scholarly journals Identification of the Potential Biomarkers in Barrett’S Esophagus Derived Esophageal Adenocarcinoma

2021 ◽  
Author(s):  
Nan Yi ◽  
Juan He ◽  
Xike Xie ◽  
Liexin Liang ◽  
Guowen Zuo ◽  
...  
Keyword(s):  
Barrett’S Esophagus ◽  
Esophageal Adenocarcinoma ◽  
Barrett's Esophagus ◽  
Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Bioinformatics Analyses ◽  
Dismal Prognosis ◽  
Cancer Genome Atlas ◽  
Public Datasets ◽  
Potential Biomarkers

Abstract Clinically, almost 50% of esophageal adenocarcinoma (EAC) originates from the progression of Barrett’s esophagus (BE). EAC is often diagnosed at late stages and is related to dismal prognosis. However, there are still no effective strategies for stratification and therapy in BE derived EAC (BE-EAC). Two public datasets (GSE26886 and GSE37200) are analyzed to identify differentially expressed genes (DEGs) between BE and EAC. A series of bioinformatics analyses are performed to explore potential biomarkers associated with BE-EAC. 27 up- and 104 down-regulated genes are identified between GSE26886 and GSE37200. The GO and KEGG enrichment analysis indicate that the DEGs are highly involved in tumorigenesis. Subsequently, Weighted Gene Co-Expression Network Analysis (WGCNA) is performed to explore the potential genes related to BE-EAC, which are further validated in The Cancer Genome Atlas (TCGA) database. 5 up-regulated genes (MYO1A, ACE2, COL1A1, LGALS4, and ADRA2A) and 3 down-regulated genes (AADAC, RAB27A, and P2RY14) were found in BE-EAC. Among them, the expression level of AADAC, ACE2 and ADRA2A show a significant correlation with patients’ survival probability. In conclusion, MYO1A, ACE2, COL1A1, LGALS4, ADRA2A, AADAC, RAB27A, and P2RY14 are potential diagnostic and prognostic biomarkers in BE-EAC.

scholarly journals Identification of the Potential Biomarkers in Barrett’S Esophagus Derived Esophageal Adenocarcinoma

2021 ◽  
Author(s):  
Nan Yi ◽  
Juan He ◽  
Xike Xie ◽  
Liexin Liang ◽  
Guowen Zuo ◽  
...  
Keyword(s):  
Barrett’S Esophagus ◽  
Esophageal Adenocarcinoma ◽  
Barrett's Esophagus ◽  
Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Bioinformatics Analyses ◽  
Dismal Prognosis ◽  
Cancer Genome Atlas ◽  
Public Datasets ◽  
Potential Biomarkers

Abstract BackgroundClinically, almost 50% of esophageal adenocarcinoma (EAC) originates from the progression of Barrett’s esophagus (BE). EAC is often diagnosed at late stages and is related to dismal prognosis. However, there are still no effective strategies for stratification and therapy in BE derived EAC (BE-EAC).MethodsTwo public datasets (GSE26886 and GSE37200) are analyzed to identify differentially expressed genes (DEGs) between BE and EAC. A series of bioinformatics analyses are performed to explore potential biomarkers associated with BE-EAC.Results27 up- and 104 down-regulated genes are identified between GSE26886 and GSE37200. The GO and KEGG enrichment analysis indicate that the DEGs are highly involved in tumorigenesis. Subsequently, Weighted Gene Co-Expression Network Analysis (WGCNA) is performed to explore the potential genes related to BE-EAC, which are further validated in The Cancer Genome Atlas (TCGA) database. 5 up-regulated genes (MYO1A, ACE2, COL1A1, LGALS4, and ADRA2A) and 3 down-regulated genes (AADAC, RAB27A, and P2RY14) were found in BE-EAC. Among them, the expression level of AADAC, ACE2 and ADRA2A show a significant correlation with patients’ survival probability .Conclusion MYO1A, ACE2, COL1A1, LGALS4, ADRA2A, AADAC, RAB27A, and P2RY14 are potential diagnostic and prognostic biomarkers in BE-EAC.

scholarly journals Circulating exosomal miRNAs as potential biomarkers for Barrett's esophagus and esophageal adenocarcinoma

2020 ◽  
Vol 26 (22) ◽  
pp. 2889-2901 ◽  
Author(s):  
Jing Lv ◽  
He-Ping Zhao ◽  
Kun Dai ◽  
Yan Cheng ◽  
Jun Zhang ◽  
...  
Keyword(s):  
Barrett’S Esophagus ◽  
Esophageal Adenocarcinoma ◽  
Barrett's Esophagus ◽  
Exosomal Mirnas ◽  
Potential Biomarkers

