Evolution of oncogenic signatures of mutation hotspots in tyrosine kinases supports the atavistic hypothesis of cancer.

ABSTRACT: Cancer has been shown as an evolutionary process emerging hallmarks that are reminiscent of unicellular organisms. Since cancer is mostly driven by somatic mutations, especially by oncogenic hotspot mutations, we proposed a molecular atavism of cancer caused by gain-of-function mutations in oncogenes. As tyrosine kinase (TK) family contains the largest subgroup of oncogenes with hotspot mutations, we traced the most predominant mutation hotspots of TK oncogenes across phylogeny with the domain information and adjacent sequences integrated as onco-signatures. We detected 9 out of 17 TK oncogenes with onco-homologs possessing an onco-signature, which could be divided into two classes by whether their onco-homologs existed in mammals or not. In Class I we identified mammalian onco-homologs as

SUBMITTER: Chen W 

PROVIDER: S-EPMC5974376 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature