| Shift from pStat6 to pStat3 predominance is associated with inflammatory bowel disease-associated dysplasia. | |
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MedLine Citation:
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PMID: 22021169 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-10-21 |
Journal Detail:
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Title: Inflammatory bowel diseases Volume: 18 ISSN: 1536-4844 ISO Abbreviation: Inflamm. Bowel Dis. Publication Date: 2012 Jul |
Date Detail:
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Created Date: 2012-06-12 Completed Date: 2012-10-18 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 9508162 Medline TA: Inflamm Bowel Dis Country: United States |
Other Details:
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Languages: eng Pagination: 1267-74 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Crohn's & Colitis Foundation of America, Inc. |
Affiliation:
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Department of Surgery, Johns Hopkins University School of Medicine and Bloomberg School of Public Health, Baltimore, Maryland, USA. ewick1@jhmi.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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:
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0/STAT1 Transcription Factor; 0/STAT1 protein, human; 0/STAT3 Transcription Factor; 0/STAT3 protein, human; 0/STAT6 Transcription Factor; 0/STAT6 protein, human |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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