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The cancer microenvironment, or tumour microenvironment, describes the non-cancerous cells present in the tumour. These include fibroblasts, immune cells and cells that comprise the blood vessels. It also includes the proteins produced by all of the cells present in the tumour that support the growth of the cancer cells.
Sun et al. identify fatty acid binding protein 5 (FABP5) as a driver of obesity-induced hepatocellular carcinoma in mice. FABP5 inhibition is found to predispose transformed cells to death by ferroptosis and to induce a pro-inflammatory tumour microenvironment.
Tumour-derived prostaglandin E2, signaling through its receptors EP2 and EP4, is shown to restrain the responses of tumour-infiltrating stem-like TCF1+CD8+ T lymphocytes, and modulation of T cell EP2 and EP4 can restore anticancer immunity.
This Review discusses the mechanisms by which common alterations of cancer cell metabolism interfere with immune functions to promote immunoevasion and tumour progression, and avenues to target such alterations for therapeutic purposes.
In this recent study, He et al. establish that chronic stress promotes metastasis through stress-induced formation of neutrophil extracellular traps (NETs).
Cancer cells adjust the composition of their glycocalyx to increase its thickness and create a physical barrier that shields them from immune recognition and engagement.