Dear Colleagues,

Cancer metastasis is the most serious problem in cancer patients because of its life-threatening nature owing to multiple organ dysfunctions caused by the growth of disseminated cancer. To overcome the problem of the metastasis dimension of cancer cells, a mechanistic understanding of cancer metastasis is necessary. The ‘seed and soil’ theory that was first proposed by Paget et al. (Cancer Metastasis Rev 1989) may become a critical clue for obtaining a partial understanding of the complex mechanism of cancer distant metastasis. The ‘seed’ represents cancer cells and ‘soil’ represents the cancer favorite organ for the destination of metastasis. Now, we have well documented that inflammation is the key event to raising the cancer-mediated soil field, termed the pre-metastatic niche, in distant organs. Soil also provides an immune suppressive environment so that cancers that arrive in certain soils readily initiate their growth again. Inflammation is expected to occur in not only distant pre-metastatic organs but also in cancer surrounding microenvironments at their primarily developed sites. Inflammation triggered by the primary cancer site provides cancer cells with a driving force of micro-metastasis with invasion, which causes them to travel towards their favorite distant organs more quickly. In this inflammation-mediated metastasis, multiple processes with a variety of signal mechanisms that require a large number of molecules are mutually contributed. Such intracellular and extracellular mechanisms are exerted in the field, including not only cancer cells but also multiple normal cells.

In this Special Issue, we aim to compile critical insights on the mutual relationship between inflammation and cancer metastasis; accordingly, we welcome articles on basic, preclinical, and clinical research related to this this theme. We hope that the collected results will be helpful for gaining an understanding of dimensions of cancer-mediated inflammation that require a prerequisite of metastatic malignancy and for establishing a preclinical rationale to target a newly identified axis in order to further improve clinical responses and patient survival.

Prof. Dr. Masakiyo Sakaguchi
Guest Editor

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• metastasis
• soil and seed theory
• inflammation
• cancer microenvironment
• cancer stroma
• cancer stem cells
• circulating cancer cells
• epithelial and mesenchymal transition (EMT)
• immune suppression
• damage-associated molecular patterns (DAMPs)
• cytokines
• chemokines
• growth factors