Esophageal cancer

Abstract

Carcinoma of the esophagus and gastroesophageal junction continues to be an aggressive cancer with poor prognosis, despite improved surgical results and the potential benefit of combined multimodality regimens. Additional data seem to confirm the rising incidence of adenocarcinoma, although users of nonsteroidal anti-inflammatory drugs seem to have a decreased risk. Much attention is focused on detecting high-grade dysplasia and early carcinoma with promising results using red fluorescence after preceding 5-aminolevulinic acid (ALA) sensitization. Positron emission tomography made a major breakthrough and seems to be superior to computed tomography in detecting distant metastasis as well as lymph node metastasis. Endoscopic ablation of early carcinoma results in promising early results, but a major issue remains the EUS discrimination between Tis-T1a and T1b, as the latter is frequently associated with lymph node metastasis. In the field of molecular biology, research is unraveling the role of cadherins and catenins in the mechanism underlying cell adherence, cell movement, and progress toward tumor formation. Mutations of p53 are correlated with loss of apoptosis and form an early step in progress toward carcinoma as well as mutations of other tumor-suppressing genes (eg, p16 and Rb mutations). Detection of such mutations may become useful prognostic indicators, but illustrate the genetic polymorphism influencing the susceptibility to carcinoma. Several lines of evidence suggest that the stabilizing or overriding of p53 mutant cancer cells and restoration of the wild-type tumor suppressor gene p53 may improve results of DNA damaging treatment modalities. Further research in this field may lead to new forms of anticancer therapy.