scholarly journals A pan-cancer analysis of prognostic genes

2015 ◽  
Author(s):  
Jordan Anaya ◽  
Brian J. Reon ◽  
Wei-Min Chen ◽  
Stefan Bekiranov ◽  
Anindya Dutta
Keyword(s):  
Microarray Data ◽  
The Cancer Genome Atlas ◽  
Rna Seq ◽  
Cancer Pathogenesis ◽  
Gene Sets ◽  
Protective Genes ◽  
Cancer Genome Atlas ◽  
Cancer Types ◽  
Measure Of Association ◽  
Pan Cancer

AbstractNumerous studies have identified prognostic genes in individual cancers, but a thorough pan-cancer analysis has not been performed. In addition, previous studies have mostly used microarray data instead of RNA-SEQ, and have not published comprehensive lists of associations with survival. Using recently available RNA-SEQ and clinical data from the The Cancer Genome Atlas for 6,495 patients, we have investigated every annotated and expressed gene’s association with survival across 16 cancer types. The most statistically significant harmful and protective genes were not shared across cancers, but were enriched in distinct gene sets which were shared across certain groups of cancers. These groups of cancers were independently reconstructed by unsupervised clustering of Cox coefficients (a measure of association with survival) for individual genes or for gene programs. This analysis has revealed unappreciated commonalities among cancers which may provide insights into cancer pathogenesis and rationales for co-opting treatments between cancers.

scholarly journals A pan-cancer analysis of prognostic genes

PeerJ ◽  
2016 ◽  
Vol 3 ◽  
pp. e1499 ◽  
Author(s):  
Jordan Anaya ◽  
Brian Reon ◽  
Wei-Min Chen ◽  
Stefan Bekiranov ◽  
Anindya Dutta
Keyword(s):  
Microarray Data ◽  
The Cancer Genome Atlas ◽  
Rna Seq ◽  
Cancer Pathogenesis ◽  
Gene Sets ◽  
Protective Genes ◽  
Cancer Genome Atlas ◽  
Cancer Types ◽  
Measure Of Association ◽  
Pan Cancer

Numerous studies have identified prognostic genes in individual cancers, but a thorough pan-cancer analysis has not been performed. In addition, previous studies have mostly used microarray data instead of RNA-SEQ, and have not published comprehensive lists of associations with survival. Using recently available RNA-SEQ and clinical data from The Cancer Genome Atlas for 6,495 patients, we have investigated every annotated and expressed gene’s association with survival across 16 cancer types. The most statistically significant harmful and protective genes were not shared across cancers, but were enriched in distinct gene sets which were shared across certain groups of cancers. These groups of cancers were independently recapitulated by both unsupervised clustering of Cox coefficients (a measure of association with survival) for individual genes, and for gene programs. This analysis has revealed unappreciated commonalities among cancers which may provide insights into cancer pathogenesis and rationales for co-opting treatments between cancers.

scholarly journals Pan-cancer analysis of m5C regulator genes reveals consistent epigenetic landscape changes in multiple cancers

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yuting He ◽  
Xiao Yu ◽  
Menggang Zhang ◽  
Wenzhi Guo
Keyword(s):  
Copy Number Variations ◽  
Regulatory Genes ◽  
The Cancer Genome Atlas ◽  
Cancer Pathogenesis ◽  
Cancer Genome Atlas ◽  
Cancer Types ◽  
Reversible Modification ◽  
Regulator Genes ◽  
Modified Nucleobases ◽  
Pan Cancer

Abstract Background 5-Methylcytosine (m5C) is a reversible modification to both DNA and various cellular RNAs. However, its roles in developing human cancers are poorly understood, including the effects of mutant m5C regulators and the outcomes of modified nucleobases in RNAs. Methods Based on The Cancer Genome Atlas (TCGA) database, we uncovered that mutations and copy number variations (CNVs) of m5C regulatory genes were significantly correlated across many cancer types. We then assessed the correlation between the expression of individual m5C regulators and the activity of related hallmark pathways of cancers. Results After validating m5C regulators’ expression based on their contributions to cancer development and progression, we observed their upregulation within tumor-specific processes. Notably, our research connected aberrant alterations to m5C regulatory genes with poor clinical outcomes among various tumors that may drive cancer pathogenesis and/or survival. Conclusion Our results offered strong evidence and clinical implications for the involvement of m5C regulators.

scholarly journals Pan-cancer analysis of m5C regulator genes reveals consistent epigenetic landscape changes in multiple cancers

