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Single-cell transcriptomics of normal pancreas, intraductal papillary mucinous neoplasm, and pancreatic adenosquamous carcinoma reveals the heterogeneous progression of pancreatic ductal and stromal cells

ABSTRACT: Single-cell transcriptomics of normal pancreas, intraductal papillary mucinous neoplasm, and pancreatic adenosquamous carcinoma reveals the heterogeneous progression of pancreatic ductal and stromal cells

PROVIDER: PRJNA694428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13516467_1.fastq.gz	Fastqsanger.gz
	SRR13516467_2.fastq.gz	Fastqsanger.gz
	SRR13516468_1.fastq.gz	Fastqsanger.gz
	SRR13516468_2.fastq.gz	Fastqsanger.gz
	SRR13516469_1.fastq.gz	Fastqsanger.gz

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A revised model of clonal evolution of intraductal papillary mucinous neoplasm-related pancreatic carcinogenesis

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Project description:Intraductal papillary mucinous neoplasm (IPMN) is a benign tumor that grows within the pancreatic ducts characterized by the production of thick mucinous fluid by surrounding tumor cells. IPMN is the most important precursor lesion for pancreatic cancer that is the fourth most common cause of cancer deaths. Differentiating between low-grade dysplasia (LGD), high-grade dysplasia (HGD), and invasive intraductal papillary mucinous neoplasms (IPMNs) remains a diagnostic challenge with current biomarkers, necessitating the development of novel biomarkers that can distinguish IPMN malignancy. We investigated differentially expressed proteins among pancreatic cyst fluids consisted of LGD, HGD, and invasive IPMN patients by using our novel proteomic strategy, and finally we discovered pancreatic cyst fluid protein marker candidates that can predict the malignant potential of IPMNs.

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Metabolic profiling of cyst fluid from patients with Intraductal Pancreatic Mucinous Neoplasm (part II)

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Single-cell transcriptomics of normal pancreas, intraductal papillary mucinous neoplasm, and pancreatic adenosquamous carcinoma reveals the heterogeneous progression of pancreatic ductal and stromal cells

Project description:Background: Single-cell RNA sequencing (scRNA-seq) contributes to discovering intrinsic heterogeneity of pancreatic adenosquamous carcinoma (PASC), a lethal human malignancy. However, the gene-pattern variations within ductal and stromal cells remain unclear. Methods: We fulfilled scRNA-seq profiling with one healthy donor pancreas, one intraductal papillary mucinous neoplasm (IPMN), and one PASC sample tissue. Multiple bioinformatics analyses were used to investigate the transcriptomics abnormalities from normal stage to tumor formation. Results: We identified ten subpopulations from 10,346 single cells, including myeloid, immune, ductal, fibroblast, acinar, stellate, endothelial, and malignant cells. Within our analysis, pancreatic cancer cells were further divided into five clusters; notably, cluster 1 exhibited stem-like phenotypes, such as UBE2C, ASPM, and TOP2A. We also found that S100A2 could be a specific biomarker for tumor cells, relating to PASC progression. LGALS1, NPM1, RACK1, and PERP were upregulated gradually from ductal to malignant cells. Furthermore, the level of copy number variation in ductal and cancer cells was significantly greater than reference cells. The expression of EREG, FCGR2A, FCGR2A, and CCL4L2 increased in myeloid cells along with tumor development, while cancer-associated fibroblast could induce the immunosuppressive tumor microenvironment, promoting pancreatic cancerogenesis. Finally, we demonstrated that EGFR-associated ligand-receptor pairs were activated in stromal to malignant cell communication. Conclusion: This study revealed the variations of ductal and stromal cells, defined cancer-associated signaling pathways, and deciphered cellular interactions following PASC progression. Thus, we provided valuable information to further understand the crucial regulatory mechanisms that embrace the potential therapeutic targets for PASC.

