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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Pigment+Cell+Melanoma+Res 2015 ; 28 (6): 673-84 Nephropedia Template TP
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The functional relevance of somatic synonymous mutations in melanoma and other cancers #MMPMID26300548
Gotea V; Gartner JJ; Qutob N; Elnitski L; Samuels Y
Pigment Cell Melanoma Res 2015[Nov]; 28 (6): 673-84 PMID26300548show ga
Recent technological advances in sequencing have flooded the field of cancer research with knowledge about somatic mutations for many different cancer types. Most cancer genomics studies focus on mutations that alter the amino acid sequence, ignoring the potential impact of synonymous mutations. However, accumulating experimental evidence has demonstrated clear consequences for gene function, leading to a widespread recognition of the functional role of synonymous mutations and their causal connection to various diseases. Here, we review the evidence supporting the direct impact of synonymous mutations on gene function via gene splicing; mRNA stability, folding, and translation; protein folding; and miRNA-based regulation of expression. These results highlight the functional contribution of synonymous mutations to oncogenesis and the need to further investigate their detection and prioritization for experimental assessment.The identification of cancer-causing mutations and the corresponding functionally impacted processes represents the main goal of cancer genomics. The inception of large collaborative efforts such as The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC) has led to the discovery of numerous causal or driver mutations in many cancer types. Nevertheless, tumors continue to be found in the absence of conspicuous mutational events, such as nucleotide substitutions, translocations or copy number variants involving genes with well-established tumorigenic connections. The lack of clear driver events in some cancers motivates the search for somatically acquired events that are more rare or have less obvious functional consequences but mechanistically converge on genes and pathways involved in oncogenesis and tumor progression.