Ontology highlight
ABSTRACT:
PROVIDER: PRJNA937042 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Ovarian cancer is the most frequent cause of cancer death in women and the leading cause of death related to gynecological cancer, accounting for 5% of estimated cancer deaths. Due to its asymptomatic nature at early stages, most ovarian cancers were diagnosed at an advanced stage, with distant metastasis in the abdominal cavity. Cancer metastasis is the primary cause of morbidity, and contributes to 95% of cancer-related deaths. Metastatic ovarian cancer is closely related with recurrence and drug resistance, rendering metastasis as the major challenge in the course of ovarian cancer treatment. Thorough understanding of ovarian cancer metastasis is believed to contribute to improve cancer cure rates, while it is still not well elucidated. One important aspect of ovarian cancer metastasis research is the identification of driver molecular. To identify proteins required for ovarian cancer metastasis, we carried out unbiased high-throughput screening by comparing the expression profile of ovarian cancer primary and metastasis tissues.
2023-01-20 | GSE222982 | GEO
Project description:Epithelial ovarian cancer (EOC) constitutes a major gynecological malignancy, with a reported incidence rate of 3-12/100 000 woman annually. As early symptoms of ovarian cancer are often clinically atypical or absent, the majority of ovarian cancer patients are diagnosed at a late stage, when the five-year survival rate is extremely low. This condition underscores the urgency of early detection of these patients and establishment of new therapeutic targets for successful intervention. Considering that the predominant biological characteristic that differentiates malignant from benign tumors is the ability to metastasize, it is necessary to identify novel metastasis-related molecules for ovarian cancer. In this study, we found that CAFs could significantly increase the metastatic potential of ovarian cancer cells compared with non-cancer associated fibroblasts(NAFs), which is associated with over-expression of CXCL14 in CAFs. We examined the impact of CAF-secreted CXCL14 on the lncRNA expression profiles in ovarian cancer during metastasis.
2016-06-01 | GSE82059 | GEO
Project description:Colorectal cancer is a leading cause of cancer-related deaths. Mutations in the innate immune receptor AIM2 are frequently identified in patients with colorectal cancer, but how AIM2 modulates colonic tumorigenesis is unknown. Here, we found that Aim2-deficient mice were hypersusceptible to colonic tumor development. Production of inflammasome-associated cytokines and other inflammatory mediators were largely intact in Aim2-deficient mice, however, intestinal stem cells were prone to uncontrolled proliferation. Aberrant Wnt signaling expanded a population of tumor-initiating stem cells in the absence of AIM2. Susceptibility of Aim2-deficient mice to colorectal tumorigenesis was enhanced by a dysbiotic gut microbiota, which was reduced by reciprocal exchange of gut microbiota with wild-type healthy mice. These findings uncover a synergy between a specific host genetic factor and gut microbiota in determining the susceptibility to colorectal cancer. Therapeutic modulation of AIM2 expression and microbiota has the potential to prevent colorectal cancer. We used microarrays to compare the transcriptome Aim2 deficent mice to wild type mice in colon tumor and colitis samples. Here were 12 mice in total, 3 for each genotype and tissue combination.
2015-07-15 | E-GEOD-69436 | biostudies-arrayexpress
Project description:Interventions: Control:Null;Ovarian benign tumor:Null;Ovarian cancer:Null
Primary outcome(s): Gut microbiota;Blood routine examination;Pathology report
Study Design: Factorial
| 2695049 | ecrin-mdr-crc
Project description:Understanding the regulatory landscape of the human genome is a central question in complex trait genetics. Most single nucleotide polymorphisms (SNPs) associated with cancer risk lie in non protein-coding regions, implicating regulatory DNA elements as functional targets of susceptibility variants. Here, we describe genome-wide annotation of regions of open chromatin and histone modification in fallopian tube and ovarian surface epithelial cells (FTSECs, OSECs), the debated cellular origins of high-grade serous ovarian cancers (HGSOCs), and in endometriosis epithelial cells (EECs), the likely precursor of clear cell ovarian carcinomas (CCOCs). The regulatory architecture of these cell types was compared to normal human mammary epithelial cells (HMECs) and LNCaP prostate cancer cells. We observed similar positional patterns of global enhancer signatures across the three different ovarian cancer precursor cell types, and evidence of tissues specific regulatory signatures to non-gynecological cell types. We found significant enrichment for risk-associated SNPs intersecting regulatory biofeatures at 17 known HGSOC susceptibility loci in FTSECs (P=3.8x10-30) OSECs (P=2.4x10-23) and HMECs (P=6.7x10-15) but not for EECs (P=0.45) or LNCaP cells (P=0.88). Hierarchical clustering of risk SNPs conditioned on the six different cell types indicates FTSECs and OSECs are highly related (96% of samples using multi-scale bootstrapping) indicating both cell types may be precursors of HGSOC. These data represent the first description of regulatory catalogues of normal precursor cells for different ovarian cancer subtypes, and provide unique insights into the tissue specific regulatory variation with respect to the likely functional targets germline genetic susceptibility variants for ovarian cancer FAIRE-Seq and ChIP-Seq of 2 different histone modifications in 5 cell types.
2015-04-22 | E-GEOD-68104 | biostudies-arrayexpress