Date of this Version
JOURNAL OF INTERFERON & CYTOKINE RESEARCH Volume 39, Number 1, 2019
While inflammation is a normal physiological response after tissue injury, the chemicals/mediators that are released by the damaged tissue can be toxic to the cells. This underlying inflammation increases the likelihood of cellular DNA damage and aberrant cell growth (Kiraly and others 2015). In this scenario, inflammation functions as a ‘‘behind-curtain factor’’ for many disorders. Cancer has long been known to be closely tethered to inflammation. Widespread evidence shows that inflammatory diseases such as colitis, pancreatitis, and hepatitis make their respective organs highly susceptible to eventual cancer development (Shalapour and Karin 2015). However, other studies have shown that in due course, a growing cancer starts recruiting and relying on various mediators of inflammation to promote angiogenesis, further proliferating, metastasizing, and subverting the innate and adaptive immune response (Chan and others 2012). While we continue to ponder the chicken or egg scenario of how cancer and inflammation are related, the critical role inflammation plays in cancer progression cannot be denied. For example, some studies demonstrate that antiinflammatory drugs such as aspirin not only act by reducing inflammation-related disorders, but also decrease the risk of colon cancer and gastrointestinal cancers. In colon cancer, aspirin specifically decreased the incidence of polyps, including advanced polyps, which are the precursors to colorectal cancer (Husain and others 2002; Wang and others 2018). However, experimental data from other cancers, including breast cancer, are not very promising, largely due to the differences in the inflamed tumor microenvironment (Strasser-Weippl and others 2018). Therefore, understanding the intricate cellular signaling pathways and the players involved in the smoldering inflammatory tumor microenvironment is paramount to identifying new strategies for the better management of cancers. In this special issue, several leaders in the field discuss the latest developments in our understanding of cancer-associated inflammation, with a focus on the role of inflammatory cytokines and interferons. Emphasis is also placed on identifying opportunities and developing road maps for novel treatment approaches to combine immunotherapies with direct modulation of cytokine levels in the host.