Development of blood biomarkers that distinguish pancreatic cancer from biliary tract cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE212211 | GEO | 2023/06/30
REPOSITORIES: GEO
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Project description:Development of blood biomarkers that distinguish pancreatic cancer from biliary tract cancer
| PRJNA874583 | ENA
Project description:Purpose: To analyze human and bacteria proteomic profiles in bile, exposed to a tumor vs. non-tumor microenvironment, in order to identify differences between these conditions, which may contribute to a better understanding of pancreatic carcinogenesis. Patients and Methods: Using liquid chromatography and mass spectrometry, human and bacteria proteomic profiles of a total of 20 bile samples (7 from gallstone (GS) patients, and 13 from pancreatic head ductal adenocarcinoma (PDAC) patients) that were collected during surgery, and taken directly from the gallbladder were compared. g:Profiler and KEGG (Kyoto Encyclopedia of Genes and Genomes) Mapper Reconstruct Pathway was used as the main comparative platform focusing on over-represented biological pathways among human proteins and interaction pathways among bacterial proteins. Results: Three bacterial infection pathways were over-represented in the human PDAC group of proteins. IL-8 is the only human protein that coincides in the three pathways and this protein is only present in the PDAC group. Quantitative and qualitative differences in bacterial proteins suggest a dysbiotic microenvironment in the PDAC group, supported by significant participation of antibiotic biosynthesis enzymes. Prokaryote interaction signaling pathways highlight the presence of zeatin in the GS group and surfactin in the PDAC group, the former in the metabolism of terpenoids and polyketides, and the latter in both metabolisms of terpenoids, polyketides and quorum sensing. Based on our findings, we propose a bacterial-induced carcinogenesis model for the biliary tract. Conclusion: To the best of our knowledge this is the first study with the aim of comparing human and bacteria bile proteins in a tumor vs. non-tumor microenvironment. We proposed a new carcinogenesis model for the biliary tract based on bile metaproteomic findings. Our results suggest that bacteria may be key players in biliary tract carcinogenesis, in a long-lasting dysbiotic and epithelially harmful microenvironment, in which specific bacterial species biofilm formation is of utmost importance. Our finding should be further explored in future using in vitro and in vivo investigations
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Project description:Biliary atresia (BA) is a rare cholestatic disease of unknown etiology that affects infants and shows an incidence of 1 out of 18,000 live births in Europe (1). The first therapeutic option is a timely performed portoenterostomy. However, the majority of patients suffer from a progressive inflammatory process, which leads to complete destruction of the extra- and intrahepatic biliary system followed by end-stage liver cirrhosis. Hence, BA is the leading indication for pediatric liver transplantation worldwide (2, 3). To understand the pathogenesis of the disease and improve theoutcome of BA patients, research has focused on the inflammatory process in liver and bile ducts, in which several factors are remarkably elevated, such as activated CD4 and CD8 T-cells, TNF alpha,IFN alpha and other proinflammatory TH1 cytokines (3-8). By the time of diagnosis, however, the disease has already reached an advanced state, characterized by the complete obstruction of the extrahepatic bile ducts with impaired bile flow and fibrosis or cirrhosis of the liver. Therefore, studies in humans focusing on the trigger mechanism of BA are limited due to the paucity of liver and availability of bile duct tissue for research. One infectious animal model has been developed, in which newborn Balb/c mice exclusively show the experimental BA phenotype after infection with rhesus rotavirus (RRV) (9, 10). This model allows the analysis of the inflammatory reactions in liver and bile ducts at early steps in the development of bile duct atresia (11-20). Furthermore, inbred mouse strains have been shown to have a different susceptibility for the development of experimental BA, suggesting that Balb/c mice have an immunological gap responsible for disease progression (10, 12). The aim of this study was to identify key genes responsible for the BA phenotype by comparing the transcriptomes at an early time point after virus infection, i.e. before bile duct atresia, between two mouse strains with different susceptibilities to BA. Differences in the virus titration and the clinical course of infected mice were analyzed, and variations in the hepatic gene response assessed by comparative microarray assays were correlated to variances in the hepatic inflammatory reaction. Balb/c mice and C57Black/6 (Black/6) mice were infected with RRV postpartum and signs of BA and survival were noted. Liver sections of diseased, healthy and control animals were assessed for T-cell expression, and the virus loads were determined. Second, mice were sacrificed after three days, and isolated hepatic RNA was subjected to gene expression analysis using Affymetrix Gene Chip MOE 430 2.0.We compared three individual expression profiles from RRV-infected Balb/c mice against 2 individual expression profiles from RRV-infected C57/BL6 control mice using the Affymetrix GeneChip MOE 430 2.0.
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Project description:Bile draining by the bile duct system is paramount for good liver function. Diseases which compromise the integrity of the biliary tree are common and often life-threatening. Both intrahepatic and extrahepatic bile ducts contain distinct (stem) cell niches which are important for bile duct homeostasis and repair. A detailed characterization of the cell populations in the extrahepatic bile ducts has been lacking due to the inability of cell culture propagation. The aim of this study was to expand extrahepatic bile duct stem cells using the organoid culture system developed for intrahepatic bile duct cells. Extrahepatic bile duct (eBD)-organoids and intrahepatic (iBD) liver-derived organoids were initiated from paired biopsies of human common bile duct and liver tissue. Organoids of both origins were characterized on the basis of morphology and growth characteristics, gene and protein expression profiles, and their differentiation capacity towards mature cholangiocytes and hepatocytes. Although eBD organoids were very similar to iBD liver organoids, some differences in growth rate, organoid size and gene and protein expression were found. More strikingly, although both organoids could be differentiated towards a mature cholangiocyte phenotype, only iBD organoids can be directed to a mature hepatocyte phenotype. Of note, eBD organoids derived from a cystic fibrosis (CF) patient, harboring the same CFTR mutation (dF508-R1162X) as found in the patient, showed normal Ca2+-dependent Cl- channel and MDR-1 transporter activity but no CFTR channel activity. In conclusion, we here show feasibility of expanding eBD organoids with distinct properties when compared to iBD organoids. These eBD organoids may provide an excellent model for studying bile duct diseases and regenerative medicine.
| EGAS00001003792 | EGA