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The combined expression of metaplasia biomarkers predicts the prognosis of gastric cancer.
Suh YS, Lee HJ, Jung EJ, Kim MA, Nam KT, Goldenring JR, Yang HK, Kim WH
(2012) Ann Surg Oncol 19: 1240-9
MeSH Terms: Adenocarcinoma, Biomarkers, Tumor, Cadherins, Female, Galectin 4, Gene Expression Profiling, Granulocyte Colony-Stimulating Factor, Humans, Immunohistochemistry, Keratin-20, Lectins, C-Type, Male, Metaplasia, Middle Aged, Mucin 5AC, Mucins, Neoplasm Staging, Pancreatitis-Associated Proteins, Prognosis, Stomach Neoplasms
Show Abstract · Added September 3, 2013
BACKGROUND - Our previous study indicated that gene expression profiling of intestinal metaplasia (IM) or spasmolytic polypeptide-expressing metaplasia (SPEM) can identify useful prognostic markers of early-stage gastric cancer, and seven metaplasia biomarkers (MUC13, CDH17, OLFM4, KRT20, LGALS4, MUC5AC, and REG4) were selectively expressed in 17-50% of gastric cancer tissues. We investigated whether the combined expression of these metaplasia biomarkers could predict the prognosis of advanced stage gastric cancer.
METHODS - The expression of seven metaplasia biomarkers was evaluated immunohistochemically using tissue microarrays comprised of 450 gastric cancer patients. The clinicopathologic correlations and the prognostic impact were analyzed according to the expression of multiple biomarkers.
RESULTS - MUC13, CDH17, LGALS4, and REG4 were significant prognostic biomarkers in univariate analysis. No expression of four markers was found in 56 cases (14.2%); 1 marker was seen in 67 cases (17%), 2 in 106 cases (27%), 3 in 101 cases (25.7%), and 4 in 63 cases (16%). Patients in which two or fewer proteins were expressed (group B) showed younger age, undifferentiated or diffuse type cancer, larger tumor size, larger number of metastatic lymph nodes, and more advanced stage than those in which three or more proteins were expressed (group A). In undifferentiated or stage II/III gastric cancer, the prognosis of group B was significantly poorer than that of group A by multivariate analysis.
CONCLUSIONS - The combined loss of expression of multiple metaplasia biomarkers is considered an independent prognostic indicator in undifferentiated or stage II/III gastric cancer.
0 Communities
1 Members
0 Resources
20 MeSH Terms
Hypoxia-inducible factor-1 signalling promotes goblet cell hyperplasia in airway epithelium.
Polosukhin VV, Cates JM, Lawson WE, Milstone AP, Matafonov AG, Massion PP, Lee JW, Randell SH, Blackwell TS
(2011) J Pathol 224: 203-11
MeSH Terms: Adolescent, Adult, Aged, Aged, 80 and over, Airway Remodeling, Bronchi, Cell Differentiation, Cell Hypoxia, Cells, Cultured, Enzyme Activation, Female, Goblet Cells, Humans, Hyperplasia, Hypoxia-Inducible Factor 1, Male, Middle Aged, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mucin 5AC, Pulmonary Disease, Chronic Obstructive, Respiratory Mucosa, Signal Transduction, Young Adult
Show Abstract · Added March 15, 2013
Goblet cell hyperplasia is a common feature of chronic obstructive pulmonary disease (COPD) airways, but the mechanisms that underlie this epithelial remodelling in COPD are not understood. Based on our previous finding of hypoxia-inducible factor-1α (HIF-1α) nuclear localization in large airways from patients with COPD, we investigated whether hypoxia-inducible signalling could influence the development of goblet cell hyperplasia. We evaluated large airway samples obtained from 18 lifelong non-smokers and 13 former smokers without COPD, and 45 former smokers with COPD. In these specimens, HIF-1α nuclear staining occurred almost exclusively in COPD patients in areas of airway remodelling. In COPD patients, 93.2 ± 3.9% (range 65-100%) of goblet cells were HIF-1α positive in areas of goblet cell hyperplasia, whereas nuclear HIF-1α was not detected in individuals without COPD or in normal-appearing pseudostratified epithelium from COPD patients. To determine the direct effects of hypoxia-inducible signalling on epithelial cell differentiation in vitro, human bronchial epithelial cells (HBECs) were grown in air-liquid interface cultures under hypoxia (1% O(2)) or following treatment with a selective HIF-1α stabilizer, (2R)-[(4-biphenylylsulphonyl)amino]-N-hydroxy-3-phenyl-propionamide (BiPS). HBECs grown in hypoxia or with BiPS treatment were characterized by HIF-1α activation, carbonic anhydrase IX expression, mucus-producing cell hyperplasia and increased expression of MUC5AC. Analysis of signal transduction pathways in cells with HIF-1α activation showed increased ERK1/2 phosphorylation without activation of epidermal growth factor receptor, Ras, PI3K-Akt or STAT6. These data indicate an important effect of hypoxia-inducible signalling on airway epithelial cell differentiation and identify a new potential target to limit mucus production in COPD.
Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
1 Communities
4 Members
0 Resources
24 MeSH Terms
Interleukin-9 induces mucous cell metaplasia independent of inflammation.
Reader JR, Hyde DM, Schelegle ES, Aldrich MC, Stoddard AM, McLane MP, Levitt RC, Tepper JS
(2003) Am J Respir Cell Mol Biol 28: 664-72
MeSH Terms: Animals, Asthma, Bronchial Hyperreactivity, Bronchoalveolar Lavage Fluid, Cell Differentiation, Cell Division, Immunoglobulin E, Interleukin-13, Interleukin-9, Male, Metaplasia, Mice, Mice, Inbred C57BL, Mucin 5AC, Mucins, Pneumonia, Proteins, Respiratory Mucosa, Up-Regulation
Show Abstract · Added February 26, 2014
Interleukin-9 (IL-9) has been strongly implicated in the pathogenesis of asthma, including the overproduction of mucus, in humans and in animal models. We evaluated the inflammatory changes associated with the upregulation of mucus production by examining the time course of inflammation after daily intratracheal IL-9 administration to naive C57Bl6 mice for 9 d. IL-9 induced an asthmatic phenotype, which in general took several days to develop, as assessed by the measurement of airway hyperresponsiveness, pulmonary inflammation, and serum immunoglobulin E. However, within 24 h of a single dose of IL-9, muc5ac mRNA upregulation occurred, and increased numbers of periodic acid Schiff/Alcian blue-positive mucous cells appeared. This response occurred before the development of an inflammatory cell influx and was the result of epithelial metaplasia. It seemed that IL-9 evoked mucous cell metaplasia independent of IL-13 because mRNA tissue evaluation indicated that muc5ac upregulation preceded any increase in IL-13 mRNA expression or detectable levels of IL-13 in the brochoalveolar lavage fluid. Therefore, the upregulation of IL-13 by IL-9 may be responsible for the amplification of mucus production but is not required for its initiation. IL-9 seems to directly stimulate mucous cell metaplasia without the requirement of inflammatory cell influx.
0 Communities
1 Members
0 Resources
19 MeSH Terms