ReviewJournal of clinical and experimental hematopathology : JCEH2024
Mechanisms of lymphoma-stromal interactions focusing on tumor-associated macrophages, fibroblastic reticular cells, and follicular dendritic cells.
Review in Journal of clinical and experimental hematopathology : JCEH, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Extranodal Marginal Zone Lymphoma: Integrating Etiology, Microenvironment, and Genetics Into Clinical Decision-Making.European journal of haematology · 2026Review
- Matrix Stiffness Regulates Diffuse Large B-Cell Lymphoma (DLBCL) Spheroid Formation in a Tunable 3D Chitosan Hydrogel Model.Gels (Basel, Switzerland) · 2026Article
- Emerging Biomarkers in Urological Cancers: Angiogenesis and Damage-Associated Molecular Pattern Signaling.International journal of molecular sciences · 2025Review
- Highlights: Myeloid cells in lymphoid malignancies.Journal of clinical and experimental hematopathology : JCEH · 2024Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
The interaction between cancer cells and stromal cells contributes to the pathogenesis of various types of tumors in the tumor microenvironment (TME). Macrophages (Mφs), a type of stromal cell, are transformed into tumor-associated Mφs (TAMs) after integrating within solid tumors. TAMs are known to interact with cancer cells and induce tumor progression. Thus, the cancer cells construct an organ-specific TME, which is advantageous for the survival of cancer cells in the TME. The density of stromal cells is known to be involved in the prognosis of patients with lymphomas. A higher density of stromal cells increases the interaction between lymphoma cells and stromal cells, promoting lymphoma progression. This review focuses on stromal cells in lymphoid tissues, such as TAMs, fibroblastic reticular cells (FRCs), and follicular dendritic cells (FDCs). This review also focuses on the signal transduction caused by stromal cells and tumor cells via factors such as cytokines. IL-10 and other cytokines secreted by TAMs activate the JAK/STAT pathway in lymphoma cells of follicular lymphoma, classic Hodgkin lymphoma, and diffuse large B-cell lymphoma. FRCs play roles in tumor promotion in follicular lymphoma and diffuse large B-cell lymphoma. Cytokines/chemokines secreted by FDCs play essential roles in lymphoma cell survival, proliferation, invasion, and migration in follicular lymphoma. In conclusion, TAMs, FRCs, and FDCs play crucial roles in the TME of lymphomas. Furthermore, histological spatial analysis revealing the positional relationship of each cell could highlight lymphoma-stromal interactions.
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