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.