scholarly journals Gene expression and immunohistochemical analyses identify SOX2 as major risk factor for overall survival and relapse in Ewing sarcoma patients

EBioMedicine ◽  
2019 ◽  
Vol 47 ◽  
pp. 156-162 ◽  
Author(s):  
Giuseppina Sannino ◽  
Aruna Marchetto ◽  
Andreas Ranft ◽  
Susanne Jabar ◽  
Constanze Zacherl ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Risk Factor ◽  
Ewing Sarcoma ◽  
Major Risk Factor ◽  
Immunohistochemical Analyses

scholarly journals CCT6A, a Novel Prognostic Biomarker for Ewing's Sarcoma

2020 ◽  
Author(s):  
Jie Jiang ◽  
Chong Liu ◽  
Guoyong Xu ◽  
Tuo Liang ◽  
Chaojie Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Ewing Sarcoma ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
High Expression ◽  
P Value ◽  
Event Free Survival ◽  
Free Survival ◽  
Cox Regression Analysis

Abstract Background: Ewing's sarcoma (ES) is the second most prevalent malignancy among bone tissue tumors, and there is no adequate prognosis biomarker. The protein encoded by CCT6A is a molecular chaperone. Early studies have suggested that CCT6A is involved in the development of many cancers, however, there is no clear evidence of a role for CCT6A in ES.Methods: In this study, we performed a bioinformatics analysis of 32 Ewing sarcoma specimens from the GSE17618 dataset for differences in gene expression and overall survival, event-free survival, and gene expression in different subgroups. Results: After three screenings, we identified CCT6A as highly correlated with Ewing's sarcoma prognosis. Survival analysis showed low overall survival (OS) for CCT6A high expression (P=0.024). On the other hand, Cox regression analysis showed that CCT6A expression, event-free survival (EFS), and age were strongly associated with the prognosis of Ewing sarcoma, identified as independent poor prognostic biomarkers. (CCT6A: P=0.015; Age: P-value=0.026; EFS: P-value=0.001). Conclusion: The expression level of CCT6A is strongly associated with the prognosis of Ewing's sarcoma. High expression of the CCT6A gene may serve as a biomarker for poor prognosis in patients with Ewing's sarcoma.

CCT6A, a novel prognostic biomarker for Ewing's sarcoma

2020 ◽  
Author(s):  
Jie Jiang ◽  
Chong Liu ◽  
Guoyong Xu ◽  
Tuo Liang ◽  
Chaojie Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Ewing Sarcoma ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
High Expression ◽  
P Value ◽  
Event Free Survival ◽  
Free Survival ◽  
Cox Regression Analysis

Abstract Background Ewing's sarcoma (ES) is the second most prevalent malignancy among bone tissue tumors, and there is no adequate prognosis biomarker. The protein encoded by CCT6A is a molecular chaperone. Early studies have suggested that CCT6A is involved in the development of many cancers, however, there is no clear evidence of a role for CCT6A in ES. Methods In this study, we performed a bioinformatics analysis of 32 Ewing sarcoma specimens from the GSE17618 dataset for differences in gene expression and overall survival, event-free survival, and gene expression in different subgroups. Results After three screenings, we identified CCT6A as highly correlated with Ewing's sarcoma prognosis. Survival analysis showed low overall survival (OS) for CCT6A high expression (P = 0.024). On the other hand, Cox regression analysis showed that CCT6A expression, event-free survival (EFS), and age were strongly associated with the prognosis of Ewing sarcoma, identified as independent poor prognostic biomarkers. (CCT6A: P = 0.015; Age: P-value = 0.026; EFS: P-value = 0.001). Conclusion The expression level of CCT6A is strongly associated with the prognosis of Ewing's sarcoma. High expression of the CCT6A gene may serve as a biomarker for poor prognosis in patients with Ewing's sarcoma.

