Nevertheless, available studies using biopsy specimens from patients with Barrett's esophagus support a carcinogenetic role for alterations in the same pathways that caused transformation of our non-neoplastic Barrett's epithelial cells in vitro, i.e. the p16/Rb and p53 checkpoint arrest pathways, the mitogenic Ras signaling pathway, and the telomerase-dependent replicative senescence pathway. Here, TP53 is linked to esophageal adenocarcinoma.