COMMENTS Background Gastric carcinoids (GCAs) are rare neuroendoc

COMMENTS Background Gastric carcinoids (GCAs) are rare neuroendocrine tumors (NETs) of the gastric mucosa originating from enterochromaffin like (ECL) cells. Type 1 (GCA1) represents the majority, and usually carries an excellent overall prognosis. Research frontiers Metastatic GCA1 are extremely rare and little is known about their natural Sorafenib VEGFR-2 history, treatment and prognosis. The present study represents a multicenter, retrospective analysis aiming to describe disease characteristics and treatment modalities in a group of rare patients with metastatic GCA1. Innovations and breakthroughs The authors demonstrated that the metastatic potential of GCA1 appears to be related to a tumor size of �� 1 cm, an elevated Ki-67 index and high serum gastrin levels. Endoscopic ultrasound is recommended in patients with these risk factors.

Somatostatin analogues may be used, particularly in patients with multiple relapsing tumors, and with metastatic disease. Surgical procedures should be performed only in patients in whom total tumor excision is expected. Applications By understanding the potential malignant behavior of these rare tumors, this study may represent a future strategy for therapeutic intervention in patients with metastatic GCA1. Peer review This is a useful multicenter, retrospective analysis of a rare disease and provides helpful information on risk factors, tumor characteristics, treatment procedures and prognosis in a wide and rare group of patients with metastatic GCA1.

Footnotes P- Reviewers: Deutsch JC, Massironi S, Pritchard DM, Vitale G S- Editor: Wen LL L- Editor: A E- Editor: Ma S
the two common, but disparate, forms of inflammatory bowel disease (IBD), Crohn’s disease and ulcerative colitis, are associated with increased reactive oxygen species (ROS) and decreased antioxidant enzymes in the intestinal mucosa (2, 34, 38, 41, 47). Exogenous ROS and the proinflammatory cytokine TNF��, both of which are increased during IBD, promote cellular injury via mitochondrial ROS production (12, 13, 44). Damaged mitochondria are a key source of increased intracellular ROS from respiratory chain dysfunction, disturbing cellular homeostasis, which can result in cell death (9). Prohibitin 1 (PHB) belongs to a family of proteins that share an evolutionarily conserved stomatin/PHB/flotillin/HflK/C domain and serves diverse roles in cell function.

PHB has been shown to regulate cell cycle progression, apoptosis, and transcription factor activity in multiple cell types (37, 54, 55). PHB is highly expressed in intestinal epithelial cells, with predominant subcellular localization Brefeldin_A to the mitochondria (49). Expression of PHB is decreased in mucosal biopsies from ulcerative colitis- and Crohn’s disease-afflicted patients and in animal models of colitis (16, 49). TNF�� decreases expression of intestinal epithelial PHB in vivo and in vitro (50).

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