title: The Status of STAT3 and STAT5 in Human Breast Atypical Ductal Hyperplasia.
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.
authors.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.
authors.forename: Aiping
authors.initials: A
authors.lastname: Shi
authors.affiliation: Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas, United States of America; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, United States of America.
authors.forename: Jie
authors.initials: J
authors.lastname: Dong
authors.affiliation: Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas, United States of America; Dan L Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, United States of America.
authors.forename: Susan
authors.initials: S
authors.lastname: Hilsenbeck
authors.affiliation: Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: Lirong
authors.initials: L
authors.lastname: Bi
authors.affiliation: Department of Pathology, MD Anderson Cancer Center, Houston, Texas, United States of America.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas, United States of America; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, United States of America; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, United States of America.
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
mesh_terms: D000328:Adult; D001940:Breast / Q000378:metabolism* / Q000473:pathology; D001943:Breast Neoplasms / Q000378:metabolism*; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism*; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000378:metabolism*; D005260:Female; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D008875:Middle Aged; D050796:STAT3 Transcription Factor / Q000096:biosynthesis*; D050799:STAT5 Transcription Factor / Q000096:biosynthesis*
chemical_list: D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D050799:STAT5 Transcription Factor