{"title":"Gum, Sap and Canker-Colloid Carcinoma-Pancreas","authors":"Anu Bajaj","doi":"10.56397/crms.2023.03.11","DOIUrl":null,"url":null,"abstract":"Colloid carcinoma pancreas is an infiltrative ductal epithelial neoplasm of pancreas characteristically denominating a preponderant (>80%) component of enlarged pools of extracellular stromal mucin pervaded with suspended neoplastic cells. Colloid carcinoma pancreas is a microsatellite stable tumefaction and exhibits KRAS genetic mutation confined to codon 12. Tumefaction is posited to arise from inverse polarization of cells with stromal mucin glycoproteins facing intrinsic cellular surface. Cogent clinical symptoms as abdominal or epigastric pain, pancreatitis, diarrhoea, hyperbilirubinemia or loss of weight are discerned. Tumefaction emerges as an enlarged, well demarcated lesion with a mean diameter of 5 centimetres and a solid, firm, gelatinous cut surface. Neoplasm is predominantly comprised of enlarged, extracellular accumulates of stromal mucin with minimal carcinoma cells suspended within extra-cellular mucin pools. Cuboidal or columnar epithelial cells configure cribriform or stellate cellular clusters or miniature tubules and strips of columnar cells along with signet ring cells. Colloid carcinoma pancreas is intensely immune reactive to CDX2, MUC2 and CEA. Neoplasm requires segregation from tumours as extravasation of benign stromal mucin, intra-ductal papillary mucinous neoplasm, mucinous cystic neoplasm or conventional pancreatic ductal adenocarcinoma. Colloid carcinoma pancreas is devoid of specific therapeutic guidelines or recommended treatment.","PeriodicalId":72751,"journal":{"name":"Current research in medical sciences","volume":"28 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current research in medical sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.56397/crms.2023.03.11","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Colloid carcinoma pancreas is an infiltrative ductal epithelial neoplasm of pancreas characteristically denominating a preponderant (>80%) component of enlarged pools of extracellular stromal mucin pervaded with suspended neoplastic cells. Colloid carcinoma pancreas is a microsatellite stable tumefaction and exhibits KRAS genetic mutation confined to codon 12. Tumefaction is posited to arise from inverse polarization of cells with stromal mucin glycoproteins facing intrinsic cellular surface. Cogent clinical symptoms as abdominal or epigastric pain, pancreatitis, diarrhoea, hyperbilirubinemia or loss of weight are discerned. Tumefaction emerges as an enlarged, well demarcated lesion with a mean diameter of 5 centimetres and a solid, firm, gelatinous cut surface. Neoplasm is predominantly comprised of enlarged, extracellular accumulates of stromal mucin with minimal carcinoma cells suspended within extra-cellular mucin pools. Cuboidal or columnar epithelial cells configure cribriform or stellate cellular clusters or miniature tubules and strips of columnar cells along with signet ring cells. Colloid carcinoma pancreas is intensely immune reactive to CDX2, MUC2 and CEA. Neoplasm requires segregation from tumours as extravasation of benign stromal mucin, intra-ductal papillary mucinous neoplasm, mucinous cystic neoplasm or conventional pancreatic ductal adenocarcinoma. Colloid carcinoma pancreas is devoid of specific therapeutic guidelines or recommended treatment.