544 Comprehensive Profiling of Plasma MicroRNAs Reveals Potential Biomarkers for Barrett's Esophagus and Esophageal Adenocarcinoma

2014 ◽  
Vol 146 (5) ◽  
pp. S-97 ◽  
Author(s):  
Jantine W. Van Baal ◽  
Pauline Bus ◽  
Christine Kestens ◽  
Fiebo T. Ten Kate ◽  
Wilbert H. Peters ◽  
...  
Keyword(s):  
Barrett’S Esophagus ◽  
Esophageal Adenocarcinoma ◽  
Barrett's Esophagus ◽  
Potential Biomarkers

scholarly journals CSIG-03. RECONCILING TUMOR HETEROGENEITY IN GLIOBLASTOMA USING A PATHWAY-BASED APPROACH

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii28-ii28
Author(s):  
Alvaro Alvarado ◽  
Kaleab Tessema ◽  
Kunal Patel ◽  
Riki Kawaguchi ◽  
Richard Everson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Patient Survival ◽  
Molecular Subtype ◽  
Gene List ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Molecular Architecture ◽  
Survival Pathways ◽  
Cancer Genome Atlas

Abstract Despite efforts to gain a deeper understanding of its molecular architecture, glioblastoma (GBM) remains uniformly fatal. While genome-based molecular subtyping has revealed that GBMs may be parsed into several molecularly distinct categories, this insight has yielded little progress towards extending patient survival. In particular, the great phenotypic heterogeneity of GBM – both inter and intratumorally – has hindered therapeutic efforts. To this end, we interrogated tumor samples using a pathway-based approach to resolve tumoral heterogeneity. Gene set enrichment analysis (GSEA) was applied to gene expression data and used to provide an overview of each sample that can be compared to other samples by generating sample clusters based on overall patterns of enrichment. The Cancer Genome Atlas (TCGA) samples were clustered using the canonical and oncogenic signatures and in both cases the clustering was distinct from the molecular subtype previously reported and clusters were informative of patient survival. We also analyzed single cell RNA sequencing datasets and uniformly found two clusters of cells enriched for cell cycle regulation and survival pathways. We have validated our approach by generating gene lists from common elements found in the top contributing genesets for a particular cluster and testing the top targets in appropriate gliomasphere patient-derived lines. Samples enriched for cell cycle related genesets showed a decrease in sphere formation capacity when E2F1, out top target, was silenced and when treated with fulvestrant and calcitriol, which were identified as potential drugs targeting this genelist. Conversely, no changes were observed in samples not enriched for this gene list. Finally, we interrogated spatial heterogeneity and found higher enrichment of the proliferative signature in contrast enhancing compared with non-enhancing regions. Our studies relate inter- and intratumoral heterogeneity to critical cellular pathways dysregulated in GBM, with the ultimate goal of establishing a pipeline for patient- and tumor-specific precision medicine.

scholarly journals SEMA6D Expression and Patient Survival in Breast Invasive Carcinoma

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Dongquan Chen ◽  
Yufeng Li ◽  
Lizhong Wang ◽  
Kai Jiao
Keyword(s):  
Breast Cancer ◽  
Expression Profile ◽  
Heart Development ◽  
Invasive Carcinoma ◽  
Patient Survival ◽  
The Cancer Genome Atlas ◽  
Breast Cancer Patients ◽  
Genomic Expression ◽  
Cancer Genome Atlas ◽  
Public Datasets

Breast cancer (BC) is the second most common cancer diagnosed in American women and is also the second leading cause of cancer death in women. Research has focused heavily on BC metastasis. Multiple signaling pathways have been implicated in regulating BC metastasis. Our knowledge of regulation of BC metastasis is, however, far from complete. Identification of new factors during metastasis is an essential step towards future therapy. Our labs have focused on Semaphorin 6D (SEMA6D), which was implicated in immune responses, heart development, and neurogenesis. It will be interesting to know SEMA6D-related genomic expression profile and its implications in clinical outcome. In this study, we examined the public datasets of breast invasive carcinoma from The Cancer Genome Atlas (TCGA). We analyzed the expression of SEMA6D along with its related genes, their functions, pathways, and potential as copredictors for BC patients’ survival. We found 6-gene expression profile that can be used as such predictors. Our study provides evidences for the first time that breast invasive carcinoma may contain a subtype based on SEMA6D expression. The expression of SEMA6D gene may play an important role in promoting patient survival, especially among triple negative breast cancer patients.

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