Fluorescence approach detects precancerous cells in esophagus

Using a molecular imaging approach that couples fluorescence endoscopy and fluorescently labeled wheat germ proteins, researchers at the University of Cambridge's MRC Cancer Cell Unit have identified changes in the patterns of glycans, or sugar molecules, that line precancerous cells in the esophagus, allowing easier detection and removal of the cells before cancer progression.

Using a molecular imaging approach that couples fluorescence endoscopy and fluorescently labeled wheat germ proteins, researchers at the University of Cambridge's MRC Cancer Cell Unit (Cambridge, England) have identified changes in the patterns of glycans, or sugar molecules, that line precancerous cells in the esophagus, allowing easier detection and removal of the cells before cancer progression.

In the study, the researchers examined the use of protein-specific molecular imaging methods that would permit early detection of precancerous markers in patients with Barrett’s esophagus. After analyzing the sugars present in human tissue samples obtained from various stages of cancer progression, the researchers found that there were different glycans present on the surface of precancerous cells. Because glycans have large structures and have been revealed to be altered in cancers—including pancreatic, colon, and stomach cancers—researchers theorized that these structures could be used as molecular targets for the endoscopic imaging of mucosal surfaces.

So, researchers employed their fluorescent imaging approach to detect changes in glycan expression on the cell surface that accompany the transition from Barrett’s esophagus through dysplasia to esophageal adenocarcinoma in situ. After the study analysis, four glycan pathways were revealed to exhibit coordinated increases in the expression of genes encoding proteins involved in the biosynthesis and degradation of glycan structures in the progression to esophageal adenocarcinoma. The pathway for glycan degradation was supplemented during the metaplastic transition to Barrett’s esophagus, but the majority of augmentation in the glycosphingolipid pathway lactoseries took place as Barrett’s esophagus progressed to low-grade dysplasia and neo-lactoseries increased between low-grade dysplasia and high-grade dysplasia.

The study demonstrates that coordinated changes in glycan expression begin before the development of esophageal adenocarcinoma and provides a potential biomarker for the detection of dysplasia and the identification of those at risk of progression from Barrett’s esophagus to esophageal adenocarcinoma, according to researchers.

The work has been published in Nature Medicine; for more information, please visit http://www.nature.com/nm/journal/vaop/ncurrent/abs/nm.2616.html.

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