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10.1016/j.dld.2020.05.027

http://scihub22266oqcxt.onion/10.1016/j.dld.2020.05.027
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32505565!?!32505565

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suck abstract from ncbi

pmid32505565      Dig+Liver+Dis 2020 ; 52 (10): 1188-1194
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  • TRPM7 is overexpressed in human IBD-related and sporadic colorectal cancer and correlates with tumor grade #MMPMID32505565
  • Pugliese D; Armuzzi A; Castri F; Benvenuto R; Mangoni A; Guidi L; Gasbarrini A; Rapaccini GL; Wolf FI; Trapani V
  • Dig Liver Dis 2020[Oct]; 52 (10): 1188-1194 PMID32505565show ga
  • BACKGROUND: Inflammatory bowel disease (IBD) predisposes to colorectal cancer (CRC) with some specific features that distinguish it from sporadic CRC. Magnesium (Mg) homeostasis is severely compromised in IBD patients, which may affect both inflammation and tumor development. Efficient transcellular Mg transport in intestinal cells depends on the transient receptor potential melastatin (TRPM) channels type 6 and 7, but their expression has never been investigated in the context of IBD-related CRC. AIMS: We sought to study the expression pattern of TRPM6 and TRPM7 in CRC, and to compare IBD-related cases to sporadic cases. METHODS: TRPM6 and TRPM7 protein expression was evaluated by immunohistochemistry in surgical specimens from 16 IBD and 13 NON-IBD CRC patients. RESULTS: TRPM7 expression was higher in tumor tissue than in the adjacent non-neoplastic tissue in both IBD and NON-IBD patients. Overall, adenocarcinomas showed a higher TRPM7 expression than adenomas. TRPM7 expression also positively correlated with tumor grade. Conversely, TRPM6 expression was higher in tumor tissues in both IBD and NON-IBD CRC, but it did not correlate with tumor stage or grade. CONCLUSIONS: We report a possible participation of TRPM6 and 7 in both IBD-related and sporadic CRC and suggest that TRPM7 might serve as a marker of malignant transformation and lack of differentiation.
  • |Adenocarcinoma/etiology/*genetics[MESH]
  • |Biomarkers/blood[MESH]
  • |Case-Control Studies[MESH]
  • |Colorectal Neoplasms/etiology/*genetics/pathology[MESH]
  • |Female[MESH]
  • |Gene Expression[MESH]
  • |Humans[MESH]
  • |Inflammatory Bowel Diseases/complications/*genetics[MESH]
  • |Magnesium/metabolism[MESH]
  • |Male[MESH]
  • |Protein Serine-Threonine Kinases/*genetics[MESH]


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