Interaction of microsatellite instability and loss of heterozygosity in adenocarcinoma: multiple markers in adenocarcinoma: an introduction to ‘Genetic changes in Slovenian patients with gastric adenocarcinoma evaluated in terms of microsatellite DNA’

Abstract

Gastric cancer is the second most frequent cause of cancer death worldwide, yet the precise mechanisms underlying the different subtypes of gastric carcinogenesis are poorly understood. Improvements in the diagnosis and prognosis of gastric cancer over classical clinicopathologic findings such as TNM stage, age or macroscopic tumor type, now include novel techniques for superficial endoscopic examination, and new strategies for genetically analyzing biopsied specimens. The development of gastric adenocarcinomas, such as that of many tumor classes, represents the cumulative effects of several different types of mutations, and it is now recognized that both the loss of normal DNA repair, as well as the mutation, loss or inhibition of tumor suppressor genes contribute to the genetic instability leading to cancer. It might be logically anticipated that the combined burden of these two defects would synergize in carcinogenesis, but the extent to which such pathways cooperate in promoting cancer is still not yet well understood. Clearly, an enhanced appreciation of the mechanisms and interactions of these pathways would aid development of diagnosis and treatment options.