It's a dog's life: Canine transmissible venereal tumor is one of the few cancer lineages that is transferred among individuals through contact. It arose millennia ago and has been evolving independently from its hosts ever since. Baez-Ortega et al. looked at the phylogenetic history of the cancer and describe several distinctive mutational patterns (see the Perspective by Maley and Shibata). Most notably, both positive and negative selection show only weak or distant signals. This suggests that the main driver of the lineage's evolution is neutral genetic drift. Understanding the influence of drift may reshape how we think about long-term cancer evolution. Science , this issue p. eaau9923 ; see also p. 440

Autonomous replication and segregation of mitochondrial DNA (mtDNA) creates the potential for evolutionary conflict driven by emergence of haplotypes under positive selection for ‘selfish’ traits, such as replicative advantage. However, few cases of this phenomenon arising within natural populations have been described. Here, we survey the frequency of mtDNA horizontal transfer within the canine transmissible venereal tumour (CTVT), a contagious cancer clone that occasionally acquires mtDNA from its hosts. Remarkably, one canine mtDNA haplotype, A1d1a, has repeatedly and recently colonised CTVT cells, recurrently replacing incumbent CTVT haplotypes. An A1d1a control region polymorphism predicted to influence transcription is fixed in the products of an A1d1a recombination event and occurs somatically on other CTVT mtDNA backgrounds. We present a model whereby ‘selfish’ positive selection acting on a regulatory variant drives repeated fixation of A1d1a within CTVT cells.

Distribution and prevalence of transmissible venereal tumor in the Colombian canine population