Diagnosis of colorectal cancer by serum and exosomal CEA family and detection of circulating tumo cells
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer
PROVIDER: 2629030 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
Similar Datasets
Project description:We used microarrays to detailed global expression of colorectal cancer cells that expressed high or low levels of carcinoembryonic antigen. CEA high and CEA low cells were purified from LoVo and xenograft tumor derived from colorectal cancer patient (xhCRC) and were used for RNA extraction.
2015-08-27 | E-GEOD-72398 | biostudies-arrayexpress
Project description:The central amygdala (CEA) is a brain region that consists of primarily GABAergic neurons. It has been widely investigated for its role in many innate and adaptive behaviors, such as appetitive and defensive behaviors. Despite the complex functions of CEA, the molecular diversity of CEA neurons has not been systemically examined. Here, we performed single-cell RNA-sequencing (scRNA-Seq) in the CEA to classify the molecularly defined neuron types in this region.
2023-02-03 | GSE213828 | GEO
Project description:A crucial step in understanding the sleep-control mechanism is to identify sleep neurons. In principle, a neuron could promote sleep by inhibiting wake-promoting neurons. Using rabies virus (RV)-mediated transsynaptic tracing, we identified several brain regions with GABAergic neurons that broadly inhibit multiple wake-promoting neuronal populations, and the most prominent source of GABAergic inputs was found in a posterior part of the CeA. The CeA is known to contain multiple subtypes of GABAergic neurons with distinct molecular markers, projection targets, and functional properties. Using translating ribosome affinity purification (TRAP) RNA-Seq, we identified molecular markers for the canditate sleep-promoting neurons in CeA.
2020-04-06 | GSE121888 | GEO
Project description:BackgroundA reliable noninvasive biomarker is not yet available for endometriosis diagnosis. Novel biomarkers for the diagnosis of endometriosis are urgently needed. The molecular constituents of exosomes, especially exosomal microRNAs (miRNAs), have considerable potential as novel biomarkers for clinical diagnosis. This study is aimed at exploring aberrant exosomal miRNA profiles by using miRNA microarray and at providing more accurate molecular biomarkers of endometriosis.MethodsExosomes were isolated from the serum of patients with endometriosis and negative controls and identified by electron microscopy, nanoparticle tracking analysis, and Western blot. Exosomal miRNAs were profiled by miRNA microarrays. The expression of selective serum exosomal miRNA was validated by qRT-PCR. Receiver operating characteristic (ROC) curves were established to explore the diagnostic value of selective miRNAs. Finally, GO annotation and KEGG pathway enrichment analyses were used to display possible functions associated with the two miRNAs.ResultsA total of 24 miRNAs showed differential levels of enrichment with P < 0.05 and |log2 fold change| > 1 by miRNA microarrays. Among the six selective miRNAs (i.e., miR-134-5p, miR-197-5p, miR-22-3p, miR-320a, miR-494-3p, and miR-939-5p), qRT-PCR analysis revealed that miR-22-3p and miR-320a were significantly upregulated in serum exosomes from patients with endometriosis compared with negative individuals. ROC curve revealed that the serum exosomal miR-22-3p and miR-320a yielded the area under the curve values of 0.855 and 0.827, respectively.ConclusionOur results demonstrated that exosomal miR-22-3p and miR-320a were significantly increased in the sera of patients with endometriosis. The two miRNAs may be useful potential biomarkers for endometriosis diagnosis.
| S-EPMC7008302 | biostudies-literature
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 to 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function. Differences in gene expression in the central nucleus of the amygdala (CeA) were compared in two groups of alcohol-preferring (P) rats, one given water only and the other given access to 15 & 30% ethanol during adolescence.
2013-07-20 | E-GEOD-49040 | biostudies-arrayexpress
Project description:These experiments were done as part of a larger study that investigated the mode of action of T-cell bispecific (TCB) antibodies (including CEA-TCB [cibisatamab]) by characterizing molecular and cellular features of immune cells and tumors following TCB treatment in vivo in humanized mice and syngeneic tumor models. To characterize the molecular parameters associated with CEA-TCB treatment we performed bulk RNA sequencing of CEA-TCB-treated and untreated tumors derived from MKN-45 tumor-bearing humanized mice. Tumor tissue was analyzed after seven consecutive TCB treatments and compared to matching controls. RNA sequencing analysis revealed a clear distinction between CEA-TCB-treated and control animals, with several genes being upregulated in tumors treated with CEA-TCB as compared to controls. Among the top 15 upregulated genes in CEA-TCB-treated tumors there were many reflective of a strong T-cell activation, migration, immune cell response (CXCL13, GNLY, GZMB, CXCL10, IDO1, SLA, CD2, TRBC2, TIGIT, IL2RB, CXCL9, CX3CL1, CCL4L2, and CD3E). Among the top downregulated ones we found keratin 6A and keratin 20 (KRT6A and KRT20) suggestive of the reduction of tumor cells as the result of TCB-mediated killing. A Gene Set Enrichment Analysis (GSEA) was conducted that further enabled identification of the main biological pathways upon CEA-TCB treatment and confirmed that the main Gene Ontology families that characterize the TCB response consist of T-cell activation (Response to interferon gamma; Adaptive Immune Response; T-cell activation; Inflammatory Response; Activation of Immune response; Cytokine secretion) and migration (Leukocyte Migration; Regulation of Cell Adhesion). We also noticed upregulation of many major histocompatibility class II molecules that are known to be expressed on antigen presenting cells (HLA-DRA, HLA-DRB5, and HLA-DRB1) along with CX3CL1 (fractalkine, a known monocyte/T-cell attractant molecule) and CSF1 (colony stimulating factor 1, macrophage) suggestive of myeloid cell recruitment and activation at tumor sites post TCB treatment. The signature appeared to be robust, as components of the signature were confirmed using complementary techniques: RNA expression analysis and protein expression as determined by flow cytometry and multiplex analysis.
