Multicellular organisms undergo millions to trillions of cell divisions during their lifetime, all their cells ultimately being derived from a single zygote. At every cell division, the entire genome is being copied, nucleotide by nucleotide, and although the precision of this copy mechanism is extremely high, mistakes do occur. Most of these copy errors are eliminated by very efficient and sophisticated DNA repair mechanisms that ultimately ensure almost perfect DNA replication1. Nonetheless, some errors slip through the repair machinery and become permanent mutations. Somatic mutations accumulate throughout life, particularly quickly if genes of the repair mechanisms themselves are affected by mutations, potentially resulting in the emergence of cancer. Cancer starts when a combination of somatic mutations produces cells that slip out of cell cycle control, making them able to grow and proliferate uncontrollably with rapidly accumulating genetic variation, and to invade tissues at the expense of the host organism. Cancer cells are genetically heterogeneous, often carrying different nucleotide sequences, methylation patterns of their DNA or even different chromosome numbers. These cells compete with each other for resources and space, where cells that most efficiently compete and evade programmed cell death will increase in number and frequency. Consequently, each cancer is an example of clonal evolution that is fueled by mutations and genetic diversity within the malignancy, a perfect example of a micro-evolutionary process. Hence, it is not surprising that adopting an evolutionary perspective is now regarded as key for a better understanding of oncogenic processes. Evolution not only explains how cancer emerges and progresses, but also explains why some individuals or species face lower cancer risks than others, how cancer resistance unfolded over time and predicts the age when cancer is most likely to emerge. Thus, implementing evolutionary theory in oncology promises better insight into oncogenic phenomena, potentially aiding the prevention, early detection as well as treatment of this major disease. However, despite recent progress towards greater convergence and dialogue between scientists working on oncology, ecology and evolutionary sciences, much remains to be done to achieve full integration of these disciplines. Similarly, while ecologists have ignored oncogenic phenomena, their roles in ecosystem functioning could be significant due to carcinogenesis influencing individual competitive and dispersal abilities, susceptibility to pathogens and vulnerability to predation. These processes are currently exacerbated given that most, if not all, ecosystems of our planet are now polluted with mutagenic substances.