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Recent attention has focused on targeting the tumor microenvironment (TME), which largely consists of infiltrating immune cells, notably T-regulatory cells (Tregs), neo-vascular cells, stromal cells, and tumor cells. Adverse events include autoimmune disease, cardiotoxicity, and cytokine release syndrome. Further, ICIs have unavoidable adverse events because they act broadly on the immune system. While ICIs may prolong survival, tumors often acquire primary or secondary resistance to them. ICIs harness the human immune system to attack tumors, predominantly by enhancing the anti-tumor activity of cytotoxic T lymphocytes (i.e., effector T cells, Teffs). Cancer immunotherapy using immune checkpoint inhibitors (ICIs) such as anti-programmed cell death protein 1 (PD-1) drugs or anti-cytotoxic T lymphocytes-associated protein 4 (CTLA-4) drugs have become common in the clinical setting. Since the identification of nitrogen mustard as an anti-cancer drug in 1940s, pharmaceutical options for malignant disease have remarkably progressed to increasingly targeted therapies. This review traces the origins of our understanding of TNFR2’s multifaceted roles in the TME and discusses the therapeutic potential of agents designed to block TNFR2 as the cornerstone of a TME-specific strategy. Novel antibodies have been developed that expressly kill only rapidly proliferating cells expressing newly synthesized TNFR2 protein.

Novel therapies that block TNFR2 signaling show promise in cell culture studies, animal models, and human studies. TNFR2 is an attractive molecular target because it is rarely expressed in normal tissues (thus, has low potential for systemic toxicity) and because it is overexpressed on many types of cancer cells as well as on associated TME components, such as T regulatory cells (Tregs), tumor-associated macrophages, and other cells that facilitate tumor progression and spread.

Another approach is to target the TME with greater specificity by taking aim at the tumor necrosis factor receptor 2 (TNFR2) signaling pathway. Although promising, many experimental therapies targeted at the TME have systemic toxicity. New therapies include agents that activate quiescent T effector cells and agents that interfere with abnormal neovascularity.

The appreciation that cancer growth is promoted by a dynamic tumor microenvironment (TME) has spawned novel approaches to cancer treatment.

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