Cellular Dynamics within the Tumor Microenvironment

Dear Colleagues, 

The evolution of a solid tumor is not only a consequence of genetic mutations but also depends on the presence and activity of normal, infiltrating cells. As cancer cells proliferate, they impose physical and metabolic stresses on the surrounding tissue. This initiates tissue repair mechanisms and inflammatory responses that recruit stromal and immune cells to the growing tumor.

Fibroblasts and cells of the innate immune system, such as macrophages, survey tissue, searching for pathogens and damaged cells and attempting to repair the tissue structure by producing and remodeling matrix components. Physical and metabolic stresses induce the production of growth factors that recruit additional cells and blood vessels. In some tumors, adaptive immune cells are recruited and can mount anticancer immune responses. These responses depend on physical interactions between multiple cell types as well as secreted cytokines or chemokines.

This creates a complex and dynamic microenvironment driven by heterogeneous interactions between various cell types and between cells and matrix structures. A further complication comes from recent evidence that tumor growth and response to treatment can also be affected by the systemic or local microbiome. Whether this is due to specific bacterial metabolites or through direct interactions with the innate or adaptive immune responses is currently an open question. Given that communication between cells can be mediated by direct contact or by soluble or matrix-bound species, a better understanding of the tumor microenvironment requires the integration of information over multiple size scales.

The purpose of this Special Issue is to provide a more comprehensive understanding of tumor cell dynamics. The focus will be on the dynamics of the host cells that infiltrate into tumors, and their interactions with each other, with cancer cells, and with matrix structures. Of particular interest are 1) the mechanisms involved in recruiting cells to tumors; 2) tumor-induced mechanisms of inflammation and immune cell recruitment; 3) fibroblast activation and matrix biology in the context of their effects on other cells; 4) interactions between cells and intra-tumor bacteria; and 5) physical interactions between immune cells that regulate antitumor immunity. Emphasis will be on the mechanisms that cells use to communicate and how physical interactions or biochemical cues either inhibit or enable tumor progression. We encourage the submission of studies based on longitudinal intravital microscopy of cell dynamics. To limit the scope, we will not examine cancer cell-autonomous mechanisms of invasion and metastasis or their interactions with the matrix.

Dr. Lance L. Munn
Guest Editor

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