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Review
. 2021 Aug 17;14(1):125.
doi: 10.1186/s13045-021-01134-x.

Targeting the tumor microenvironment in B-cell lymphoma: challenges and opportunities

Yingyue Liu  1 , Xiangxiang Zhou  2   3   4   5   6   7 , Xin Wang  8   9   10   11   12   13
Affiliations
Review

Targeting the tumor microenvironment in B-cell lymphoma: challenges and opportunities

Yingyue Liu et al. J Hematol Oncol. .

Abstract

B-cell lymphoma is a group of hematological malignancies with high clinical and biological heterogeneity. The pathogenesis of B-cell lymphoma involves a complex interaction between tumor cells and the tumor microenvironment (TME), which is composed of stromal cells and extracellular matrix. Although the roles of the TME have not been fully elucidated, accumulating evidence implies that TME is closely relevant to the origination, invasion and metastasis of B-cell lymphoma. Explorations of the TME provide distinctive insights for cancer therapy. Here, we epitomize the recent advances of TME in B-cell lymphoma and discuss its function in tumor progression and immune escape. In addition, the potential clinical value of targeting TME in B-cell lymphoma is highlighted, which is expected to pave the way for novel therapeutic strategies.

Keywords: B-cell lymphoma; Immunosuppression; Targeted therapy; Tumor microenvironment.

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Conflict of interest statement

The authors have no relevant conflicts.

Figures

Fig. 1
Fig. 1
Major constituents of the TME and targeted therapies. The figure depicts the typical microenvironment of B-cell lymphoma. Tumor microenvironment refers to the internal environment in which tumor cells produce and live, major cellular and noncellular components. It includes not only the tumor cells but also the immune and inflammatory cells, fibroblasts and other cells around them. It also comprises the intercellular substance, micro-vessels and biological molecules infiltrated in the nearby area. Current strategies targeting TME components are also highlighted
Fig. 2
Fig. 2
TME targeting strategies to treat B-cell lymphoma. MDSC, TAM (M2), TAN (N2) and Treg inhibit the process of the antitumor immune response through several inhibition pathways and establish an immunosuppressive TME
Fig. 3
Fig. 3
Impact of hypoxic TME and targeted therapy. Growth factors regulate HIF-1α through MAPK/ERK and PI3K/AKT/mTOR pathway, consequently induce the simulation of HIF-1α mRNA transactivation. Under the hypoxic microenvironment, HIF-1α in cells up-regulates the expression of PD-L1 in hypoxic tumor cells, prevents MDSC from maturation at the tumor site and involves the up-regulation of CD47 on the surface of tumor cells. After CD47 combines with SIRPα on the surface of macrophages, tumor cells provide a robust “don't phagocytize me” signal, thus preventing the phagocytosis of macrophages
See this image and copyright information in PMC

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