B-cell malignancies are a heterogeneous group of hematological neoplasms derived from cells at different stages of B-cell development. Malignant B cells develop in specialized tissue microenvironments, such as bone marrow and secondary lymphoid organs, where they receive supportive signals promoting tumor proliferation and survival.
The tumor microenvironments of B-cell malignancies are highly variable in terms of spatial organization and composition of accessory cells, which include immune and inflammatory cells, in addition to blood and lymphatic vascular meshwork.
The cellular components of the microenvironment generally reflect those of the normal counterpart and interact with malignant B cells through a complex network of soluble factors, chemokine receptors, and adhesion molecules. Furthermore, antigenic stimulation mediated by the B-cell receptor (BCR) plays a prominent pathogenetic role in mature B-cell malignancies.
The degree of interactions and dependance of malignant cells on the microenvironments for survival and proliferation deeply differ across types of B-cell malignancies, extending from a high dependence on the microenvironment for growth to an autonomous, microenvironment-independent growth. Several lines of evidence support the crucial role of microenvironment signals in controlling the pathogenesis, development, and drug resistance of B-cell malignancies.
On the other hand, malignant cells can shape the microenvironment to promote immunosuppressive and escaping mechanisms aimed at avoiding immune surveillance. Increasing evidence also indicates that the tumor microenvironment can induce treatment resistance.
The elucidation of mechanisms involved in the crosstalk between tumor cells and microenvironment is of preeminent importance to understand the biological mechanisms of diseases and develop novel treatments of patients with hematologic malignancies.
This Special Issue intends to provide an Open Access forum collecting original research and review articles addressing cellular and molecular pathways involved in the crosstalk between malignant B cells and their microenvironments.