A new tool for an old problem

Cancer is characterized by somatic mutations that provide a growth and survival advantage. The mutations are a function of chance because of the random nature of mutagenesis. However, the biology in the tumor cells drives the selection of mutations that are advantageous to the cancer. 1 in addition, the tumor environment exerts a selective pressure on the tumor. For example, the hypoxic environment of a tumor induces HiF, stimulating veGF production, which signals to the non-tumor endothelial cells to stimulate angiogenesis. witkiewicz et al. have assessed the association of another non-tumor marker, MCT4, in triple-negative breast cancer (TnBC). 2 Triple-negative breast cancers are estro-gen and progesterone receptor-negative and HeR-2-negative and account for 10–20% of all breast cancers. 3 standard treatment is surgery with radiotherapy and adjuvant che-motherapy, sometimes with biologic agents. Although TnBCs are generally very susceptible to chemotherapy, they are often associated with a shorter median time to relapse and early death. One important goal is to identify prognostic biomarkers to reliably select high-and low-risk subsets of TnBC. Prognostic biomarkers do not have to be limited to the tumor cell. The ratio of tumor to stroma in TnBC is a predictor of outcome; tumors with < 50% stroma have a 5-year progression free survival and overall survival of 85% and 89% compared with 45% and 65% in tumors with > 50% stroma. 4 Does the biology of the stroma predict response in TnBC? Loss of stromal caveolin-1 (Cav-1) is predictive in TnBCs; 75.5% of patients are alive at 5 y with high stromal Cav-1 compared with 9.4% of patients with low stromal Cav-1.