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Recurrent loss of heterozygosity correlates with clinical outcome in pancreatic neuroendocrine cancer

ABSTRACT: Pancreatic neuroendocrine tumors (pNETs) are uncommon cancers arising from pancreatic islet cells. Here we report analysis of gene mutation, copy number and RNA expression of 57 sporadic well-differentiated pNETs.

PROVIDER: EGAS00001003038 | EGA |

REPOSITORIES: EGA

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Recurrent loss of heterozygosity correlates with clinical outcome in pancreatic neuroendocrine cancer.

Project description:Pancreatic neuroendocrine tumors (pNETs) are uncommon cancers arising from pancreatic islet cells. Here we report the analysis of gene mutation, copy number, and RNA expression of 57 sporadic well-differentiated pNETs. pNET genomes are dominated by aneuploidy, leading to concordant changes in RNA expression at the level of whole chromosomes and chromosome segments. We observed two distinct patterns of somatic pNET aneuploidy that are associated with tumor pathology and patient prognosis. Approximately 26% of the patients in this series had pNETs with genomes characterized by recurrent loss of heterozygosity (LoH) of 10 specific chromosomes, accompanied by bi-allelic MEN1 inactivation and generally poor clinical outcome. Another ~40% of patients had pNETs that lacked this recurrent LoH pattern but had chromosome 11 LoH, bi-allelic MEN1 inactivation, and universally good clinical outcome. The somatic aneuploidy allowed pathogenic germline variants (e.g., ATM) to be expressed unopposed, with RNA expression patterns showing inactivation of downstream tumor suppressor pathways. No prognostic associations were found with tumor morphology, single gene mutation, or expression of RNAs reflecting the activity of immune, differentiation, proliferative or tumor suppressor pathways. In pNETs, single gene mutations appear to be less important than aneuploidy, with MEN1 the only statistically significant recurrently mutated driver gene. In addition, only one pNET in the series had clearly actionable single nucleotide variants (SNVs) (in PTEN and FLCN) confirmed by corroborating RNA expression changes. The two clinically relevant patterns of LoH described here define a novel oncogenic mechanism and a plausible route to genomic precision oncology for this tumor type.

| S-EPMC6054670 | biostudies-literature

DNA methylation and Panel sequencing for pancreatic neuroendocrine carcinomas (PanNECs) and pancreatic neuroendocrine tumors (PanNETs)

Project description:Pancreatic Neuroendocrine Neoplasms (PanNENs) are two subclasses: the well-differentiated, low to high-grade Pancreatic Neuroendocrine Tumors (PanNETs) and the poorly-differentiated, high-grade Pancreatic Neuroendocrine Carcinomas (PanNECs). DNA methylation and sequencing was performed for 57 PanNEN samples to decipher distinct methylation profiles separating PanNENs. Our study provides a robust and clinically applicable method to clearly distinguish PanNECs from PanNETG3s and improve patient stratification.

| EGAS00001005731 | EGA

Gene expression of pancreatic tumors

Project description:Solid-pseudopapillary neoplasm of pancreas(SPN), ductal adenocarcinoma(PCA), neuroendocrine tumor(NET) and non-neoplastic pancreas. To investigate the specific gene expression of SPN compared to other types of pancreatic tumor, we analyzed large-scale gene expressioin analysis to identify the molecular signature that may affect SPN tumorigenesis. Differentially expressed genes were analyzed on SPNs, PCAs, NETs and Non-neoplastic tissues. Solid-pseudopapillary neoplasm (SPN) is an uncommon pancreatic tumor with distinct clinicopathologic features. SPNs are characterized by mutations in exon 3 of CTNNB1. However, little is known about the gene and microRNA expression profiles of SPNs. Thus, we sought to characterize SPN-specific gene expression and identify the signaling pathways activated in these tumors. The mRNA expression profile of 14 SPNs, 6 pancreatic adenocarcinomas (PCAs), 6 pancreatic neuroendocrine tumors (NETs), and five non-neoplastic pancreatic tissues were analyzed.

2013-12-31 | E-GEOD-43795 | biostudies-arrayexpress

Proteogenomic characterization of pancreatic neuroendocrine tumor

Project description:To characterize pancreatic neuroendocrine tumor at protein level, we performed mass spectromery-based proteome analysis using clinical FFPE tissue samples.

2024-07-10 | PXD034571 | Pride

Gene expression profiling of pancreatic neuroendocrine carcinoma and mixed neuroendocrine-non-neuroendocrine neoplasm

Project description:Pancreatic neuroendocrine carcinoma (NEC) and mixed neuroendocrine-non-neuroendocrine neoplasm (MiNEN) are rare pancreatic malignant tumors, and comprehensive gene analyses are scarce. In this study, six NECs and six MiNENs were collected, immunohistochemistry for synaptophysin, chromogranin A, INSM1, Ki-67, and Rb was conducted, and KRAS mutational status was examined. Among these cases, comprehensive gene expression analysis of oncogene pathways using nCounter® were performed with six NECs and four MiNENs, and those data were compared with that of three pancreatic ductal adenocarcinomas (PDACs), with that of three normal pancreatic ducts, and with each other. By dividing NEC and MiNEN cases into KRAS-mutated group and KRAS-wild group, the difference of clinicopathological data and gene expression profiling data were examined between the two groups. Compared to the data of normal pancreatic epithelium, all 13 cancer-related pathways were upregulated in PDAC, MiNEN, and NEC group with more upregulation in this order. Compared to the data of PDAC, genes of DNA Damage repair pathway was most upregulated both in NECs and MiNENs. Regarding the difference between KRAS-mutated and KRAS-wild groups, several genes were differentially expressed between the two, where MMP7 was the upregulated gene with highest p-value and NKD1 was the downregulated gene with highest p-value in KRAS-mutated group. From the extent of upregulation of 13 pathways, MiNEN was considered more progressed stage than PDAC, and NEC was considered more progressed than MiNEN. From the comparison of KRAS-mutated and KRAS-wild NECs and MiNENs, several differentially expressed genes were identified in this study.

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Project description:Pancreatic neuroendocrine neoplasms (PNENs) are biologically and clinically heterogeneous neoplasms. We used quantitative global proteomic analysis on 40 PNENs to compliment paired transcriptome data.

2021-11-30 | PXD024175 | Pride

RHAMMB promotes metastasis of pancreatic neuroendocrine tumor

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2024-04-16 | GSE200497 | GEO

GCGR Loss-of-Function Mutations Promote Amino Acid-Dependent Pancreatic Neuroendocrine Tumor Initiation from a Subpopulation of Alpha Cells [single-cell RNA-seq]

Project description:Evaluating cell subpopulations in mouse pancreatic islets and pancreatic tumors

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Pancreatic Stellate Cells Promote Growth and Metastasis of Pancreatic Neuroendocrine Tumor

Project description:We aimed to study the interaction of PNETs and pancreatic stellate cells (PSCs) in PNET progression through exploring specific gene expression of PNETs cultured with conditional media of PSCs.

2024-02-22 | GSE167321 | GEO

GATA4 and GATA6 loss-of-expression is associated with extinction of the "classical" programme and poor outcome in pancreatic ductal adenocarcinoma

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