Topic Highlight
Copyright ©2011 Baishideng Publishing Group Co.
World J Gastroenterol. Aug 28, 2011; 17(32): 3672-3683
Published online Aug 28, 2011. doi: 10.3748/wjg.v17.i32.3672
Figure 1
Figure 1 Clonal evolution models in Barrett’s esophagus. A: The current model of clonal evolution adapted from Maley et al[66]. Founder mutation (red cross) occurs in a single progenitor and provides a growth advantage that predisposes to a selective sweep. Successive selective sweeps result in progression along the metaplasia dysplasia pathway. Clone bifurcation is responsible for the genetic heterogeneity in this model; B: The newly proposed model of evolution based on the mutation of multiple progenitor cells situated in esophageal gland squamous ducts located throughout the length of the esophagus (red crosses). Multiple independent clones then arise and evolve separately. The presence of multiple different clones gives rise to a mosaic interdigitating clonal pattern of the Barrett’s segment represented as the striped areas[65].
Figure 2
Figure 2 Age distribution of cases diagnosed with oesophageal adenocarcinoma (A) and gastric cardia adenocarcinoma (B) in the USA between 1977-1996, displaying the "birth cohort effect". Each individual curve represents the age-specific incidence rates in a five year period (from El-Serag et al[70]).