2021 ◽  
Author(s):  
Yuting He ◽  
Xiao Yu ◽  
Menggang Zhang ◽  
Wenzhi Guo
Keyword(s):  
Copy Number Variations ◽  
Regulatory Genes ◽  
The Cancer Genome Atlas ◽  
Cancer Pathogenesis ◽  
Cancer Genome Atlas ◽  
Cancer Types ◽  
Reversible Modification ◽  
Regulator Genes ◽  
Modified Nucleobases ◽  
Pan Cancer

Abstract Backgroud5-methylcytosine (m5C) is a reversible modification to both DNA and various cellular RNAs. However, its roles in developing human cancers are poorly understood, including the effects of mutant m5C regulators and the outcomes of modified nucleobases in RNAs. Methods Based on The Cancer Genome Atlas (TCGA) database, we uncovered that mutations and copy number variations (CNVs) of m5C regulatory genes were significantly correlated across 33 cancer types. We then assessed the correlation between the expression of individual m5C regulators and the activity of related hallmark pathways of cancers. After validating m5C regulators' expression based on their contributions to cancer development and progression, we observed their up-regulation within tumor-specific processes. Results Notably, our research connected aberrant alterations to m5C regulatory genes with poor clinical outcomes among various tumors that may drive cancer pathogenesis and/or survival. Conclusions Our results offered strong evidence and clinical implications for the involvement of m5C regulators.

scholarly journals PR/SET Domain Family and Cancer: Novel Insights from the Cancer Genome Atlas

2018 ◽  
Vol 19 (10) ◽  
pp. 3250 ◽  
Author(s):  
Anna Sorrentino ◽  
Antonio Federico ◽  
Monica Rienzo ◽  
Patrizia Gazzerro ◽  
Maurizio Bifulco ◽  
...  
Keyword(s):  
Family Members ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Driver Gene ◽  
Rna Seq ◽  
Set Domain ◽  
Primary Tumors ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

The PR/SET domain gene family (PRDM) encodes 19 different transcription factors that share a subtype of the SET domain [Su(var)3-9, enhancer-of-zeste and trithorax] known as the PRDF1-RIZ (PR) homology domain. This domain, with its potential methyltransferase activity, is followed by a variable number of zinc-finger motifs, which likely mediate protein–protein, protein–RNA, or protein–DNA interactions. Intriguingly, almost all PRDM family members express different isoforms, which likely play opposite roles in oncogenesis. Remarkably, several studies have described alterations in most of the family members in malignancies. Here, to obtain a pan-cancer overview of the genomic and transcriptomic alterations of PRDM genes, we reanalyzed the Exome- and RNA-Seq public datasets available at The Cancer Genome Atlas portal. Overall, PRDM2, PRDM3/MECOM, PRDM9, PRDM16 and ZFPM2/FOG2 were the most mutated genes with pan-cancer frequencies of protein-affecting mutations higher than 1%. Moreover, we observed heterogeneity in the mutation frequencies of these genes across tumors, with cancer types also reaching a value of about 20% of mutated samples for a specific PRDM gene. Of note, ZFPM1/FOG1 mutations occurred in 50% of adrenocortical carcinoma patients and were localized in a hotspot region. These findings, together with OncodriveCLUST results, suggest it could be putatively considered a cancer driver gene in this malignancy. Finally, transcriptome analysis from RNA-Seq data of paired samples revealed that transcription of PRDMs was significantly altered in several tumors. Specifically, PRDM12 and PRDM13 were largely overexpressed in many cancers whereas PRDM16 and ZFPM2/FOG2 were often downregulated. Some of these findings were also confirmed by real-time-PCR on primary tumors.

scholarly journals Integrated Dissection of lncRNA-Perturbated Triplets Reveals Novel Prognostic Signatures Across Cancer Types

2020 ◽  
Vol 21 (17) ◽  
pp. 6087
Author(s):  
Yunzhen Wei ◽  
Limeng Zhou ◽  
Yingzhang Huang ◽  
Dianjing Guo
Keyword(s):  
Cancer Biology ◽  
Noncoding Rna ◽  
The Cancer Genome Atlas ◽  
Dynamic Changes ◽  
Computational Framework ◽  
Potential Biomarker ◽  
Cancer Genome Atlas ◽  
Cancer Types ◽  
Tcga Dataset ◽  
Pan Cancer

