VIMM scientist Dr. Masoud Manjili published an invited review paper in Cancer Research in which he proposed an intriguing concept regarding tumor dormancy (1). He suggested that tumor dormancy is a natural byproduct of evolutionary mechanisms of cell survival, such as gene mutations and epigenetic modifications, which are detectable in both healthy individuals and in cancer survivors. He went on to suggest that tumor metastasis may be an early dissemination event that occurs during malignant dormancy even before primary cancer is clinically detectable. Finally, he suggested that chronic inflammation is a key factor in awakening dormant malignant cells at the primary site in advanced stage disease (1). In a separate paper published in Cancer Research (2), he argued that since cellular dormancy is an evolutionarily conserved survival mechanism in biological systems, any stress or cytotoxic therapy could trigger cellular dormancy. Therefore, a successful cancer therapy is likely to be achieved by controlling or maintaining malignant dormancy, rather than attempting to destroy dormant malignant cells. This could be accomplished by cancer immunotherapy because of the establishment of long-term memory responses (Figure 1).
