Epigenetic Inactivation of the CpG Demethylase TET1 as a DNA Methylation Feedback Loop in Upper Aerodigestive Tract and Gastrointestinal Cancers

2017 ◽  
Vol 15 (1) ◽  
pp. e46
Author(s):  
Lili Li ◽  
Chen Li ◽  
Haitao Mao ◽  
Zhenfang Du ◽  
Wai Yee Chan ◽  
...  
Epigenetics ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. 270-277 ◽  
Author(s):  
Samson Mani ◽  
Kasia Szymańska ◽  
Cyrille Cuenin ◽  
David Zaridze ◽  
Karen Balassiano ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3014
Author(s):  
Sheila Coelho Soares-Lima ◽  
Hisham Mehanna ◽  
Diego Camuzi ◽  
Paulo Thiago de Souza-Santos ◽  
Tatiana de Almeida Simão ◽  
...  

Upper aerodigestive tract (UADT) tumors present different biological behavior and prognosis, suggesting specific molecular mechanisms underlying their development. However, they are rarely considered as single entities (particularly head and neck subsites) and share the most common genetic alterations. Therefore, there is a need for a better understanding of the global DNA methylation differences among UADT tumors. We performed a genome-wide DNA methylation analysis of esophageal (ESCC), laryngeal (LSCC), oral (OSCC) and oropharyngeal (OPSCC) squamous cell carcinomas, and their non-tumor counterparts. The unsupervised analysis showed that non-tumor tissues present markedly distinct DNA methylation profiles, while tumors are highly heterogeneous. Hypomethylation was more frequent in LSCC and OPSCC, while ESCC and OSCC presented mostly hypermethylation, with the latter showing a CpG island overrepresentation. Differentially methylated regions affected genes in 127 signaling pathways, with only 3.1% of these being common among different tumor subsites, but with different genes affected. The WNT signaling pathway, known to be dysregulated in different epithelial tumors, is a frequent hit for DNA methylation and gene expression alterations in ESCC and OPSCC, but mostly for genetic alterations in LSCC and OSCC. UADT tumor subsites present differences in genome-wide methylation regarding their profile, intensity, genomic regions and signaling pathways affected.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Lili Li ◽  
Chen Li ◽  
Haitao Mao ◽  
Zhenfang Du ◽  
Wai Yee Chan ◽  
...  

1980 ◽  
Vol 13 (3) ◽  
pp. 403-412 ◽  
Author(s):  
Charles W. Vaughan ◽  
Freddy Homburger ◽  
Stanley M. Shapshay ◽  
Enrique Soto ◽  
Peter Bernfeld

Author(s):  
Edward Odell ◽  
Nina Gale ◽  
Selvam Thavaraj ◽  
Alfons Nadal ◽  
Nina Zidar ◽  
...  

2021 ◽  
Vol 10 (11) ◽  
pp. 2439
Author(s):  
Jerome R. Lechien ◽  
Stéphane Hans ◽  
Francois Bobin ◽  
Christian Calvo-Henriquez ◽  
Sven Saussez ◽  
...  

Background: Laryngopharyngeal reflux (LPR) is a common disease in otolaryngology characterized by an inflammatory reaction of the mucosa of the upper aerodigestive tract caused by digestive refluxate enzymes. LPR has been identified as the etiological or favoring factor of laryngeal, oral, sinonasal, or otological diseases. In this case series, we reported the atypical clinical presentation of LPR in patients presenting in our clinic with reflux. Methods: A retrospective medical chart review of 351 patients with LPR treated in the European Reflux Clinic in Brussels, Poitiers and Paris was performed. In order to be included, patients had to report an atypical clinical presentation of LPR, consisting of symptoms or findings that are not described in the reflux symptom score and reflux sign assessment. The LPR diagnosis was confirmed with a 24 h hypopharyngeal-esophageal impedance pH study, and patients were treated with a combination of diet, proton pump inhibitors, and alginates. The atypical symptoms or findings had to be resolved from pre- to posttreatment. Results: From 2017 to 2021, 21 patients with atypical LPR were treated in our center. The clinical presentation consisted of recurrent aphthosis or burning mouth (N = 9), recurrent burps and abdominal disorders (N = 2), posterior nasal obstruction (N = 2), recurrent acute suppurative otitis media (N = 2), severe vocal fold dysplasia (N = 2), and recurrent acute rhinopharyngitis (N = 1), tearing (N = 1), aspirations (N = 1), or tracheobronchitis (N = 1). Abnormal upper aerodigestive tract reflux events were identified in all of these patients. Atypical clinical findings resolved and did not recur after an adequate antireflux treatment. Conclusion: LPR may present with various clinical presentations, including mouth, eye, tracheobronchial, nasal, or laryngeal findings, which may all regress with adequate treatment. Future studies are needed to better specify the relationship between LPR and these atypical findings through analyses identifying gastroduodenal enzymes in the inflamed tissue.


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