The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Shift from pStat6 to pStat3 predominance is associated with inflammatory bowel disease-associated dysplasia.
Elizabeth C Wick; Robert E LeBlanc; Guillermo Ortega; Chelsea Robinson; Elizabeth Platz; Drew M Pardoll; Chris Iacobuzio-Donahue; Cynthia L Sears (Profiled Authors: Elizabeth Platz; Chris Iacobuzio-Donahue; Cynthia Sears; Elizabeth Wick; Drew Pardoll)
Department of Surgery, Johns Hopkins University School of Medicine and Bloomberg School of Public Health, Baltimore, Maryland, USA. firstname.lastname@example.org
Inflammatory bowel diseases 2012;18(7):1267-74.
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.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Marco Dal Molin; Seung-Mo Hong; Sachidanand Hebbar; Rajni Sharma; Francesca Scrimieri; Roeland F de Wilde; Skye C Mayo; Michael Goggins; Christopher L Wolfgang; Richard D Schulick; et al.Human pathology 2012;43(4):585-91.
Antoun Toubaji; Siobhan Sutcliffe; Alcides Chaux; Kristen Lecksell; Jessica Hicks; Angelo M De Marzo; Elizabeth A Platz; George J Netto
Immunohistochemical expression of minichromosome maintenance complex protein 2 predicts biochemical recurrence in prostate cancer: a tissue microarray and digital imaging analysis-based study of 428 cases.Human pathology 2012;43(11):1852-65.
Z Q Ning; J Li; M McGuinness; R J ArceciOncogene 2001;20(33):4528-36.
Appears in this Publication
Author of this Publication