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Neuroendocrine carcinomas arising in ulcerative colitis:Coincidences or possible correlations?

World Journal of Gastroenterology 2009年第33期15卷 4193-4195页

作者： Roberto Grassia Paolo Bodini Paolo Dizioli Teresa Staiano Elena Iiritano guglielmo bianchi Federico Buffoli Digestive Endoscopy and Gastroenterology Unit A.O. "Istituti Ospitalieri di Cremona"

Patients with in· ammatory bowel disease (IBD) are at increased risk of colorectal malignancies. Adenocarcinoma is the commonest type of colorectal neoplasm associated with ulcerative colitis (UC) and Crohn's disease, but other types of epithelial and non-epithelial tumors have also been described in inflamed bowel. With regards to non-epithelial malignancies, lymphomas and sarcomas represent the largest group of tumors reported in association with IBD, especially in immunosuppressed patients. Carcinoids and in particular neuroendocrine neoplasms other than carcinoids (NENs) are rare tumors and are infrequently described in the setting of IBD. Thus, this association requires further investigation. We report two cases of neoplasms arising in mild left-sided UC with immuno-histochemical staining for neuroendocrine markers: a large cell and a small cell neuroendocrine carcinoma of the rectum. The two patients were different in age (35 years vs 77 years) and disease duration (11 years vs 27 years), and both had never received immuno-suppressant drugs. Although the patients underwent regular endoscopic and histological follow-up, the two neoplasms were locally advanced at diagnosis. One of the two patients developed multiple liver metastases and died 15 mo after diagnosis. These findings confirm the aggressiveness and the poor prognosis of NENs compared to colorectal adenocarcinoma. While carcinoids seem to be coincidentally associated with IBD, NENs may also arise in this setting. In fact, long-stand-ing in· ammation could be directly responsible for thedevelopment of pancellular dysplasia involving epithelial, goblet, Paneth and neuroendocrine cells. It has yet to be established which IBD patients have a higher risk of developing NENs.

关键词：溃疡性结肠炎神经内分泌癌

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S100B protein in tissue development,repair and regeneration

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World Journal of Biological Chemistry 2013年第1期4卷 1-12页

作者： guglielmo Sorci Francesca Riuzzi Cataldo Arcuri Claudia Tubaro Roberta bianchi Ileana Giambanco Rosario Donato Department of Experimental Medicine and Biochemical Sciences University of Perugia06122 PerugiaItaly Francesca Riuzzi Rosario DonatoInteruniversity Institute for MyologyUniversity of Perugia06122 PerugiaItaly

The Ca 2+-binding protein of the EF-hand type,S100B,exerts both intracellular and extracellular regulatory *** an intracellular regulator,S100B is involved in the regulation of energy metabolism,transcription,protein phosphorylation,cell proliferation,survival,differentiation and motility,and Ca 2+ homeostasis,by interacting with a wide array of proteins(i.e.,enzymes,enzyme substrates,cytoskeletal subunits,scaffold/adaptor proteins,transcription factors,ubiquitin E3 ligases,ion channels) in a restricted number of cell *** an extracellular signal,S100B engages the pattern recognition receptor,receptor for advanced glycation end-products(RAGE),on immune cells as well as on neuronal,astrocytic and microglial cells,vascular smooth muscle cells,skeletal myoblasts and ***,RAGE may not be the sole receptor activated by S100B,the protein being able to enhance bFGF-FGFR1 signaling by interacting with FGFR1-bound bFGF in particular cell ***,extracellular effects of S100B vary depending on its local *** evidence suggests that at the concentration found in extracellular fluids in normal physiological conditions and locally upon acute tissue injury,which is up to a few nM levels,S100B exerts trophic effects in the central and peripheral nervous system and in skeletal muscle tissue thus participating in tissue *** present commentary summarizes results implicating intracellular and extracellular S100B in tissue development,repair and regeneration.

关键词： S100B Cell proliferation Cell differentiation Cell survival Cell motility Development Tissue homeostasis Tissue repair Tissue regeneration

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