In vitro and in vivo models provide the better knowledge on the pathogenesis of esophagitis-Barret’-carcinoma
progression that can results in promising treatment strategies for esophageal cancer.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Seminars in Thoracic and Cardiovascular SurgeryAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Esophageal cancer: an updated surveillance epidemiology and end results database analysis.World J Oncol. 2020; 11: 55-64
- From Reflux Esophagitis to Esophageal Adenocarcinoma.Dig Dis. 2016; 34: 483-490
- Toll-like Receptor 4 Mediates Reflux-Induced Inflammation in a Murine Reflux Model.Semin Thorac Cardiovasc Surg. 2022; 34: 1324-1335
- Bile acid-induced “Minority MOMP” promotes esophageal carcinogenesis while maintaining apoptotic resistance via Mcl-1.Oncogene. 2020; 39: 877-890
- Prolonged exposure to acid and bile induces chromosome abnormalities that precede malignant transformation of benign Barrett's epithelium.Mol Cytogenet. 2012; 5
Article info
Publication history
Published online: September 12, 2021
Footnotes
Conflicts of Interest: No conflict of interests to disclose.
Identification
Copyright
© 2021 Elsevier Inc. All rights reserved.
ScienceDirect
Access this article on ScienceDirectLinked Article
- Toll-like Receptor 4 Mediates Reflux-Induced Inflammation in a Murine Reflux ModelSeminars in Thoracic and Cardiovascular SurgeryVol. 34Issue 4
- PreviewDysregulation of toll-like receptor (TLR) signaling within the gastrointestinal epithelium has been associated with uncontrolled inflammation and tumorigenesis. We sought to evaluate the role of TLR4 in the development of gastroesophageal reflux-mediated inflammation and mucosal changes of the distal esophagus. Verified human esophageal Barrett's cells with high grade dysplasia (CPB) and esophageal adenocarcinoma cells (OE33) were treated with deoxycholic acid for 24 hours. Cells were pretreated with a TLR4-specific inhibitor peptide 2 hours prior to deoxycholic acid treatment.
- Full-Text
- Preview
