Affiliation:
1. Department of Pathology, University of California, San Francisco, California, USA; email: thea.tlsty@ucsf.edu
Abstract
Cancer research seeks to understand the biology underlying the progression to malignant transformation. Recently, the incidence of esophageal adenocarcinoma (EAC) has increased dramatically, and if we understand why and how, we will be better equipped for diagnosis, prognosis, detection, prevention, and intervention. The earliest steps in progression for most malignancies are the most difficult to study. The initiation of cancer is believed to be a relatively rare and sporadic event, the locations and timings of which are most often unknown. Of the trillions of somatic cells in our bodies, only a few ever find themselves on a path to malignancy. However, chronic inflammation generates a metaplastic lesion that is directly linked to increased incidence of EAC and thus alerts us to the time and place that progression is initiated and allows us to study the biology. We describe recent studies that identify coordinated actions between stromal and epithelial cells that progress to EAC.
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