In this chapter we describe the state of the art knowledge of the role played by myeloid cells in promoting and supporting the growth and the invasive properties of a deadly brain tumor, glioblastoma. We provide a review of the works describing the intercellular communication among glioma and associated microglia/macrophage cells (GAMs) using in vitro cellular models derived from mice, rats and human patients and in vivo animal models using syngeneic or xenogeneic experimental systems. Special emphasis will be given to 1) the timing alteration of brain microenvironment under the influence of glioma, 2) the bidirectional communication among tumor and GAMs, 3) possible approaches to interfere with or to guide these interactions, with the aim to identify molecular and cellular targets which could revert or delay the vicious cycle that favors tumor biology.
Role of Infiltrating Microglia/Macrophages in Glioma / Catalano, M.; D'Alessandro, G.; Trettel, F.; Limatola, C.. - (2020), pp. 281-298. [10.1007/978-3-030-30651-9_14].
Role of Infiltrating Microglia/Macrophages in Glioma
Catalano M.Primo
Writing – Original Draft Preparation
;D'Alessandro G.Secondo
Writing – Original Draft Preparation
;Trettel F.Penultimo
Writing – Original Draft Preparation
;Limatola C.
Ultimo
Writing – Original Draft Preparation
2020
Abstract
In this chapter we describe the state of the art knowledge of the role played by myeloid cells in promoting and supporting the growth and the invasive properties of a deadly brain tumor, glioblastoma. We provide a review of the works describing the intercellular communication among glioma and associated microglia/macrophage cells (GAMs) using in vitro cellular models derived from mice, rats and human patients and in vivo animal models using syngeneic or xenogeneic experimental systems. Special emphasis will be given to 1) the timing alteration of brain microenvironment under the influence of glioma, 2) the bidirectional communication among tumor and GAMs, 3) possible approaches to interfere with or to guide these interactions, with the aim to identify molecular and cellular targets which could revert or delay the vicious cycle that favors tumor biology.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
