Stay pruned for summer.

August 1, 2017. This decade in oncology will be remembered for its vast headways made in our knowledge of the complex interplay between tumors and the immune system. This week’s report in JAMA Onc expands our understanding (and confusion?) of how triple negative breast cancers (TNBC) and the immune system interact, specifically by exploring the association between tumor infiltrating lymphocytes (TIL) and tumor genetic heterogeneity. Didn’t we just talk about TILs? Well, here’s a new take: Some think that tumors with lots of mutations produce lots of different antigens that stimulate the immune system (bad tumor→ immune response). Others think the reverse happens, where a strong immune system essentially “prunes” the tumor of its heterogeneity (immune response→ good tumor). Using data from the Cancer Genome Atlas, this report supports the latter hypothesis: TNBCs with the best prognosis had lots of TIL, lower mutations and neoantigens, and less clonal heterogeneity. In other words, the immune system appears to drive, at least in part, the behavior of TNBC by prohibiting mutations that could result in aggressive behavior. So regardless of which comes first, the lymphocyte infiltrating chicken or the genetically homogenous egg, TILs mean good prognosis and good response to targeted therapy. Which is sTIL more good news for lymphocyte infiltration.