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

Shi A, Dong J, Hilsenbeck S, Bi L, Zhang H, Li Y - PLoS ONE (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China; Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas, United States of America.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

pSTAT5 and pSTAT3 status in human ADH.A. H&E staining (top panel), pSTAT5 (mid panel), and pSTAT3 IHC staining (bottom panel) of normal TDLU, ADH, UDH, and ADH-adjacent ducts. B. Quantification of pSTAT5 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. C. Paired comparison for percentage of pSTAT5 positive cells in ADH and corresponding ADH-adjacent normal ducts. D. Quantification of pSTAT3 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. E. Paired comparison for percentage of pSTAT3-positive cells in ADH and corresponding ADH-adjacent normal ducts.
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pone.0132214.g001: pSTAT5 and pSTAT3 status in human ADH.A. H&E staining (top panel), pSTAT5 (mid panel), and pSTAT3 IHC staining (bottom panel) of normal TDLU, ADH, UDH, and ADH-adjacent ducts. B. Quantification of pSTAT5 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. C. Paired comparison for percentage of pSTAT5 positive cells in ADH and corresponding ADH-adjacent normal ducts. D. Quantification of pSTAT3 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. E. Paired comparison for percentage of pSTAT3-positive cells in ADH and corresponding ADH-adjacent normal ducts.

Mentions: We obtained from the First Hospital of Jilin University 59 ADHs (31 of which were from breasts without an invasive cancer while 28 of which were adjacent to an invasive cancer), and for comparison 31 normal breast tissues and 21 UDH samples. We stained them by immunohistochemistry for both pSTAT5 and pSTAT3. The median percentage of pSTAT5-positive cells was 15.0%, 11.7%, 19.2%, and 8.7% in normal TDLUs (terminal ductal lobular units), pure ADH, tumor-adjacent ADH, and UDH, respectively, and were not significantly different from each other (Fig 1A and 1B). However, among the 19 cases of ADH (including both types of ADH) that also had ADH-adjacent, histologically normal epithelia, paired comparison of pSTAT5 in ADH vs. normal ducts detected higher levels in ADH (31.65% vs. 17.10%, p = 0.0069, Fig 1C), which was similar to normal breast epithelia from benign breast.


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

Shi A, Dong J, Hilsenbeck S, Bi L, Zhang H, Li Y - PLoS ONE (2015)

pSTAT5 and pSTAT3 status in human ADH.A. H&E staining (top panel), pSTAT5 (mid panel), and pSTAT3 IHC staining (bottom panel) of normal TDLU, ADH, UDH, and ADH-adjacent ducts. B. Quantification of pSTAT5 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. C. Paired comparison for percentage of pSTAT5 positive cells in ADH and corresponding ADH-adjacent normal ducts. D. Quantification of pSTAT3 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. E. Paired comparison for percentage of pSTAT3-positive cells in ADH and corresponding ADH-adjacent normal ducts.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4492667&req=5

pone.0132214.g001: pSTAT5 and pSTAT3 status in human ADH.A. H&E staining (top panel), pSTAT5 (mid panel), and pSTAT3 IHC staining (bottom panel) of normal TDLU, ADH, UDH, and ADH-adjacent ducts. B. Quantification of pSTAT5 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. C. Paired comparison for percentage of pSTAT5 positive cells in ADH and corresponding ADH-adjacent normal ducts. D. Quantification of pSTAT3 staining in normal TDLU, pure ADH, tumor-adjacent ADH (TA-ADH), and UDH, and pairwise comparisons shown by horizontal lines. E. Paired comparison for percentage of pSTAT3-positive cells in ADH and corresponding ADH-adjacent normal ducts.
Mentions: We obtained from the First Hospital of Jilin University 59 ADHs (31 of which were from breasts without an invasive cancer while 28 of which were adjacent to an invasive cancer), and for comparison 31 normal breast tissues and 21 UDH samples. We stained them by immunohistochemistry for both pSTAT5 and pSTAT3. The median percentage of pSTAT5-positive cells was 15.0%, 11.7%, 19.2%, and 8.7% in normal TDLUs (terminal ductal lobular units), pure ADH, tumor-adjacent ADH, and UDH, respectively, and were not significantly different from each other (Fig 1A and 1B). However, among the 19 cases of ADH (including both types of ADH) that also had ADH-adjacent, histologically normal epithelia, paired comparison of pSTAT5 in ADH vs. normal ducts detected higher levels in ADH (31.65% vs. 17.10%, p = 0.0069, Fig 1C), which was similar to normal breast epithelia from benign breast.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China; Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas, United States of America.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus