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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

Cell apoptosis rates in human ADH and their relationships with pSTAT5 and pSTAT3.A. Quantification of TUNEL assay in normal ducts, ADH, and UDH. B-C. B-C. No association between percentages of pSTAT5+ (B) and TUNEL+ cells or between pSTAT3+ (C) and TUNEL+ cells in ADH. Each dot represents an individual ADH lesion.
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pone.0132214.g004: Cell apoptosis rates in human ADH and their relationships with pSTAT5 and pSTAT3.A. Quantification of TUNEL assay in normal ducts, ADH, and UDH. B-C. B-C. No association between percentages of pSTAT5+ (B) and TUNEL+ cells or between pSTAT3+ (C) and TUNEL+ cells in ADH. Each dot represents an individual ADH lesion.

Mentions: We also asked whether in these ADH samples, the rates of pSTAT5 or pSTAT3 were inversely correlated with cell apoptosis. Apoptosis was previously found to be low (0.2–0.3%) in ADH [47, 48]. We found that in our ADH samples (n = 59), the apoptosis rate was also low, ranging from 0 to 2.34% with the medium value at approximately 0.16%. Similar lower rates of apoptosis were also found in normal breast tissues (n = 31) and UDH cases (n = 15) (Fig 4A). There was no significant association between the rates of pSTAT5-postive cells or pSTAT3-positive cells and cell apoptosis (Fig 4B and 4C).


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)

Cell apoptosis rates in human ADH and their relationships with pSTAT5 and pSTAT3.A. Quantification of TUNEL assay in normal ducts, ADH, and UDH. B-C. B-C. No association between percentages of pSTAT5+ (B) and TUNEL+ cells or between pSTAT3+ (C) and TUNEL+ cells in ADH. Each dot represents an individual ADH lesion.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0132214.g004: Cell apoptosis rates in human ADH and their relationships with pSTAT5 and pSTAT3.A. Quantification of TUNEL assay in normal ducts, ADH, and UDH. B-C. B-C. No association between percentages of pSTAT5+ (B) and TUNEL+ cells or between pSTAT3+ (C) and TUNEL+ cells in ADH. Each dot represents an individual ADH lesion.
Mentions: We also asked whether in these ADH samples, the rates of pSTAT5 or pSTAT3 were inversely correlated with cell apoptosis. Apoptosis was previously found to be low (0.2–0.3%) in ADH [47, 48]. We found that in our ADH samples (n = 59), the apoptosis rate was also low, ranging from 0 to 2.34% with the medium value at approximately 0.16%. Similar lower rates of apoptosis were also found in normal breast tissues (n = 31) and UDH cases (n = 15) (Fig 4A). There was no significant association between the rates of pSTAT5-postive cells or pSTAT3-positive cells and cell apoptosis (Fig 4B and 4C).

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