Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1041943 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26866802_1.fastq.gz | Fastqsanger.gz | |||
| SRR26866802_2.fastq.gz | Fastqsanger.gz | |||
| SRR26866803_1.fastq.gz | Fastqsanger.gz | |||
| SRR26866803_2.fastq.gz | Fastqsanger.gz | |||
| SRR26866804_1.fastq.gz | Fastqsanger.gz |
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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:Pancreatic cancer is among the deadliest cancers that affects almost 54,000 patients in United States alone, with 90% of them succumbing to the disease. Lack of early detection is considered to be the foremost reason for such dismal survival rates. Our study shows that resident gut microbiota is altered at the early stages of tumorigenesis much before development of observable tumors in a spontaneous, genetically engineered mouse model for pancreatic cancer. In the current study, we analyzed the microbiome of in a genetic mouse model for PDAC (KRASG12DTP53R172HPdxCre or KPC) and age-matched controls using WGS at very early time points of tumorigenesis. During these time points, the KPC mice do not show any detectable tumors in their pancreas. Our results show that at these early time points, the histological changes in the pancreas correspond to a significant change in certain gut microbial population. Our predictive metabolomic analysis on the identified bacterial species reveal that the primary microbial metabolites involved in progression and development of PDAC tumors are involved in polyamine metabolism.
2019-07-07 | E-MTAB-6921 | biostudies-arrayexpress
Project description:Cancer is a disease of the genome. Many genomic abnormalities have been found in a variety of cancer types, which are believed to be attributable to tumorigenesis as well as resistance to treatment and recurrence. Genomic heterogeneity in the same type of cancer or within a tumor reveals the complexity of cancer biology so that intratumor heterogeneity has become an inherent feature of cancer. In this study, we use whole-exome sequencing and array comparative genomic hybridization technology to examine the mutational profiling and copy number changes from multi-region samples within an esophageal cancer in order to understand the genomic phylogeny in the evolution of intratumor heterogeneity in esophageal cancer.
2014-12-31 | GSE60625 | GEO
Project description:We classified samples and deciphered a key genes signature of intratumor heterogeneity by Principal Component Analysis and Weighted Gene Co-expression Network Analysis. Transcriptome analysis highlighted a pronounced intratumor architecture reflecting the surgical sampling plan of the study and identified gene modules associated with hallmarks of cancer.
2016-09-19 | E-MTAB-5092 | biostudies-arrayexpress
Project description:We classified samples and deciphered a key genes signature of intratumor heterogeneity by Principal Component Analysis and Weighted Gene Co-expression Network Analysis. We provide a signature of key cancer-heterogeneity genes highly associated with the intratumor spatial gradient and show that it is enriched in genes with correlation between methylation and expression levels.
2016-09-19 | E-MTAB-5109 | biostudies-arrayexpress
Project description:Background: Mortality rates of pancreatic cancer remain high, which is mainly due to advanced disease and metastasis. We hypothesized that DNA copy number alteration are enriched in metastatic cells compared to autologous primary tumors, which may inform on cancer-related pathways possibly serving as potential targets for specific therapies. We investigated 18 pancreatic ductal adenocarcinomas, including 39 lymph node and 5 distant metastases after surgical resection. Analysis was performed with array-based comparative genomic hybridization. Results: Metastases acquire a higher frequency of CNAs with the highest in distant metastasis (OM: median=42, LNM: median=23, PT: median=17). In LNM, gains were prevalent on chromosome bands 8q11.23-q24.3, 12q14.1, 17p12.1, 21q22.12, and losses on 3p21.31, 4p14, 8p23.3-p11.21,17p12-11.2. Genes on amplified regions are involved in cancer-related pathways such as WNT-signaling, also involved in metastasis. Conclusions: Pancreatic cancers show a high degree of intratumor heterogeneity, which could lead to resistance of chemotherapy and worse outcome. ACGH analysis reveals regions preferentially gained or lost in synchronous metastases encoding for genes involved in cancer-related pathways, which could lead to novel therapeutic opportunities.
2017-10-01 | GSE103787 | GEO
Project description:This project is reporting on microdissection proteomics of human operable, non-neoadjuvant treated pancreatic ductal adenocarcinomas (PDAC) with deep coverage of histologically neoplastic and adjacent healthier exocrine glands as well as stromal regions surrounding both. Through proteomic analysis, the parenchymal sample types differed significantly, with the malignant regions characterized by a broad downregulation of digestive enzymes. Instead, the stromal areas were alike, dominated by extracellular matrix proteins and lower expression of most metabolic pathways compared to the exocrine areas. Cholesterol synthesizing enzymes were more abundant in the tumor than stroma, as confirmed by an independent PDAC dataset and immunohistochemistry of PDAC microarrays. However, this was not accompanied by intratumor lipid deposition. Pathways most prognostic for survival were unexpectedly enriched in the histologically healthier exocrine glands, with a specific prognostic marker. Systematic analysis of pancreatic cancer transcriptomes from The Cancer Genome Atlas revealed that increased transcriptional complexity confers poor prognosis in PDAC.
2022-09-05 | PXD026371 | Pride
Project description:Leveraging the cGAS-STING DNA sensing pathway in dendritic cells (DCs) for anti-pancreatic tumor immunity is challenging due to activation constraints, particularly in the context of pancreatic cancer's immunotherapeutic resistance. Recent research indicates that magnesium (Mn2+) enhances cGAS sensitivity to DNA, although the precise mechanism remains unclear. In this study, we demonstrate that the addition of Mn2+ increases the affinity of tumor cell-DNA binding to cGAS. Utilizing a Raft-Ultra method, we engineered immunogenic extracellular vesicles (EVs) derived from tumor cell lysate-pulsed DCs, loaded with Mn-DNA complexes (EVDC@Mn-DNA). These EVs efficiently deliver DNA to DCs, activating the cGAS-STING pathway both in vitro and in vivo. Animal experiments reveal that administering EVDC@Mn-DNA enhances vascular function, as evidenced by increased blood flow/perfusion, improved anti-PD-L1 delivery, reduced hypoxia, and elevated endothelial expression of the T cell adhesion molecule ICAM1. Furthermore, this treatment promotes the intratumor population of activated DCs and T cells and increases the sizes of tertiary lymphoid structures, thereby restraining orthotopic pancreatic tumor growth. Overall, our EVDC@Mn-DNA strategy activates intratumor DCs, restoring vascular-immune cell homeostasis and stimulating anti-tumor immunity in pancreatic cancer.
2024-04-15 | PXD051467 |