Biology of esophageal cancer: Mechanisms of resistance and metastases

Cancer of the esophagus comes in two different types: adenocarcinoma (EAC) and squamous cell carcinoma (SCC). Multiple genetic changes, leading to genetic instability, and epigenetic phenomena, have been described to explain the malignant transformation. Recently we have started understanding the basis regulating tumorigenic processes in esophageal cancer but still, there is a lot to discover concerning to two of the most interesting questions in the field: the mechanisms of resistance to treatment and the process of metastases. Several mechanisms of resistance to treatment in esophageal cancer have been described in the literature. Some of them refer to resistance to induction of DNA damage an others to the induction of an apoptotic response. Many studies have tried to demonstrate a relation between a determined tumor phenotype and ability to form metastases. As a result many different markers have been stablished as prognosis factors. Recently, a brand new kind of studies defining gene expression signatures by cDNA microarray technology and tissue arrays are replacing the classic strategies in esophageal cancer. A new generation of studies with a more mechanistic approach has also arised during the latest years. Those studies are looking for determining the relationship between the presence of circulating or disseminated tumor cells and the ability to form metastases. Also, the emergence of new concepts are slowly revolutioning the understanding of tumor biology.