2020-10-29 | GSE155887 | GEO
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 – 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function.
2013-07-20 | GSE49040 | GEO
Project description:Background: Safe and sensitive methods for glioblastoma diagnosis and disease monitoring are urgently needed. Exosomes are nano-sized extracellular vesicles that contain molecules characteristic of their cell-of-origin, including microRNA. Exosomes released by glioblastoma tumors cross the blood-brain-barrier ino the peripheral circulation. Methods: Serum exosomal-microRNA isolated from IDH-wildtype glioblastoma (n=12) and IDH-mutant glioma grades II-III (n=10) were analyzed using small-RNA next generation sequencing and compared to age- and gender-matched healthy controls. Differentially expressed miRNAs (|fold change|³2 and p-value ≤ 0.05 in three statistical tests, Fischer-exact, t-test, and Wilcoxon) were identified and the predictive power of individual and subsets of miRNAs were tested using univariate (logistic regression) and multivariate (Random Forest) analyses. Additional glioblastoma sera (n=4) and independent sets of healthy (n=9) and non-glioma (n=10) controls were used to further test the predictive power of our glioblastoma miRNA signature. Results: Twenty-six miRNAs were differentially expressed in glioblastoma relative to healthy controls. Seven miRNAs (miR-182-5p, miR-328-3p, miR-339-5p, miR-340-5p, miR-485-3p, miR-486-5p and miR-543) were the most stable for classifying glioblastoma, achieving a predictive power of 91.7%. Strikingly, the combined expressions of miR-182-5p, miR-328-3p miR-485-3p miR-486-5p distinguished glioblastoma patients from controls with perfect accuracy. This miRNA panel was able to correctly classify all specimens in validation cohorts (n=23). An analogous approach was used to identify 23 dysregulated miRNAs in IDH-mutant gliomas, including a distinct subset of stable miRNAs for classifying patients with lower-grade IDH-mutant gliomas. Conclusions: Our serum exosomal-miRNA signature can accurately diagnose glioblastoma preoperatively. These findings have significant scope to revolutionize glioblastoma tumor diagnosis and disease monitoring. IMPORTANCE OF STUDY: There is a real need for accurate biomarkers that can measure glioblastoma disease activity and treatment response in a safe and timely manner. This study demonstrates that exosome-associated microRNAs have exceptional utility as blood-based biomarkers in glioma patients. This work also shows the potential for exosomal microRNA profiles to be used for glioma subtyping, grading and determining mutational states. The development of specific, sensitive and non-invasive screening tests would have significant clinical benefit by reducing costs of treatment monitoring, improving accessibility and quality-of-life measures. Moreover, such tests have the potential to provide objectively measured surrogate endpoints to allow clinical trial protocols to be more dynamic and adaptive.
2018-11-14 | GSE122488 | GEO
Project description:Exosomes are nano-sized extracellular vesicles released by many cells that contain molecules characteristic of their cell of origin, including microRNA. Exosomes released by glioblastoma cross the blood-brain barrier into the peripheral circulation and carry molecular cargo distinct to that of "free-circulating" miRNA. In this pilot study, serum exosomal microRNAs were isolated from glioblastoma (n = 12) patients and analyzed using unbiased deep sequencing. Results were compared to sera from age- and gender-matched healthy controls and to grade II-III (n = 10) glioma patients. Significant differentially expressed microRNAs were identified, and the predictive power of individual and subsets of microRNAs were tested using univariate and multivariate analyses. Additional sera from glioblastoma patients (n = 4) and independent sets of healthy (n = 9) and non-glioma (n = 10) controls were used to further test the specificity and predictive power of this unique exosomal microRNA signature. Twenty-six microRNAs were differentially expressed in serum exosomes from glioblastoma patients relative to healthy controls. Random forest modeling and data partitioning selected seven miRNAs (miR-182-5p, miR-328-3p, miR-339-5p, miR-340-5p, miR-485-3p, miR-486-5p, and miR-543) as the most stable for classifying glioblastoma. Strikingly, within this model, six iterations of these miRNA classifiers could distinguish glioblastoma patients from controls with perfect accuracy. The seven miRNA panel was able to correctly classify all specimens in validation cohorts (n = 23). Also identified were 23 dysregulated miRNAs in IDHMUT gliomas, a partially overlapping yet distinct signature of lower-grade glioma. Serum exosomal miRNA signatures can accurately diagnose glioblastoma preoperatively. miRNA signatures identified are distinct from previously reported "free-circulating" miRNA studies in GBM patients and appear to be superior.
| S-EPMC6290767 | biostudies-literature
Project description:Single cell RNA-sequencing in the mouse central amygdala (CEA)
| PRJNA882498 | ENA