Dataset Information

Profiling of Kallikrein Proteases and Global Proteome Biology of PDAC, Chronic Pancreatitis and Normal Pancreas

ABSTRACT: Cell conditioned medium from human pancreatic cancer cell lines MiaPaCa-2, AsPC-1, primary pancreatic cell lines as well as human FFPE tissue samples from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), ampullary cancer, non-malignant adjacent pancreas and normal pancreas were analyzed via targeted (SRM, PRM) and/or explorative (DIA) mass spectrometry.

INSTRUMENT(S): TSQ Vantage, Q Exactive Plus

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Prof. Oliver Schilling

PROVIDER: MSV000090255 | MassIVE |

REPOSITORIES: MassIVE

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Publications

Targeted and explorative profiling of kallikrein proteases and global proteome biology of pancreatic ductal adenocarcinoma, chronic pancreatitis, and normal pancreas highlights disease-specific proteome remodelling.

Werner Janina J Bernhard Patrick P Cosenza-Contreras Miguel M Pinter Niko N Fahrner Matthias M Pallavi Prama P Eberhard Johannes J Bronsert Peter P Rückert Felix F Schilling Oliver O

Neoplasia (New York, N.Y.) 20230105

Pancreatic ductal adenocarcinoma (PDAC) represents one of the most aggressive and lethal malignancies worldwide with an urgent need for new diagnostic and therapeutic strategies. One major risk factor for PDAC is the pre-indication of chronic pancreatitis (CP), which represents highly inflammatory pancreatic tissue. Kallikreins (KLKs) are secreted serine proteases that play an important role in various cancers as components of the tumor microenvironment. Previous studies of KLKs in solid tumors ...[more]

PMID: 36610378

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Project description:This is the experiment set used for a paper written in collaboration with Hopkins. It compares genes that are differentially expressed between normal pancreas, pancreatic cell lines and pancreatic adenocarcinoma. Pancreatic cancer is the fifth leading cause of cancer death in the United States. We used cDNA microarrays to analyze global gene expression patterns in 14 pancreatic cancer cell lines, 17 resected infiltrating pancreatic cancer tissues, and 5 samples of normal pancreas to identify genes that are differentially expressed in pancreatic cancer. We found more than 400 cDNAs corresponding to genes that were differentially expressed in the pancreatic cancer tissues and cell lines as compared to normal pancreas. These genes that tended to be expressed at higher levels in pancreatic cancers were associated with a variety of processes, including cell-cell and cell-matrix interactions, cytoskeletal remodeling, proteolytic activity, and Ca(++) homeostasis. Two prominent clusters of genes were related to the high rates of cellular proliferation in pancreatic cancer cell lines and the host desmoplastic response in the resected pancreatic cancer tissues. Of 149 genes identified as more highly expressed in the pancreatic cancers compared with normal pancreas, 103 genes have not been previously reported in association with pancreatic cancer. The expression patterns of 14 of these highly expressed genes were validated by either immunohistochemistry or reverse transcriptase-polymerase chain reaction as being expressed in pancreatic cancer. The overexpression of one gene in particular, 14-3-3 sigma, was found to be associated with aberrant hypomethylation in the majority of pancreatic cancers analyzed. The genes and expressed sequence tags presented in this study provide clues to the pathobiology of pancreatic cancer and implicate a large number of potentially new molecular markers for the detection and treatment of pancreatic cancer. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Using regression correlation