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The Status of STAT3 and STAT5 in Human Breast Atypical Ductal Hyperplasia.

Signal Transducer and Activation of Transcription factors (STAT3 and STAT5) play important roles in breast epithelial cell differentiation, proliferation, and apoptosis. They have been investigated extensively in established breast cancer, but their activation status in precancerous lesions has not... Full description

Journal Title: PloS one 2015, Vol.10(7), p.e0132214
Main Author: Shi, Aiping
Other Authors: Dong, Jie , Hilsenbeck, Susan , Bi, Lirong , Zhang, Hong , Li, Yi
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0132214
Link: http://search.proquest.com/docview/1694963061/?pq-origsite=primo
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recordid: proquest1694963061
title: The Status of STAT3 and STAT5 in Human Breast Atypical Ductal Hyperplasia.
format: Article
creator:
  • Shi, Aiping
  • Dong, Jie
  • Hilsenbeck, Susan
  • Bi, Lirong
  • Zhang, Hong
  • Li, Yi
subjects:
  • Adult–Metabolism
  • Breast–Pathology
  • Breast Neoplasms–Metabolism
  • Carcinoma, Ductal, Breast–Metabolism
  • Carcinoma, Intraductal, Noninfiltrating–Metabolism
  • Female–Biosynthesis
  • Humans–Biosynthesis
  • Hyperplasia–Biosynthesis
  • Immunohistochemistry–Biosynthesis
  • Middle Aged–Biosynthesis
  • Stat3 Transcription Factor–Biosynthesis
  • Stat5 Transcription Factor–Biosynthesis
  • Stat3 Transcription Factor
  • Stat3 Protein, Human
  • Stat5 Transcription Factor
ispartof: PloS one, 2015, Vol.10(7), p.e0132214
description: Signal Transducer and Activation of Transcription factors (STAT3 and STAT5) play important roles in breast epithelial cell differentiation, proliferation, and apoptosis. They have been investigated extensively in established breast cancer, but their activation status in precancerous lesions has not been reported. Formalin-fixed, paraffin-embedded archival tissues from 59 cases of atypical ductal hyperplasia (ADH) and 31 cases of normal human breast tissue as well as 21 cases of usual ductal hyperplasias (UDH) were obtained from the First Hospital of Jilin University, China, and stained for pSTAT3 and pSTAT5 by immunohistochemistry. The median percentage of pSTAT5+ cells in ADH was 12%, not significantly deviant from that in normal breast. The median percentage of pSTAT3+ cells in ADH was 30%, significantly higher than that of normal breast. pSTAT3 and pSTAT5 were exclusive of each other--they were detected in different ADHs or in different cells within the same ADHs. In addition, both pSTAT3 and pSTAT5 were produced in similar percentages of cells in ADHs from cancer-free patients vs. ADHs that were adjacent to an invasive cancer. Our finding of a complementary expression pattern of pSTAT3 and pSTAT5 in ADH suggests that these two transcription factors may have feedback inhibitory effects on each other during early stages of breast cancer evolution, and that disruption of this inverse relationship may be important in the progression from early lesions to cancer, which exhibits positive association between pSTAT3 and pSTAT5.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0132214
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleThe Status of STAT3 and STAT5 in Human Breast Atypical Ductal Hyperplasia.
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0132214
subjectAdult–Metabolism ; Breast–Pathology ; Breast Neoplasms–Metabolism ; Carcinoma, Ductal, Breast–Metabolism ; Carcinoma, Intraductal, Noninfiltrating–Metabolism ; Female–Biosynthesis ; Humans–Biosynthesis ; Hyperplasia–Biosynthesis ; Immunohistochemistry–Biosynthesis ; Middle Aged–Biosynthesis ; Stat3 Transcription Factor–Biosynthesis ; Stat5 Transcription Factor–Biosynthesis ; Stat3 Transcription Factor ; Stat3 Protein, Human ; Stat5 Transcription Factor
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descriptionSignal Transducer and Activation of Transcription factors (STAT3 and STAT5) play important roles in breast epithelial cell differentiation, proliferation, and apoptosis. They have been investigated extensively in established breast cancer, but their activation status in precancerous lesions has not been reported. Formalin-fixed, paraffin-embedded archival tissues from 59 cases of atypical ductal hyperplasia (ADH) and 31 cases of normal human breast tissue as well as 21 cases of usual ductal hyperplasias (UDH) were obtained from the First Hospital of Jilin University, China, and stained for pSTAT3 and pSTAT5 by immunohistochemistry. The median percentage of pSTAT5+ cells in ADH was 12%, not significantly deviant from that in normal breast. The median percentage of pSTAT3+ cells in ADH was 30%, significantly higher than that of normal breast. pSTAT3 and pSTAT5 were exclusive of each other--they were detected in different ADHs or in different cells within the same ADHs. In addition, both pSTAT3 and pSTAT5 were produced in similar percentages of cells in ADHs from cancer-free patients vs. ADHs that were adjacent to an invasive cancer. Our finding of a complementary expression pattern of pSTAT3 and pSTAT5 in ADH suggests that these two transcription factors may have feedback inhibitory effects on each other during early stages of breast cancer evolution, and that disruption of this inverse relationship may be important in the progression from early lesions to cancer, which exhibits positive association between pSTAT3 and pSTAT5.
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