Tasmanian devils, the largest marsupial carnivores, have lived in relative isolation on the island of Tasmania. Consequently, there is limited genetic diversity within the devil population, reducing the population's overall fitness and making them more susceptible to the spread of infectious disease. In the past 30 years one such disease, a contagious cancer, has emerged posing an existential threat to the species. The cancer, devil tumor facial disease, is of non-viral origin and is spread by biting which has enabled it to disseminate throughout the devil population, in-and-between different geographic loci. Under this intense selective pressure an evolutionary arms race emerged between the contagious disease and the genetics of the devil host. Aided by the efforts of conscientious scientists there is now hope for the future of the Tasmanian devil population. Furthermore, the Tasmanian devil facial tumor has served as a case study in the value of interdisciplinary science, bringing together ecologists, immunologists, cell biologists, epidemiologists, and cancer biologist, all with the combined goal of saving the Tasmanian devil species.

The HeLa cell line, named after the patient Henrietta Lacks, was one the first human cell lines to be used for tissue culture. In the decades since its origin, it has become a feature in labs across the world. Despite its longevity, repeated detection of most HeLa marker chromosomes have lead the scientific community to view HeLa as a stable cell line and its corresponding findings to be reproducible. However, to date no investigation has examined other meaningful aspects of HeLa's genomic variability, such has whether HeLa's modal chromosome number remains constant. Considering the importance of a cell line's karyotype with respect to reproducibility, I sought to examine the stability of HeLa's karyotype by examining HeLa's modal chromosome number as reported in the literature.