期刊
CELL
卷 156, 期 6, 页码 1324-1335出版社
CELL PRESS
DOI: 10.1016/j.cell.2014.01.051
关键词
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资金
- Marie Curie Actions (INTERPOD)
- ERC Starting Grant
- ERASysBio+ ERANET
- MICINN [BFU2011-26206, BIO2012-37161]
- AGAUR
- EMBO Young Investigator Program
- EU Framework 7 project [277899 4DCellFate]
- EMBL-CRG Systems Biology Program
- ERC
- Fundacion Botin
- Fundacion Alicia Koplowicz
- Consolider RNAREG
- MINECO
- ICREA Funding Source: Custom
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 similar 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.
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