Cancer cells have many abnormal characteristics enabling tumours to grow, spread and avoid immunological and therapeutic destruction. Central to this is the innate ability of populations of cancer cells to rapidly evolve. One feature of many cancers is that they activate genes that are normally associated with distinct developmental states, including germ cell specific genes. This has historically led to the proposal that tumours take on embryonal characteristics, the so called embryonal theory of cancer. However, one group of germline genes, not directly associated with embryonic somatic tissue genesis, are those that encode the specific factors to drive the unique reductional chromosome segregation of meiosis I, which also results in chromosomal exchanges. Here we propose that meiosis I-specific modulators of reductional segregation can contribute to oncogenic chromosome dynamics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, as meiotic factors are not a feature of most embryonic tissue development. We postulate that some meiotic chromosome regulatory functions contribute to a soma-to-germline model for cancer, in which activation of germline (including meiosis) functions drive oncogenesis, and we extend this to propose that meiotic factors could be a powerful sources of targets for therapeutics and biomonitoring in oncology.