The molecular biology of esophageal carcinoma.

摘要: There have been many new developments in our understanding of esophageal carcinoma biology over the past several years. Information regarding both major forms this disease, adenocarcinoma and squamous cell carcinoma, has accumulated conjunction with data on precursor conditions such as Barrett’s esophagus. Some most interesting promising findings included aneuploidy (abnormal DNA content), amplification overexpression proto-oncogenes, loss heterozygosity at multiple chromosomal loci, tumor suppressor gene inactivation. Of particular importance is mutation deletion involving p53, but abnormalities retinoblastoma, deleted colon cancer, adenomatous polyposis coli genes described well. Recently, two important cancer pathways implicated genesis types also inculpated carcinogenesis: cyclin kinase inhibitor cascade mismatch repair process. Alterations p16 p15 inhibitors, including point homozygous deletion, reported primary tumors and/or tumor-derived lines. Microsatellite instability, hallmark defects, detected cancers, particularly those associated metaplasia (where it may represent an early event). Further field molecular carcinogenesis malignancies promise to yield improvements detection, prognostic categorization, perhaps eventual gene-based therapy deadly disease.