ArticleScientific reports2018
Evolution of oncogenic signatures of mutation hotspots in tyrosine kinases supports the atavistic hypothesis of cancer.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
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- Disruption of metazoan gene regulatory networks in cancer alters the balance of co-expression between genes of unicellular and multicellular origins.Genome biology · 2024Article
- The evolutionary cancer genome theory and its reasoning.Genetics in medicine open · 2023Review
- What Are the Reasons for Continuing Failures in Cancer Therapy? Are Misleading/Inappropriate Preclinical Assays to Be Blamed? Might Some Modern Therapies Cause More Harm than Benefit?International journal of molecular sciences · 2022Review
- Cancer progression as a sequence of atavistic reversions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Article
- Intratumor Heterogeneity and Therapy Resistance: Contributions of Dormancy, Apoptosis Reversal (Anastasis) and Cell Fusion to Disease Recurrence.International journal of molecular sciences · 2020Review
- Towards quantitative and multiplexed in vivo functional cancer genomics.Nature reviews. Genetics · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 assuming oncogenic functions with onco-signatures always intact in cancer, such as HCK and LYN. In Class II with no bona fide mammalian onco-homologs, Pyk2, a protist onco-homolog with an onco-signature of BRAF was found assuming oncogenic-like functions. Onco-signatures in both classes root deep in the primitive system. Together, these evidences supported our proposal that cancer can be driven by reverse evolution of oncogenes through gain-of-function mutations. And also for the first time, we provided the specific targets for experimental verification of the atavistic hypothesis of cancer.
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