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Autophagy, a lysosomal degradation system, has both cell survival and cell death-promoting capabilities, and its versatility is exploited in many pathologic entities. In neoplastic processes, autophagy has been demonstrated to contribute to both tumor suppression and tumorigenesis in a relatively tumor-specific fashion. Beclin-1 is a protein involved in the formation of the autophagosome, the core unit of autophagy, and serves as one of the general markers for this process. Previous studies have shown Beclin-1 overexpression in both pre-neoplastic and invasive colon carcinoma but weak to absent expression in normal colonic mucosa.

Serrated polyps (SPs) of the colon represent morphologically and molecularly unique precursor lesions in the serrated adenoma-carcinoma pathway. The pathophysiology of the serrated pathway and its natural progression is of great interest. The specific role of autophagy in SPs is not fully described.

We evaluated SPs and autophagy using Beclin-1 protein, a general autophagy marker, to aid in the assessment of autophagy along the serrated pathway. Difference in Beclin-1 staining may represent variation in autophagy among polyp subtypes, exposing biological and possible clinically useful properties.