Author 2012. Published by Oxford University Press. All rights reserved.
Note:
Related Files :
Animals
apoptosis
Cell Proliferation
Female
gene expression
lactation
pregnancy
Review
Show More
Related Content
More details
DOI :
10.1093/carcin/bgs362
Article number:
Affiliations:
Database:
Scopus
Publication Type:
Review
;
.
Language:
English
Editors' remarks:
ID:
19538
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:29
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Scientific Publication
Stat5 in breast cancer: Potential oncogenic activity coincides with positive prognosis for the disease
33
Barash, I., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Ireland
Stat5 in breast cancer: Potential oncogenic activity coincides with positive prognosis for the disease
Nuclear localization of signal transducer and activator of transcription (Stat) 5 marks good prognosis in estrogen receptor/progesterone receptor-positive breast tumors. This positive characteristic is counteracted by studies in laboratory animals demonstrating that deregulated Stat5 activity may convert proper mammary development into a latent oncogenic process. Tumorigenesis is initiated during the parity cycles, most probably during pregnancy, when the activated Stat5 antagonizes or manipulates parity's protective mechanisms. For example, it can alter the differentiation/proliferation balance, induce growth hormone signaling, cause specific alteration in chromatin structure, inhibit tumor-suppressor activity and induce DNA damage that counteracts the enhanced DNA-damage response exerted by parity. Palpable tumors develop after a latent period from individual cells. This happens in the estropausal period in transgenic mice maintaining deregulated Stat5 activity in the mammary gland, or during involution, months after transplantation of transfected cells with constitutively active Stat5. Candidate vulnerable cells are those which maintain high nuclear Stat5 activity. Due to the hazardous outcome of deregulated Stat5 activity in these cells, such as induced DNA damage or high cyclin D1 activity, the gland is prone to transformation. The developing tumors are mostly adenocarcinomas or their subtypes. They are estrogen receptor-positive and maintain a specific Stat5 gene signature that allows tracking their inducer. From a clinical point of view, deregulated Stat5 activity represents a genuine risk factor for breast cancer. Monitoring Stat5 activity during vulnerable periods and developing specific tools for its suppression in breast epithelial cells could potentially limit new incidence of the disease. © The Author 2012. Published by Oxford University Press. All rights reserved.
Scientific Publication
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