Interaction of tumor-associated macrophages and cancer chemotherapy

Abstract

It has been recently recognized that the tumor microenvironment (TME) is an essential factor that defines the efficiency of chemotherapy. The local TME, consisting of immune cells with diverse phenotypes and functions, can strongly modulate the response to chemotherapy. Tumor-associated macrophages (TAMs) that display pronounced heterogeneity and phenotypic plasticity are the major innate immune component in the microenvironment of solid tumors. In our review, we elucidate the complex role of TAMs in the progression of different types of solid tumors, summarize the current knowledge about the effects of different anticancer chemotherapeutic agents on monocytes/macrophages, and describe the mechanisms of chemotherapy resistance mediated by TAMs.

Immune Landscape in Burkitt Lymphoma reveals M2-macrophage polarization and Correlation between PD-L1 expression and Non-Canonical EBV latency program

“…12,13 In the recent decade a model has been developed to describe the complex mechanism of macrophage activation as a polarization towards two opposite states, namely M1 and M2, with proinflammatory and pro-tumoral properties respectively. [32][33][34][35][36] TAM density in particular M2-TAMs have been associated with tumor progression and poor prognosis in DLBCL. 37,38 In the present work, we identified a polarization towards a M2 phenotype of TAMs in all cases by applying three different approaches (CIBERSORT, mIHC and mIF) regardless of the subtype of BL, and thus, of EBV status.…”

Tumor microenvironment complexity and therapeutic implications at a glance

“…Similar to CAFs, TAMs are heterogeneous and available in different types depending on their origin and function [88]. Based on their origin and half-life, they are (i) long-living embryonically (yolk sac)-derived tissue-resident macrophages and (ii) short-lived circulating monocyte-derived macrophages derived from bone marrow and recruited to tumor tissue by growth factors and chemokines, such as, CCL2, CCL5, and macrophage colony-stimulating factor (M-CSF) [89][90][91].…”

“…Clinical studies and experimental animal models suggest that TAM commonly plays a pro-tumoral role in various ways [89,96,97]. For one, TAM strengthens angiogenesis by production of VEGF-A, TNFα, urokinase plasminogen activator (uPA), FGF, adrenomedullin (ADM), and semaphorin 4D (Sema4D) thymidine phosphorylase (TP), lymphangigensis (secretion of VEGF-A, VEGF-C, VEGF-D, CXCL8, MMP2, MMP9) fueling cancer invasion and metastasis [96,98,99].…”

Tumor‐infiltrating M2 macrophage in pretreatment biopsy sample predicts response to chemotherapy and survival in esophageal cancer

“…In addition to the biological malignancy of tumor cells and the influence of genetic characteristics on sensitivity to therapeutic agents, the immune condition of the tumor microenvironment (TME), consisting of varieties of immune cells, was recently recognized to modulate the efficiency of chemotherapy . Among the components of the TME, tumor‐infiltrating macrophages (TAM) have been reported to contribute to chemoresistance by modulating the cytotoxicity of tumor‐infiltrating T cells . We previously reported the association between TAM and chemotherapy efficacy in EC patients by analyzing the immunohistochemistry (IHC) of resected specimens .…”