Long noncoding RNA (lncRNA)/microRNA(miRNA)/mRNA triplets contribute to cancer biology. However, identifying significative triplets remains a major challenge for cancer research. The dynamic changes among factors of the triplets have been less understood. Here, by integrating target information and expression datasets, we proposed a novel computational framework to identify the triplets termed as “lncRNA-perturbated triplets”. We applied the framework to five cancer datasets in The Cancer Genome Atlas (TCGA) project and identified 109 triplets. We showed that the paired miRNAs and mRNAs were widely perturbated by lncRNAs in different cancer types. LncRNA perturbators and lncRNA-perturbated mRNAs showed significantly higher evolutionary conservation than other lncRNAs and mRNAs. Importantly, the lncRNA-perturbated triplets exhibited high cancer specificity. The pan-cancer perturbator OIP5-AS1 had higher expression level than that of the cancer-specific perturbators. These lncRNA perturbators were significantly enriched in known cancer-related pathways. Furthermore, among the 25 lncRNA in the 109 triplets, lncRNA SNHG7 was identified as a stable potential biomarker in lung adenocarcinoma (LUAD) by combining the TCGA dataset and two independent GEO datasets. Results from cell transfection also indicated that overexpression of lncRNA SNHG7 and TUG1 enhanced the expression of the corresponding mRNA PNMA2 and CDC7 in LUAD. Our study provides a systematic dissection of lncRNA-perturbated triplets and facilitates our understanding of the molecular roles of lncRNAs in cancers.

scholarly journals Pan-cancer analysis reveals complex tumor-specific alternative polyadenylation

2017 ◽  
Author(s):  
Zhuyi Xue ◽  
René L Warren ◽  
Ewan A Gibb ◽  
Daniel MacMillan ◽  
Johnathan Wong ◽  
...  
Keyword(s):  
Alternative Polyadenylation ◽  
Length Change ◽  
The Cancer Genome Atlas ◽  
Cancer Type ◽  
Rna Seq ◽  
Multiple Cancer ◽  
Tissue Samples ◽  
Cancer Genome Atlas ◽  
Specific Alternative ◽  
Cancer Types

AbstractAlternative polyadenylation (APA) of 3’ untranslated regions (3’ UTRs) has been implicated in cancer development. Earlier reports on APA in cancer primarily focused on 3’ UTR length modifications, and the conventional wisdom is that tumor cells preferentially express transcripts with shorter 3’ UTRs. Here, we analyzed the APA patterns of 114 genes, a select list of oncogenes and tumor suppressors, in 9,939 tumor and 729 normal tissue samples across 33 cancer types using RNA-Seq data from The Cancer Genome Atlas, and we found that the APA regulation machinery is much more complicated than what was previously thought. We report 77 cases (gene-cancer type pairs) of differential 3’ UTR cleavage patterns between normal and tumor tissues, involving 33 genes in 13 cancer types. For 15 genes, the tumor-specific cleavage patterns are recurrent across multiple cancer types. While the cleavage patterns in certain genes indicate apparent trends of 3’ UTR shortening in tumor samples, over half of the 77 cases imply 3’ UTR length change trends in cancer that are more complex than simple shortening or lengthening. This work extends the current understanding of APA regulation in cancer, and demonstrates how large volumes of RNA-seq data generated for characterizing cancer cohorts can be mined to investigate this process.

scholarly journals Pan-cancer driver copy number alterations identified by joint expression/CNA data analysis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Gaojianyong Wang ◽  
Dimitris Anastassiou
Keyword(s):  
Gene Expression ◽  
Copy Number ◽  
The Cancer Genome Atlas ◽  
Copy Number Alterations ◽  
Multiple Cancer ◽  
Cancer Driver ◽  
Large Gene ◽  
Cancer Genome Atlas ◽  
Cancer Types ◽  
Pan Cancer

Abstract Analysis of large gene expression datasets from biopsies of cancer patients can identify co-expression signatures representing particular biomolecular events in cancer. Some of these signatures involve genomically co-localized genes resulting from the presence of copy number alterations (CNAs), for which analysis of the expression of the underlying genes provides valuable information about their combined role as oncogenes or tumor suppressor genes. Here we focus on the discovery and interpretation of such signatures that are present in multiple cancer types due to driver amplifications and deletions in particular regions of the genome after doing a comprehensive analysis combining both gene expression and CNA data from The Cancer Genome Atlas.

scholarly journals Clinical and Prognostic Significance of TZAP Expression in Cervical Cancer

Medicina ◽  
2020 ◽  
Vol 56 (5) ◽  
pp. 207
Author(s):  
Won-Jin Park ◽  
Jae-Hee Park ◽  
Ho-Yong Shin ◽  
Jae-Ho Lee
Keyword(s):  
Cervical Cancer ◽  
Survival Analysis ◽  
Prognostic Value ◽  
Prognostic Significance ◽  
Telomeric Repeat ◽  
The Cancer Genome Atlas ◽  
Genetic Changes ◽  
Cancer Pathogenesis ◽  
Cancer Genome Atlas ◽  
Cancer Types

