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The role of altered long noncoding RNAs in overall survival of ovarian cancer: A systematic review and meta-analysis.
Seyed Hosseini, E, Alizadeh Zarei, M, Haddad Kashani, H, Milajerdi, A, Zare Dehghanani, Z, Hassani Bafrani, H, Nikzad, H
Pathology, research and practice. 2021;:153363
Abstract
In recent years, tremendous research efforts have been focused on investigating the effect of dysregulation of lncRNAs on cancer progression, most of which confirm a positive link. This inspired us to conduct the present meta-analysis to explore whether aberrant expression of multiple lncRNAs has a role in patients' outcome in ovarian cancer. This comprehensive meta-analysis pertains to the evaluation of association between dysregulated lncRNAs expression level with eventual outcome and clinicopathological characteristics of ovarian cancer patients. We systematically searched PubMed, Web of Science, and Scopus to find all eligible articles. Pooled hazard ratios (HRs) and 95% confidence intervals (95% CIs) for overall survival, disease-free survival and progression-free survival were measured with a fixed or random effects model. A total of 34 studies were included in the meta-analysis. Dysregulation of lncRNAs were contributed to shorter overall survival (34 studies, 1180 patients HR = 2.12, 95% CI: 1.73 ± 2.60, random-effects) in ovarian cancer. Furthermore, altered lncRNAs were also related to decreased progression-free survival (8 studies, 1180 patients HR: 1.88, 95% CI: (1.35-2.62) and disease-free survival (2 studies, 285 patients, HR: 6.07, 95% CI: 1.28-28.78) in this disease. Our analyses supported the robust prognostic significance of altered lncRNAs in ovarian cancer. However, more extended studies are encouraged to evaluate the clinical application potential of these lncRNAs in the prognosis evaluation of ovarian cancer.
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Prospective validation in epithelial tumors of a gene expression predictor of liver metastasis derived from uveal melanoma.
Tsantoulis, P, Delorenzi, M, Bièche, I, Vacher, S, Mariani, P, Cassoux, N, Houy, A, Stern, MH, Roman-Roman, S, Dietrich, PY, et al
Scientific reports. 2019;(1):17178
Abstract
Predicting the risk of liver metastasis can have important prognostic and therapeutic implications, given the availability of liver-directed therapy. Uveal melanoma has a striking predisposition for liver metastasis despite the absence of anatomical proximity. Understanding its biology may uncover factors promoting liver metastasis in other malignancies. We quantified gene expression by RNAseq in 76 uveal melanomas and combined with public data in a meta-analysis of 196 patients. The meta-analysis of uveal melanoma gene expression identified 63 genes which remained prognostic after adjustment for chromosome 3 status. Two genes, PTP4A3 and JPH1, were selected by L1-penalized regression and combined in a prognostic score. The score predicted liver-specific relapse in a public pan-cancer dataset and in two public colorectal cancer datasets. The score varied between colorectal consensus molecular subtypes (CMS), as did the risk of liver relapse, which was lowest in CMS1. Additional prospective validation was done by real-time PCR in 463 breast cancer patients. The score was significantly correlated with liver relapse in hormone receptor positive tumors. In conclusion, the expression of PTP4A3 and JPH1 correlates with risk of liver metastasis in colorectal cancer and breast cancer. The underlying biological mechanism is an interesting area for further research.
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Ranking candidate genes of esophageal squamous cell carcinomas based on differentially expressed genes and the topological properties of the co-expression network.
Shen, Y, Tantai, J, Zhao, H
European journal of medical research. 2014;(1):52
Abstract
BACKGROUND The aim of this study was to identify the candidate genes of esophageal squamous cell carcinoma (ESCC). METHODS Gene expression profiling of 17 ESCC samples and 17 adjacent normal samples, GSE20347, was downloaded from Gene Expression Omnibus database. The raw data were preprocessed, and the differentially expressed genes (DEGs) between ESCC and normal samples were identified by using SAM software (false discovery rate <0.001). Then, the co-expression network of DEGs was constructed based on Pearson's correlation test (r-value ≥0.8). Furthermore, the topological properties of the co-expression network were analyzed through NetworkAnalyzer (default settings) of Cytoscape. The expression fold changes of DEGs and topological properties were utilized to identify the candidate genes of ESCC (Crin score >4), which were further analyzed based on DAVID functional enrichment analysis (P-value <0.05). RESULTS A total of 1,063 DEGs were identified, including 490 up-regulated and 573 down-regulated DEGs. Then, the co-expression network of DEGs was constructed, containing 999 nodes and 46,323 edges. Based on the expression fold changes of DEGs and the topological properties of the co-expression network, DEGs were ranked, and the top 24 genes were candidate genes of ESCC, such as CRISP3, EREG, CXCR2, and CRNN. Furthermore, the 24 genes were significantly enriched in bio-functions regarding cell differentiation, glucan biosynthetic process and immune response. CONCLUSION The present study suggested that CRISP3, EREG, CXCR2, and CRNN might be causative genes of ESCC, and play vital roles in the development of ESCC. However, further experimental studies are needed to confirm our results.
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Functional polymorphisms of folate metabolism and response to chemotherapy for colorectal cancer, a systematic review and meta-analysis.
Jennings, BA, Kwok, CS, Willis, G, Matthews, V, Wawruch, P, Loke, YK
Pharmacogenetics and genomics. 2012;(4):290-304
Abstract
OBJECTIVES Many primary studies have considered the association of polymorphisms of folate metabolism and response to 5-fluorouracil (5-FU) and capecitabine in patients with colorectal cancer. The conclusions from these studies have been conflicting and few have considered large cohorts of patients. Therefore, we have completed a systematic review and meta-analyses to summarize some of the findings to date. We conducted searches for any studies that had addressed the prognostic value of genotype analysis of thymidylate synthetase (TYMS), Methylenetetrahydrofolate reductase (MTHFR) and dihydrofolate reductase (DHFR). METHODS We collected data on the study designs, and completed meta-analyses to pool congruent data about treatment effect. A narrative summary is presented for 39 studies that describe three TYMS genotypes and two MTHFR genotypes associated with response to 5-FU-based chemotherapy. RESULTS Data were synthesized from up to 2402 patients for the most commonly studied markers TYMS 5' UTR repeat polymorphism (rs45445694) and MTHFR 677 C>T (rs1801133). We found that the TYMS genotype associated with the lowest protein expression (2R/2R) was significantly associated with improved clinical benefit; the pooled risk ratio was relative risk=1.36 [1.11, 1.65]; P=0.003. Moreover, the same trend was observed for adverse effects; the pooled risk ratio was 2.04 [1.42, 2.95]; P=0.0001. CONCLUSION There is a small but statistically significant association between treatment effect (both intended effects and adverse events) and a TYMS genotype associated with low protein expression; however, the effect size is small and therefore indicates limited clinical utility.