Abstract：
:Synonymous mutations change the sequence of a gene without directly altering the sequence of the encoded protein. Here, we present evidence that these "silent" mutations frequently contribute to human cancer. Selection on synonymous mutations in oncogenes is cancer-type specific, and although the functional consequences of cancer-associated synonymous mutations may be diverse, they recurrently alter exonic motifs that regulate splicing and are associated with changes in oncogene splicing in tumors. The p53 tumor suppressor (TP53) also has recurrent synonymous mutations, but, in contrast to those in oncogenes, these are adjacent to splice sites and inactivate them. We estimate that between one in two and one in five silent mutations in oncogenes have been selected, equating to ~6%- 8% of all selected single-nucleotide changes in these genes. In addition, our analyses suggest that dosage-sensitive oncogenes have selected mutations in their 3' UTRs.
journal_name
Celljournal_title
Cellauthors
Supek F,Miñana B,Valcárcel J,Gabaldón T,Lehner Bdoi
10.1016/j.cell.2014.01.051subject
Has Abstractpub_date
2014-03-13 00:00:00pages
1324-1335issue
6eissn
0092-8674issn
1097-4172pii
S0092-8674(14)00145-7journal_volume
156pub_type
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