Abstract 465: Nicotine Differentially Influences Segmental Aortic Stiffening

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Markus U Wagenhaeuser ◽  
Isabel N Schellinger ◽  
Sabina P Guenther ◽  
Takuya Yoshino ◽  
Kensuke Toyama ◽  
...  
Keyword(s):  
Gene Expression ◽  
Risk Factor ◽  
Time Course ◽  
Collagen Type ◽  
Collagen Type I ◽  
Aortic Aneurysms ◽  
Major Risk Factor ◽  
Type I ◽  
Type Iii ◽  
Aortic Stiffening

Background: Arterial stiffness is a major risk factor for various cardiovascular diseases and contributes to the development of abdominal aortic aneurysms (AAA). In this context, differential aortic stiffening of adjacent aortic segments increases aortic wall stress and accelerates the disease. Smoking is a major risk factor for AAA, in part due to nicotine. In this study, we investigated aortic stiffening of the thoracic and abdominal aorta and analyzed stiffness-related gene expression. Methods: 36 WT mice (C57BL/6) mice were infused with nicotine or PBS using osmotic mini pumps for 42 days. Thoracic segment (TS) and abdominal segment (AS) aortic stiffness were analyzed using ultrasound (M-Mode and PW). TS and AS were further investigated by ex vivo myograph measurements. Gene expression for TMIP2, MT1-MMP, MMP2, collagen type I and type III was performed for both segments separately. Results: Myograph measurements revealed increased strain within the AS after 2 weeks (p<.05) in response to nicotine (vs. PBS), but no stiffening of the TS. After 6 weeks, the AS showed additional increases in strain with nicotine (p<.05); however, only minor increases in stiffness could be observed for the TS. Ultrasound M-Mode results confirmed the myograph results. Nicotine treatment also led to increased aortic pulse wave velocity (PWV) after 2 weeks (p<.05) and 6 weeks (p<.05). Gene expression analysis revealed up-regulation in the TS and AS of MT1-MMP and MMP2 after 2 weeks of nicotine, while TIMP2 was downregulated, and collagen type I and type III were up-regulated in both TS and AS (p<.05). After 6 weeks, there were no longer significant differences in either segment for any of these genes. Discussion: Aortic stiffening in response to nicotine varies between the TS and AS segment over a time course of 6 weeks. This leads to an increased stiffness gradient between the TS and AS. Gene expression changes in stiffness-related genes occurred in response to nicotine, although no difference appeared between the segments. We conclude that the difference in stiffness development for TS and AS could be based on a different basic morphological structure involving elastin and collagen load, and that these responses may in part explain nicotine’s role in promoting AAA.

scholarly journals Clinical, pathological, and PAM50 gene expression features of HER2-low breast cancer

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Francesco Schettini ◽  
Nuria Chic ◽  
Fara Brasó-Maristany ◽  
Laia Paré ◽  
Tomás Pascual ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Overall Survival ◽  
High Activity ◽  
Triple Negative ◽  
Her2 Expression ◽  
Drug Conjugates ◽  
Molecular Features ◽  
Biological Heterogeneity ◽  
Antibody Drug

AbstractNovel antibody-drug conjugates against HER2 are showing high activity in HER2-negative breast cancer (BC) with low HER2 expression (i.e., 1+ or 2+ and lack of ERBB2 amplification). However, the clinical and molecular features of HER2-low BC are yet to be elucidated. Here, we collected retrospective clinicopathological and PAM50 data from 3,689 patients with HER2-negative disease and made the following observations. First, the proportion of HER2-low was higher in HR-positive disease (65.4%) than triple-negative BC (TNBC, 36.6%). Second, within HR-positive disease, ERBB2 and luminal-related genes were more expressed in HER2-low than HER2 0. In contrast, no gene was found differentially expressed in TNBC according to HER2 expression. Third, within HER2-low, ERBB2 levels were higher in HR-positive disease than TNBC. Fourth, HER2-low was not associated with overall survival in HR-positive disease and TNBC. Finally, the reproducibility of HER2-low among pathologists was suboptimal. This study emphasizes the large biological heterogeneity of HER2-low BC, and the need to implement reproducible and sensitive assays to measure low HER2 expression.

scholarly journals Functions and clinical significance of KLRG1 in the development of lung adenocarcinoma and immunotherapy

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaodong Yang ◽  
Yuexin Zheng ◽  
Zhihai Han ◽  
Xiliang Zhang
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Killer Cell ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Normal Lung ◽  
Using Data ◽  
Low Expression

