Esophageal Adenocarcinoma in the Proximal Esophageal Segment: A Unique Presentation in a Male With Alcohol Abuse.

Esophageal adenocarcinoma (EAC) is a malignancy classically seen in the distal esophagus. While many risk factors associated with the condition have been reported, the most common among them are gastroesophageal reflux disease (GERD) and obesity. Histological changes range from metaplasia within the esophagus from stratified squamous epithelium to non-ciliated columnar cells with goblet cells.

Inhibition of cholinergic signaling causes apoptosis in human bronchioalveolar carcinoma.

Recent case-controlled clinical studies show that bronchioalveolar carcinomas (BAC) are correlated with smoking. Nicotine, the addictive component of cigarettes, accelerates cell proliferation through nicotinic acetylcholine receptors (nAChR). In this study, we show that human BACs produce acetylcholine (ACh) and contain several cholinergic factors including acetylcholinesterase (AChE), choline acetyltransferase (ChAT), choline transporter 1 (CHT1, SLC5A7), vesicular acetylcholine transporter (VAChT, SLC18A3), and nACh receptors (AChRs, CHRNAs).

MG624, an α7-nAChR antagonist, inhibits angiogenesis via the Egr-1/FGF2 pathway.

Small cell lung cancer (SCLC) demonstrates a strong etiological association with smoking. Although cigarette smoke is a mixture of about 4,000 compounds, nicotine is the addictive component of cigarette smoke. Several convergent studies have shown that nicotine promotes angiogenesis in lung cancers via the α7-nicotinic acetylcholine receptor (α7-nAChR) on endothelial cells.