There is a strong association between cancer and inflammation. Dysregulated inflammatory responses play a pivotal role in tumor initiation, promotion, and progression through different pathways. Over the past decade, pharmacological inhibition of inflammatory cells and their products, together with manipulation of genes involved in their functions, has been shown to participate in tumor incidence and progression. In consequence, cancer-promoting inflammation is an encouraging target of therapy in oncology. The list of tumor promoting inflammatory cells includes tumor associated macrophages (TAMs), dendritic cells, neutrophils, immature myeloid cells, mast cells, eosinophils, and lymphocytes. These cells are present at the tumor microenvironment and produce a variety of cytotoxic and inflammatory mediators, thus sustaining immunosuppression, tumor cell proliferation and survival, angiogenesis, extracellular matrix breakdown, metastasis, chemoresistance, and radioresistance. Thus, understanding how inflammation in the whole tumor microenvironment can be targeted into more effective ways may give a better chance to obtain durable antitumor responses.

In this special issue, we seek research aimed to understand how the complex network of inflammatory circuits in the tumor microenvironment could be used for new therapeutic modalities. Research should explore interactions between chronic inflammation modulation and its consequences in carcinogenesis; original research and review papers are welcome.

Potential topics include but are not limited to the following:

• Targeting tumor-induced immune suppression
• Modulation of mitochondrial signaling pathways in damaged cells
• Immunotherapy based on immune-checkpoint inhibitors and inflammatory signaling
• Targeting of myeloid cells
• Mechanisms of potential drugs targeting dysregulated inflammatory responses
• Therapeutic interventions targeting specific STATs-dependent pathways
• Strategies to modulate the microbiome with consequences in inflammation and carcinogenesis
• Blockage of inflammation-related products that promote metastasis