Research Topic

Tumor Microenvironment

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Carcinogenesis is a multistage process consisting of tumor initiation, promotion and progression. While tumor initiation may be a brief and irreversible process, tumor promotion and progression are long lasting and potentially reversible processes. These phases, critically depend on the interaction between ...

Carcinogenesis is a multistage process consisting of tumor initiation, promotion and progression. While tumor initiation may be a brief and irreversible process, tumor promotion and progression are long lasting and potentially reversible processes. These phases, critically depend on the interaction between cancer cells and microenvironment, which contains a variety of myeloid cells including macrophages, neutrophils, dendritic cells and myeloid-derived suppressor cells, and lymphoid cells of the adaptive and innate immune system. The immune system might play opposite roles in tumor development. Whereas a full activation can lead to the eradication of malignant cells, chronic activation of various immune cell types in and around pre-malignant tissue might actually promote oncogenic transformation and tumor growth by producing pro-inflammatory cytokines, chemokines and reactive oxygen species. Understanding the molecular mechanisms underlying the tumor promoting properties of the immune system is critical to any effort to slow down or prevent tumor progression. Most importantly, the prognostic impact of the in situ immune cell infiltrate has been demonstrated in different tumor types. In particular, an innovative methodology designed as 'Immunoscore' has been recently defined to quantify the in situ immune infiltrate in colorectal cancer.

This Research Topic aims to present novel insights on the prognostic significance of the tumor microenvironment in different cancer subtypes, and on its predictive relevance, as related to responsiveness to targeted drugs and chemotherapy.

Major components of tumor microenvironment, including tumor-associated macrophages, lymphocytes and cancer-associated fibroblasts will be evaluated. Furthermore pro-angiogenic factors, cytokines, and chemokines potentially involved and their mechanisms of action and signalling pathways will also be discussed. Increasing our understanding on how the different components of the tumor microenvironment interact with tumor cells and on the molecular background underlying their cross-talk could help to identify novel therapeutic and chemopreventive targets.


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