Abstract
cells displayed cytoprotection through crinophagy. The longer gastrin stimulation (months), the more accumulation of lipofuscin bodies, leading to an impaired function and eventually, cell death. The poorly differentiated cells within the ECL cell tumor are probably derived directly or indirectly via runaway autophagy which is associated with anti-apoptotic pathways. We suggest that autophagy-targeted therapy should focus on this runaway pathway in gastrin-driven neoplasia.
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