Abstract
Diffuse large B-cell lymphoma (DLBCL) represents 30-40% of all non-Hodgkin lymphomas (NHL) and is a disease with an aggressive behavior. Because about one-third of DLBCL patients will be refractory or resistant to standard therapy, several studies focused on identification of new individual prognostic and risk stratification biomarkers and new potential therapeutic targets. In contrast to other types of cancers like carcinomas, where tumor microenvironment was widely investigated, its role in DLBCL pathogenesis and patient survival is still poorly understood, although few studies had promising results. The composition of TME and its interaction with neoplastic cells may explain the role of several genes (beta2-microglobulin gene, CD58 gene), receptor-like programmed cell death-1 (PD-1) and its ligand (PD-L1), or other cell components (Treg) in tumor evasion of immune surveillance, resulting in tumor progression. Also, it was found that “gene expression profile” of the microenvironmental cells, the phenotype of tumor-associated macrophages (TAM), the expression of matricellular proteins like SPARC and fibronectin, the overexpression of several types of matrix metalloproteinases (MMPs) like MMP-2 and MMP-9, or the tissue inhibitors of matrix metalloproteinases (TIMPs) may lead to a favorable or adverse outcome. With this review, we try to highlight the influence of microenvironment components over lymphoid clone progression and their prognostic impact in DLBCL patients.
Highlights
Diffuse large B-cell lymphoma (DLBCL) represents about 3040% of non-Hodgkin lymphomas (NHL) [1]
CD58, the receptor of the natural killer (NK) cells or T cell CD2+, has an important role in this process. 21% of DLBCLs, more frequently the activated B-cell (ABC) subtype, were found to have inactivation of the CD58 gene (CD58) that is implied in the loss of recognition of tumor cells by circulating T-lymphocytes (CTL) and NK cells [22]
They concluded that since the expression of CD68 or CD163 is associated with an adverse outcome in patients treated with R-CHOP, double staining for CD68 and CD163 may be a better method of predicting outcomes of DLBCL [60]
Summary
Diffuse large B-cell lymphoma (DLBCL) represents about 3040% of non-Hodgkin lymphomas (NHL) [1]. New molecular findings in DLBCL genetics have shown that these lymphomas comprise a group of disorders with specific signaling programs [1], and their first target was to identify new potential therapies with greater specificity and with lower toxicity [2]. Current research in this field is focused on identification of new individual prognostic and risk stratification biomarkers in order to predict the outcome and therapy response or that could indicate the patients who may be eligible for more aggressive therapies. The composition and spatial characteristics of the TME and the interaction between its components and lymphoma cells demonstrate significant heterogeneity depending on the type of lymphoma or the tissue or organ in which lymphoma arises and may have an important impact in the patient’s survival, therapy response, and disease progression or relapse
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