Background and Objectives: Telomeric zinc finger-associated protein (TZAP) is a telomere-associated factor that was previously called ZBTB48. This protein binds preferentially to long telomeres, competing with telomeric repeat factors 1 and 2. Genetic changes in TZAP may be associated with cancer pathogenesis; however, this relationship has not yet been elucidated for any type of cancer. In this study, we aimed to examine the clinicopathologic and prognostic value of TZAP expression in cervical cancer (CC). Materials and Methods: The data were extracted from The Cancer Genome Atlas cohorts by OncoLnc (21 cancer types, 7700 cancers). The prognostic value of TZAP for different stages of 264 CCs was examined using survival analysis. Results: The TZAP expression did not differ significantly between CC and normal matched tissues. Age, cancer stage, and viral infection were not associated with TZAP expression. Survival analysis revealed a shorter overall survival in CC patients with a lower TZAP expression (χ2 = 3.62, p = 0.057). The prognostic value of TZAP expression was greater in patients with N1 stage CC (χ2 = 5.64, p = 0.018). Conclusion: TZAP expression is a possible prognostic marker for CC, especially stage N1 CC.

scholarly journals Pan-cancer analysis of non-coding recurrent mutations and their possible involvement in cancer pathogenesis

NAR Cancer ◽  
2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Chie Kikutake ◽  
Minako Yoshihara ◽  
Mikita Suyama
Keyword(s):  
The Cancer Genome Atlas ◽  
Whole Genome Sequencing Data ◽  
Sequencing Data ◽  
Huge Number ◽  
Protein Coding ◽  
Coding Regions ◽  
Cancer Pathogenesis ◽  
Recurrent Mutations ◽  
Cancer Genome Atlas ◽  
Pan Cancer

Abstract Cancer-related mutations have been mainly identified in protein-coding regions. Recent studies have demonstrated that mutations in non-coding regions of the genome could also be a risk factor for cancer. However, the non-coding regions comprise 98% of the total length of the human genome and contain a huge number of mutations, making it difficult to interpret their impacts on pathogenesis of cancer. To comprehensively identify cancer-related non-coding mutations, we focused on recurrent mutations in non-coding regions using somatic mutation data from COSMIC and whole-genome sequencing data from The Cancer Genome Atlas (TCGA). We identified 21 574 recurrent mutations in non-coding regions that were shared by at least two different samples from both COSMIC and TCGA databases. Among them, 580 candidate cancer-related non-coding recurrent mutations were identified based on epigenomic and chromatin structure datasets. One of such mutation was located in RREB1 binding site that is thought to interact with TEAD1 promoter. Our results suggest that mutations may disrupt the binding of RREB1 to the candidate enhancer region and increase TEAD1 expression levels. Our findings demonstrate that non-coding recurrent mutations and coding mutations may contribute to the pathogenesis of cancer.

scholarly journals Comprehensive Analysis of Immune Correlation of KIF20A in Pan-cancer

2020 ◽  
Author(s):  
Xiao-Han Cui ◽  
Qiu-Ju Peng ◽  
Peng Gao ◽  
Xu-Dong Zhang ◽  
Ren-Zhi Li ◽  
...  
Keyword(s):  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Immune Checkpoints ◽  
Rna Seq ◽  
Gene Set Enrichment ◽  
Related Information ◽  
Common Causes ◽  
Cancer Genome Atlas ◽  
Pan Cancer

Abstract Background: Cancer is one of the most common causes of death, and the morbidity and mortality are gradually increasing in the world. KIF20A plays an important role in tumors, but its immune relevance in pan-cancer needs to be further studied.Methods: KIF20A-related information was download from The Cancer Genome Atlas (TCGA). Collecting RNA-seq data is fragments per kilobase million (FPKM) style data. The ESTIMATE algorithm was used for estimating the stromal and immune scores for 33 tumors. Then, we analyzed the correlation between KIF20A in pan-cancer and immune checkpoints and performed gene set enrichment analysis (GSEA) analysis on the co-expressed genes of KIF20A in pan-cancer.Results: We have confirmed that the expression of KIF20A has a intensive correlation with prognosis in 33 kinds of tumors. Its expression of KIF20A was related to a variety of immune cells and immune checkpoints. Based on the results of GSEA for further analysis, in multiple tumors, KIF20A is related to immune-related pathways.Conclusion: We have demonstrated that KIF20A played an important role in pan-cancer and could affect the occurrence or development of a variety of tumors. Moreover, KIF20A was related to immunity, and KIF20A- related immune research in pan-cancer also needs to be further demonstrate.

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