Molecular and biologic basis of upper gastrointestinal malignancy--esophageal carcinoma.
Esophageal cancer is one of the most deadly forms of gastrointestinal cancer. Even though the incidence of esophageal adenocarcinoma has been rising in Western populations over the past two decades, esophageal squamous cell carcinoma remains the predominant type of esophageal malignancy in the remainder of the world. With the recent advances in molecular biology, high-output genome wide screening has provided comprehensive profiles of molecular alterations in human esophageal carcinomas. The elucidation of the basic mechanisms of esophageal carcinogenesis brings with it the promise of developing treatment and preventive strategies that are based on the molecular biology of these tumors. The genetic alterations discussed in this article are not unique to the formation of esophageal carcinomas and represent only a fraction of the molecular changes found in these tumors. The goal of this article is to provide the clinician with a useful conceptual basis for evaluating studies on the molecular mechanisms underlying the development of esophageal carcinomas.
Souza
Rhonda F
RF
Department of Medicine, Dallas VA Medical Center, Dept. of GI, Harold C. Simmons Comprehensive Cancer Center, University of Texas-Southwestern Medical Center at Dallas, TX, USA. rsouza@airmail.net
D000230:Adenocarcinoma / Q000235:genetics / Q000503:physiopathology*; D017209:Apoptosis; D001471:Barrett Esophagus / Q000503:physiopathology; D002453:Cell Cycle / Q000502:physiology; D016213:Cyclins / Q000502:physiology; D004938:Esophageal Neoplasms / Q000235:genetics / Q000503:physiopathology*; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D006801:Humans; D016160:Retinoblastoma Protein / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D018631:ras Proteins / Q000502:physiology
D016213:Cyclins; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D018631:ras Proteins