Figure 1.

The complex relation and balance between genomic instability, inflammation and cancer promotion and control [adapted from (19) and (20)]. An increasing body of research suggests that two additional hallmarks of cancer are involved in the pathogenesis of some and perhaps all cancers. One involves the capability to modify, or reprogram, cellular metabolism in order to most effectively support neoplastic proliferation. The second allows cancer cells to evade immunological destruction, in particular by T and B lymphocytes, macrophages, and natural killer cells. Additionally, two consequential characteristics (lower half of figure) of neoplasia facilitate acquisition of both core and emerging hallmarks. Genomic instability endows cancer cells with genetic alterations that drive tumor progression. Inflammation by innate immune cells designed to fight infections and heal wounds can instead result in their inadvertent support of multiple hallmark capabilities, thereby manifesting the now widely appreciated tumor-promoting consequences of inflammatory responses.