Differentiation and cancer

Cancers are, in most cases, the outcome of unlimited proliferation but also deregulated differentiation and apoptosis, resulting in disruption of tissue microarchitecture. In fact, one of the challenges of adult tissues, particularly epithelial ones, is to maintain the normal differentiation as cells renew and, more importantly, upon injury. Many tissues fail the later and regenerate changing differentiation – a process designated metaplasia – which is, in some cases, the first step in a carcinogenic cascade. Metaplasia is a frequent event throughout the gastrointestinal tract, most significantly in the anterior part with the appearance of intestinal differentiation in esophagus and stomach upon chronic injury, but it is also present in intestine, with the appearance of esophageal and gastric differentiation under chronic inflammatory conditions and in different polypoid syndromes.
It is our main goal to understand how these differentiation shifts predispose and progress to cancer and ultimately identify novel biomarkers and therapeutic targets to improve diagnostic screening, prevention, patient stratification and treatment of cancers of the GI tract.

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