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Comprehensive Proteomic Characterization of Human Pancreatic Cyst Fluid from Intraductal Papillary Mucinous Neoplasm by LC-MS/MS

Project description:Intraductal papillary mucinous neoplasm (IPMN) is a duct-dilating precancerous lesion that grows in pancreatic ducts and is accompanied by the production of mucinous fluid. In recent years, its cystic fluid has been used molecularly for the differential diagnosis of other cystic tumors and malignancies. Thus, proteomic research of IPMN cyst fluid must be performed to identify an effective diagnostic biomarker. We examined the IPMN cyst fluid proteome using a novel proteomic strategy, combined with high-resolution LC-MS/MS. Although we did not deplete any high-abundance proteins, our dataset consistently detected thousands of proteins including pancreatic tumor markers, such as mucin family members, S100 proteins, and CEA-related proteins. In addition, we found 590 protein mutations through a variant sequence database search. Bioinformatics analyses were performed to determine biological functions and clinical meanings of canonical IPMN proteins and mutated proteins. Our proteomic platform and in-depth proteome dataset are valuable references that can be used in future studies.

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Project description:The increased number of pancreatic cyst lesions (PCLs) have been detected through the development of abdominal imaging techniques, such as computed tomography (CT), magnetic resonance imaging (MRI), and endoscopic ultrasound (EUS). However, accurate classification of cystic lesions is difficult because of the lack of standardized diagnostic methods, and thus potentially unnecessary surgical resection has been performed on pancreatic cyst patients. Among four most common types of cystic lesions of pancreas, intraductal papillary mucinous neoplasms (IPMNs), mucinous cystic neoplasms (MCN), serous cystic neoplasms (SCN), and solid pseudopapillary neoplasms (SPNs), IPMNs, the precursor lesion of pancreatic cancer, have been detected most frequently, and are subdivided into low-grade dysplasia (LGD), high-grade dysplasia (HGD), and invasive IPMN in accordance with their malignancy. To discover the potential biomarkers of the histological grades of IPMN, we investigated pancreatic cyst fluid proteins that are differentially expressed in accordance with the IPMN malignancy by LC-MS/MS analysis.

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A revised model of clonal evolution of intraductal papillary mucinous neoplasm-related pancreatic carcinogenesis

Project description:A revised model of clonal evolution of intraductal papillary mucinous neoplasm-related pancreatic carcinogenesis

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Improved Detection of Circulating Epithelial Cells in Patients with Intraductal Papillary Mucinous Neoplasms

Project description:Circulating epithelial cells (CECs) were purified using a microfluidic device from healthy donors, patients bearing intraductal papillary mucinous neoplasms, or pancreatic ductal adenocarcinoma and their transcriptomes were sequenced.

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miRNA expression profiles in Pancreatic Cystic tumours and Pancreatic Cancer

Project description:MicroRNA (miRNA) expression profiles have been described in pancreatic ductal adenocarcinoma (PDAC), but these have not been compared with premalignant lesions. We wished to identify miRNA expression profiles in pancreatic cystic tumors with low malignant potential (serous microcystic adenomas) and high malignant potential (mucinous cystadenoma and intraductal papillary mucinous neoplasm (IPMN)) and compare these to PDAC and carcinoma-ex-IPMN (CEI). n= 20 samples Benign Pancreatic Cystic Tumour (n=7 Microcystic, n= 6 Mucinous, n= 7 IPMN) were compared with n= 9 samples of carcinoma ex IPMN and n= 14 samples of pancreatic cancer (adenocarcinoma) for known homo sapiens miRNAs (mirbase 13).

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Nuclear GSK-3β and Oncogenic KRas Promote Expansion of Terminal Duct Cells and the Development of Intraductal Papillary Mucinous Neoplasm

Project description:Intraductal papillary mucinous neoplasm (IPMN) represents one precursor lesion of pancreatic ductal adenocarcinoma (PDA), but the cell-of-origin remains unclear. Here we describe a new mouse model in which pancreas-specific Cre activation of a nuclear glycogen synthase kinase-3β transgene is combined with oncogenic KRas (referred to as KNGC). KNGC mice show accumulation of neoplastic ductal cells at 4-weeks that progressively develop into IPMN with low-grade dysplasia in advanced age. RNA-sequencing identified expression of several genes found in the terminal duct cell lineage including Agr2 and Aqp5. Interestingly, Aqp5, a water channel, was found to be required for the development of IPMN lesions in KNGC mice. Staining of human IPMN samples indicates that these preneoplastic lesions also arise from expansion of the terminal duct population. Altogether, these data highlight the utility of the KNGC model for understanding the biology of IPMN and potential utility in defining predictive biomarkers of IPMN – PDA development.

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