Ahmed AZHARUDDIN, Ehtesham Ahmed SHARIFF, Raiyan Ehtesham Ahmed SHARIEFF, Farahnaz MUDDEBIHAL, Mohammed Daham ALANAZI, Saleh Hamdan ALANAZI
Annals of Clinical and Analytical Medicine - 2026;17(10):1094-1098
Aim: This study seeks to elucidate the evolutionary trajectory of MYC proto-oncogenes across vertebrate lineages, with particular emphasis on the role of gene duplication events in shaping their diversification. By examining conserved functional domains, the research aims to generate insights that may advance our understanding of oncogenic mechanisms and inform future directions in cancer biology. Methods: Phylogenetic analyses were conducted on MYC protein sequences derived from 37 representative vertebrate species to investigate evolutionary relationships. Multiple sequence alignment was performed using the MUSCLE program with default parameters to ensure accurate positional homology across taxa. Neighbor Joining (NJ) and Maximum Likelihood (ML) methods were employed to infer phylogenetic trees. Statistical robustness of the inferred clades was evaluated by calculating bootstrap support values based on 1,000 replicates, thereby providing confidence estimates for major branching patterns. Results: Comparative phylogenetic analyses revealed that gene duplication events in early vertebrate evolution gave rise to the c-MYC lineage, establishing a foundation for subsequent diversification. Strong sequence conservation was observed among hominids, with human, bonobo, and chimpanzee MYC proteins exhibiting 98.7% similarity. Human MYC sequences shared 87% identity with gorilla homologs and 83% with orangutan homologs, reflecting gradual divergence among great apes. Conclusion: Elevated evolutionary rates in key functional domains indicate positive selection driving adaptive changes in oncogenic regulation. The ability of MYC to change and adapt across species (its evolutionary plasticity) may help explain why it can act as an oncogene. The resulting phylogenetic patterns provide essential context for interpreting MYC-driven tumorigenesis.
