Data on the function of CDH17 in pancreatic cancer growth
DATA IN BRIEF
Authors: Yuan, Hao; Stenberg, Joseph; Li, Guangfu
Abstract
Data presented in this article are related to the research article entitled "Disruption of oncogenic liver-intestine cadherin (CDH17) drives apoptotic pancreatic cancer death". To investigate the influence of CDH17 on human pancreatic cancer (PC), we performed gain and loss of CDH17 function with siRNA and recombinant plasmid to evaluate its impact on PC cell proliferation, colony formation, and migration. The data can be valuable for researchers interested in the study of oncogenic activity related to the CDH17 gene in PC growth and motility. (c) 2019 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
FABP1 and Hepar expression levels in Barrett's esophagus and associated neoplasia in an Asian population
DIGESTIVE AND LIVER DISEASE
Authors: Srivastava, Supriya; Kern, Florian; Sharma, Neel; McKeon, Frank; Xian, Wa; Yeoh, Khay Guan; Ho, Khek Yu; Teh, Ming
Abstract
Introduction: Barrett's esophagus (BE) is a premalignant condition associated with esophageal adenocarcinoma (EAC). Evidence highlights that EAC is associated with an estimated 5-year survival of approximately 10-15%. Therefore, there is a need to determine which biomarkers are of value in the diagnosis of BE and beyond. The aim of our study was to evaluate the clinical significance of markers known to be expressed across BE and associated neoplasia. Methods: Retrospective tissues were obtained from columnar lined esophagus (CLE) without goblet cells (n = 22), BE (n = 29), dysplasia (n = 14), and EAC (n = 10). Standardised immunohistochemistry for FABP1, Hepar, CDH17, and CDX2 were performed followed by quantitative staining and statistical analysis. Results: FABP1 expression was negligible in CLE and was highest in BE, with a further decrease in expression in dysplasia and EAC. Hepar expression was also negligible in CLE and was highest in dysplasia and BE, with a reduced expression in EAC. CDH17 and CDX2 showed a significantly higher expression in BE, dysplasia, and EAC compared to CLE. Conclusion: All 4 markers were excellent diagnostic panels to clearly discriminate BE from CLE. Moreover, as FABP1 and Hepar have different expression levels in dysplasia and EAC, these markers could function as key diagnostic aids in helping to determine the state of disease progression. (C) 2017 Published by Elsevier Ltd on behalf of Editrice Gastroenterologica Italiana S.r.l.