Cancer-related
inflammation is considered the "seventh hallmark of
cancer"; numerous studies demonstrate that
tumors develop and progress within inflammatory diseases. Central to the development of
cancer are genetic changes that endow these
cancer cells with many of the hallmarks of
cancer, such as self-sufficient growth and resistance to anti-growth and pro-death signals. However, while the genetic changes that occur within
cancer cells themselves, such as activated oncogenes or dysfunctional
tumor suppressors, are responsible for many aspects of
cancer development, they are not sufficient.
Tumor promotion and progression are dependent on ancillary processes involving cells of the
tumor environment that are not necessarily cancerous themselves. Infiltration of immune cells facilitates
tumor development through the production of factors that promote
carcinogenesis and by enabling
tumors to evade the host immune response. Small molecules including
cytokines,
chemokines, and
growth factors play key roles in both
inflammation and
cancer by promoting proliferation, angiogenesis, and
carcinogenesis and by recruiting immune cells. The extracellular matrix is altered in
inflammation and provides structural support to developing
tumors.
Hypoxia is a common state in
cancers and inflamed tissues which causes DNA damage and induces tumorigenic factors. Finally, tissue vasculature is a vital part of its microenvironment, supplying
oxygen, nutrients, and
growth factors to rapidly dividing cells and providing a mechanism for metastatic spread. This review will discuss the reflexive relationship between
cancer and
inflammation with particular focus on how by considering the role of
inflammation in physiologic processes such as the maintenance of tissue homeostasis and repair may provide a logical framework for understanding the connection between the inflammatory response and
cancer. The cells and molecules outlined here represent potential targets for the treatment of
head and neck cancer.