Document Detail


Shift from pStat6 to pStat3 predominance is associated with inflammatory bowel disease-associated dysplasia.
MedLine Citation:
PMID:  22021169     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Activated Stat3 is an important mediator of oncogenesis in the colon. To test the hypothesis that select Stat activation and/or the pattern of Stat activation serves as a marker for early neoplastic transformation, we examined the distribution of activated Stat1(pStat1), Stat6(pStat6), and Stat3(pStat3) in colitis along the continuum of inactive disease to colitis-associated cancer.
METHODS: Tissue microarrays were constructed using colonoscopy biopsy and surgical specimens from 67 patients with ulcerative colitis or Crohn's colitis and 11 controls. In all, 111 sets of samples were analyzed representing normal tissue, active disease, low-grade dysplasia, high-grade dysplasia, and colitis-associated cancer. Immunohistochemistry to detect pStat1, pStat6, and pStat3 in colonic epithelial and mucosal immune cells was then correlated with clinical and pathological data (tumor location, histologic type, grade, and lymph node involvement).
RESULTS: In 50% of colitis-associated cancer samples, pStat3 was detected prominently in epithelial cells, where it was routinely associated with intense pStat3 staining in surrounding immune cells. Stat3 activation was greater in low-grade tumors than in high-grade ones (P < 0.05). pStat6 expression was more common in normal tissues than in colitis-associated cancer (P < 0.05). pStat1 was detected in a small subset of immune cells in patients with chronic inactive and active colitis, low- and high-grade dysplasia, but not in colitis-associated cancer.
CONCLUSIONS: pStat3 may be a marker for neoplastic transformation in patients with colitis. A shift from predominant immune cell Stat6 activation to Stat3 activation accompanies the onset of dysplasia with concomitant increased epithelial cell Stat3 activation in a subset of patients.
Authors:
Elizabeth C Wick; Robert E LeBlanc; Guillermo Ortega; Chelsea Robinson; Elizabeth Platz; Drew M Pardoll; Chris Iacobuzio-Donahue; Cynthia L Sears
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-10-21
Journal Detail:
Title:  Inflammatory bowel diseases     Volume:  18     ISSN:  1536-4844     ISO Abbreviation:  Inflamm. Bowel Dis.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-06-12     Completed Date:  2012-10-18     Revised Date:  2013-04-16    
Medline Journal Info:
Nlm Unique ID:  9508162     Medline TA:  Inflamm Bowel Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1267-74     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Crohn's & Colitis Foundation of America, Inc.
Affiliation:
Department of Surgery, Johns Hopkins University School of Medicine and Bloomberg School of Public Health, Baltimore, Maryland, USA. ewick1@jhmi.edu
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / etiology,  metabolism,  secondary
Adenocarcinoma, Mucinous / etiology,  metabolism,  secondary
Case-Control Studies
Cell Transformation, Neoplastic / metabolism,  pathology*
Colitis, Ulcerative / complications*,  metabolism,  pathology
Colorectal Neoplasms / etiology*,  metabolism,  pathology
Crohn Disease / complications*,  metabolism,  pathology
Epithelial Cells / metabolism,  pathology*
Female
Humans
Immunoenzyme Techniques
Lymphatic Metastasis
Male
Middle Aged
Neoplasm Grading
Phosphorylation
Prognosis
STAT1 Transcription Factor / metabolism
STAT3 Transcription Factor / metabolism*
STAT6 Transcription Factor / metabolism*
Tissue Array Analysis
Grant Support
ID/Acronym/Agency:
K08 DK 087856/DK/NIDDK NIH HHS; R01 CA 091409/CA/NCI NIH HHS; R01 CA151393/CA/NCI NIH HHS; R01 DK 080817/DK/NIDDK NIH HHS; R01 DK 45496/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/STAT1 Transcription Factor; 0/STAT1 protein, human; 0/STAT3 Transcription Factor; 0/STAT3 protein, human; 0/STAT6 Transcription Factor; 0/STAT6 protein, human

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