ArticleFrontiers in immunology2020
Potential Oncogenic Effect of the MERTK-Dependent Apoptotic-Cell Clearance Pathway in Starry-Sky B-Cell Lymphoma.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- From pathogenesis to therapeutic targeting: new insight into TAM receptors in rheumatoid arthritis.Cell & bioscience · 2025Review
- Of Tingible Bodies and Starry Skies: Control of Normal and Malignant Tissues Through Apoptotic Cell-Dependent Communication (ACDC).Advances in experimental medicine and biology · 2025Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Hijacking homeostasis: Regulation of the tumor microenvironment by apoptosis.Immunological reviews · 2023Review
- Control of tumor-associated macrophage responses by nutrient acquisition and metabolism.Immunity · 2023Review
- The Apoptosis Paradox in Cancer.International journal of molecular sciences · 2022Review
- Editorial: New Insights Into the Complexity of Tumor Immunology in B-Cell Malignancies: Disease Biology and Signaling.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The histological architecture of certain aggressive B-cell lymphomas (prototypically Burkitt's lymphoma, BL) is characterized by a "starry-sky" (SS) appearance. This is caused by tumor-associated macrophages (TAMs), which appear in standard histological preparations as "stars" in a darkly stained "sky" of lymphoma cells. SS-TAMs accumulate in response to constitutive apoptosis in these tumors and are activated by the apoptotic tumor cells to a pro-oncogenic phenotype. The extent to which SS-TAMs contribute to lymphoma growth through responses generated by interactions with apoptotic tumor cells is unknown. Here, we demonstrate a role for the receptor tyrosine kinase, MERTK, in the oncogenic activity of SS-TAMs. We show that MERTK expression is largely restricted to the macrophages of human BL and of murine models of SS B-cell lymphoma and that it is upregulated in SS-TAMs as compared to the germinal center or paracortical macrophages of normal lymph nodes. Our results further demonstrate that MERTK is active in the phagocytosis of apoptotic lymphoma cells by macrophages and, most significantly, that SS lymphoma growth is markedly inhibited in
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