Comparative study and meta-analysis of meta-analysis studies for the correlation of genomic markers with early cancer de
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PRIMARY RESEARCH
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Comparative study and meta-analysis of meta-analysis studies for the correlation of genomic markers with early cancer detection Zoi Lanara1,2†, Efstathia Giannopoulou3†, Marta Fullen4, Evangelos Kostantinopoulos2, Jean-Christophe Nebel4, Haralabos P Kalofonos3, George P Patrinos2 and Cristiana Pavlidis2*
Abstract A large number of common disorders, including cancer, have complex genetic traits, with multiple genetic and environmental components contributing to susceptibility. A literature search revealed that even among several meta-analyses, there were ambiguous results and conclusions. In the current study, we conducted a thorough meta-analysis gathering the published meta-analysis studies previously reported to correlate any random effect or predictive value of genome variations in certain genes for various types of cancer. The overall analysis was initially aimed to result in associations (1) among genes which when mutated lead to different types of cancer (e.g. common metabolic pathways) and (2) between groups of genes and types of cancer. We have meta-analysed 150 meta-analysis articles which included 4,474 studies, 2,452,510 cases and 3,091,626 controls (5,544,136 individuals in total) including various racial groups and other population groups (native Americans, Latinos, Aborigines, etc.). Our results were not only consistent with previously published literature but also depicted novel correlations of genes with new cancer types. Our analysis revealed a total of 17 gene-disease pairs that are affected and generated gene/ disease clusters, many of which proved to be independent of the criteria used, which suggests that these clusters are biologically meaningful. Keywords: Cancer, Meta-analysis, Gene, Association, Interaction, Single-nucleotide polymorphism, Alleles, Clustering
Introduction Cancer is the result of a complicated process that involves the accumulation of both genetic and epigenetic alterations in various genes [1]. The somatic genetic alterations in cancer include point mutations, small insertion/deletion events, translocations, copy number changes and loss of heterozygosity [2]. These changes either augment the action and/or expression of an oncoprotein or silence tumour suppressor genes. Single-nucleotide polymorphism (SNP) is the most common form of genetic variation in the human genome. Although common SNPs for disease prediction are not ready for widespread use [3], recent genome-wide association studies (GWASs) using high-throughput techniques have identified regions of the * Correspondence: [email protected] † Equal contributors 2 School of Health Sciences, Department of Pharmacy, University of Patras, University Campus, Rio, Patras 26504, Greece Full list of author information is available at the end of the article
genome that contain SNPs with alleles that are associated with increased risk for cancer such as FGFR2 in breast cancer [4-7]. The knowledge on gene mutations that predispose tumour initiation or tumour development and progress will give
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