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Abstract
BackgroundSolid pseudopapillary neoplasms (SPN) are pancreatic tumors with low malignant potential and good prognosis. However, differential diagnosis between SPN and pancreatic malignancies including pancreatic neuroendocrine tumor (PanNET) and ductal adenocarcinoma (PDAC) is difficult. This study tried to identify candidate biomarkers for the distinction between SPN and the two malignant pancreatic tumors by examining the gene regulatory network of SPN.MethodsThe gene regulatory network for SPN was constructed by a co-expression model. Genes that have been reported to be correlated with SPN were used as the clues to hunt more SPN-related genes in the network according to a shortest path approach. By means of the K-nearest neighbor algorithm (KNN) classifier evaluated by the jackknife test, sets of genes to distinguish SPN and malignant pancreatic tumors were determined.ResultsWe took a new strategy to identify candidate biomarkers for differentiating SPN from the two malignant pancreatic tumors PanNET and PDAC by analyzing shortest paths among SPN-related genes in the gene regulatory network. 43 new SPN-relevant genes were discovered, among which, we found hsa-miR-194 and hsa-miR-7 along with 7 transcription factors (TFs) such as SOX11, SMAD3 and SOX4 etc. could correctly differentiate SPN from PanNET, while hsa-miR-204 and 4 TFs such as SOX9, TCF7 and PPARD etc. were demonstrated as the potential markers for SPN versus PDAC. 14 genes were demonstrated to serve as the candidate biomarkers for distinguishing SPN from PanNET and PDAC when considering them as malignant pancreatic tumors together.ConclusionThis study provides new candidate genes related to SPN and the potential biomarkers to differentiate SPN from PanNET and PDAC, which may help to diagnose patients with SPN in clinical setting. Furthermore, candidate biomarkers such as SOX11 and hsa-miR-204 which could cause cell proliferation but inhibit invasion or metastasis may be of importance in understanding the molecular mechanism of pancreatic oncogenesis and could be possible therapeutic targets for malignant pancreatic tumors.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-015-0718-3) contains supplementary material, which is available to authorized users.
Highlights
Solid pseudopapillary neoplasms (SPN) are pancreatic tumors with low malignant potential and good prognosis
By linking the members through shortest path method, we obtained new candidate SPN genes which are on the shortest paths
The strategy we proposed to discover candidate biomarkers to discriminate SPN from pancreatic neuroendocrine tumor (PanNET) or pancreatic ductal adenocarcinoma (PDAC) was to search for the candidate SPN-related genes through SPN gene regulatory network firstly, and to analyze the expression profiles by focusing on the resulted SPN genes in order to decrease the noise that most of the current large scale gene expression analysis are confronted with
Summary
Solid pseudopapillary neoplasms (SPN) are pancreatic tumors with low malignant potential and good prognosis. SPNs are most commonly confused with PanNETs which could occur at pancreatic tail, body and head like SPNs. The difficulty in diagnosis lies in that the two kinds of tumors have histological commonalities, including small- to medium-sized uniform cells with scanty cytoplasm, indiscernible nucleoli, hyaline globules, and numerous small blood vessels with hyalinized walls [9] and both of them behave monomorphous growth and rosette-like structures in morphology [7, 10]. The difficulty in diagnosis lies in that the two kinds of tumors have histological commonalities, including small- to medium-sized uniform cells with scanty cytoplasm, indiscernible nucleoli, hyaline globules, and numerous small blood vessels with hyalinized walls [9] and both of them behave monomorphous growth and rosette-like structures in morphology [7, 10] Both of them can express some neuroendocrine markers, such as CDH1, MME, VIM and CD56 [11]. We speculated that overexpression of SOX11 may contribute to the tumorigenesis but less malignant behaviours of SPN, the detailed mechanisms need further investigation
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