Esophageal cancer

Citation
T. Lerut et G. Decker, Esophageal cancer, CURR OPIN G, 15(4), 1999, pp. 364-369
Citations number
41
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
CURRENT OPINION IN GASTROENTEROLOGY
ISSN journal
02671379 → ACNP
Volume
15
Issue
4
Year of publication
1999
Pages
364 - 369
Database
ISI
SICI code
0267-1379(199907)15:4<364:EC>2.0.ZU;2-9
Abstract
Carcinoma of the esophagus and gastroesophageal junction continues to be an aggressive cancer with poor prognosis, despite improved surgical results a nd the potential benefit of combined multimodality regimens. Additional dat a seem to confirm the rising incidence of adenocarcinoma, although users of nonsteroidal anti-inflammatory drugs seem to have a decreased risk. Much a ttention is focused on detecting high-grade dysplasia and early carcinoma w ith promising results using red fluorescence after preceding 5-aminolevulin ic acid (ALA) sensitization. Positron emission tomography made a major brea kthrough and seems to be superior to computed tomography in detecting dista nt metastasis as well as lymph node metastasis. Endoscopic ablation of earl y carcinoma results in promising early results, but a major issue remains t he EUS discrimination between Tis-T1a and T1b, as the latter is frequently associated with lymph node metastasis. In the field of molecular biology, r esearch is unraveling the role of cadherins and catenins in the mechanism u nderlying cell adherence, cell movement, and progress toward tumor formatio n. 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-supp ressing genes (eg, p16 and Rb mutations). Detection of such mutations may b ecome useful prognostic indicators, but illustrate the genetic polymorphism influencing the susceptibility to carcinoma. Several lines of evidence sug gest that the stabilizing or overriding of p53 mutant cancer cells and rest oration of the wild-type tumor suppressor gene p53 may improve results of D NA damaging treatment modalities. Further research in this field may lead t o new forms of anticancer therapy. (C) 1999 Lippincott Williams & Wilkins, Inc.