Purpose of review: Loss of cell growth control is not sufficient to explain why tumours form as the immune system recognizes many malignant cells and keeps them in check. The local inflammatory microenvironment is a pivotal factor in tumour formation, as tumour-associated inflammation actively suppresses antitumour immunity. The purpose of this review is to evaluate emerging evidence that amino acid catabolism is a key feature of tumour-associated inflammation that supports tumour progression and immune resistance to therapy.
Recent findings: Enhanced amino acid catabolism in inflammatory tumour microenvironments correlates with carcinogen resistance and immune regulation mediated by tumour-associated immune cells that protect tumours from natural and vaccine-induced immunity. Interfering with metabolic pathways exploited by tumours is a promising antitumour strategy, especially when combined with other therapies. Moreover, molecular sensors that evolved to detect pathogens may enhance evasion of immune surveillance to permit tumour progression.
Summary: Innate immune sensing that induces amino acid catabolism in tumour microenvironments may be pivotal in initiating and sustaining local inflammation that promotes immune resistance and attenuates antitumour immunity. Targeting molecular sensors that mediate these metabolic changes may be an effective strategy to enhance antitumour immunity that prevents tumour progression, as well as improving the efficacy of cancer therapy.