Inflammatory markers have a role in renal cell carcinoma prognosis

The cause is unclear for most renal cell cancers (RCCs), although inactivation of the von Hippel-Lindau tumor-suppressor gene plays a key role for some clear-cell variants. The resulting elevation of hypoxia-inducible factor and subsequent dysregulation of cell growth is well documented. The role of inflammation as a cause or promoter of cancer cell growth has been appreciated better in the laboratory than in the clinic, but in recent years the spotlight has turned to inflammation, fueled primarily by two observations: (1) recognition of the neutrophil/lymphocyte ratio (NLR) as a marker of inflammation for many cancers, including renal cancer [1,2]; and (2) the extraordinarily rapid development of PD1/L1 inhibitors [3–5], which has highlighted the importance of immune function in some cancers. The biological mechanisms for the interplay between inflammation and immune function are still unclear, but there is increasing evidence that perturbations to many parts of the immune and inflammation signaling pathways aid in the promotion of angiogenesis and immune surveillance tolerance.