Abstract Background As a marker of differentiation, Killer cell lectin like receptor G1 (KLRG1) plays an inhibitory role in human NK cells and T cells. However, its clinical role remains inexplicit. This work intended to investigate the predictive ability of KLRG1 on the efficacy of immune-checkpoint inhibitor in the treatment of lung adenocarcinoma (LUAD), as well as contribute to the possible molecular mechanisms of KLRG1 on LUAD development. Methods Using data from the Gene Expression Omnibus, the Cancer Genome Atlas and the Genotype-Tissue Expression, we compared the expression of KLRG1 and its related genes Bruton tyrosine kinase (BTK), C-C motif chemokine receptor 2 (CCR2), Scm polycomb group protein like 4 (SCML4) in LUAD and normal lung tissues. We also established stable LUAD cell lines with KLRG1 gene knockdown and investigated the effect of KLRG1 knockdown on tumor cell proliferation. We further studied the prognostic value of the four factors in terms of overall survival (OS) in LUAD. Using data from the Gene Expression Omnibus, we further investigated the expression of KLRG1 in the patients with different responses after immunotherapy. Results The expression of KLRG1, BTK, CCR2 and SCML4 was significantly downregulated in LUAD tissues compared to normal controls. Knockdown of KLRG1 promoted the proliferation of A549 and H1299 tumor cells. And low expression of these four factors was associated with unfavorable overall survival in patients with LUAD. Furthermore, low expression of KLRG1 also correlated with poor responses to immunotherapy in LUAD patients. Conclusion Based on these findings, we inferred that KLRG1 had significant correlation with immunotherapy response. Meanwhile, KLRG1, BTK, CCR2 and SCML4 might serve as valuable prognostic biomarkers in LUAD.

Pre-transplant hypertension: a major risk factor for chronic progressive renal allograft dysfunction?

1995 ◽  
Vol 10 (7) ◽  
pp. 1206-1211 ◽  
Author(s):  
U. Frei ◽  
R. Schindler ◽  
D. Wieters ◽  
U. Grouven ◽  
R. Brunkhorst ◽  
...  
Keyword(s):  
Risk Factor ◽  
Renal Allograft ◽  
Major Risk Factor ◽  
Allograft Dysfunction

scholarly journals Construction of a competitive endogenous RNA network and analysis of potential regulatory axis targets in glioblastoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kai Yu ◽  
Huan Yang ◽  
Qiao-li Lv ◽  
Li-chong Wang ◽  
Zi-long Tan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Differentially Expressed Genes ◽  
Pearson Correlation ◽  
Differentially Expressed ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Network Chain ◽  
Cerna Network ◽  
Potential Marker

Abstract Background Glioblastoma is the most common primary malignant brain tumor. Because of the limited understanding of its pathogenesis, the prognosis of glioblastoma remains poor. This study was conducted to explore potential competing endogenous RNA (ceRNA) network chains and biomarkers in glioblastoma by performing integrated bioinformatics analysis. Methods Transcriptome expression data from The Cancer Genome Atlas database and Gene Expression Omnibus were analyzed to identify differentially expressed genes between glioblastoma and normal tissues. Biological pathways potentially associated with the differentially expressed genes were explored by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis, and a protein-protein interaction network was established using the STRING database and Cytoscape. Survival analysis using Gene Expression Profiling Interactive Analysis was based on the Kaplan–Meier curve method. A ceRNA network chain was established using the intersection method to align data from four databases (miRTarBase, miRcode, TargetScan, and lncBace2.0), and expression differences and correlations were verified by quantitative reverse-transcription polymerase chain reaction analysis and by determining the Pearson correlation coefficient. Additionally, an MTS assay and the wound-healing and transwell assays were performed to evaluate the effects of complement C1s (C1S) on the viability and migration and invasion abilities of glioblastoma cells, respectively. Results We detected 2842 differentially expressed (DE) mRNAs, 2577 DE long non-coding RNAs (lncRNAs), and 309 DE microRNAs (miRNAs) that were dysregulated in glioblastoma. The final ceRNA network consisted of six specific lncRNAs, four miRNAs, and four mRNAs. Among them, four DE mRNAs and one DE lncRNA were correlated with overall survival (p < 0.05). C1S was significantly correlated with overall survival (p= 0.015). In functional assays, knockdown of C1S inhibited the proliferation and invasion of glioblastoma cell lines. Conclusions We established four ceRNA networks that may influence the occurrence and development of glioblastoma. Among them, the MIR155HG/has-miR-129-5p/C1S axis is a potential marker and therapeutic target for glioblastoma. Knockdown of C1S inhibited the proliferation, migration, and invasion of glioblastoma cells. These findings clarify the role of the ceRNA regulatory network in glioblastoma and provide a foundation for further research.

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