ArticleFrontiers in oncology2019
Mast Cells May Differentially Regulate Growth of Lymphoid Neoplasms by Opposite Modulation of Histamine Receptors.
Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Thapsigargin triggers a non-apoptotic, caspase-independent programmed cell death in basophilic leukaemia cells.Cell death discovery · 2025Article
- Mast cell metabolism in cancer: an underexplored frontier demanding more attention.Frontiers in immunology · 2025Review
- Phytochemicals as Immunomodulatory Molecules in Cancer Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Histamine H4 Receptor Agonism Induces Antitumor Effects in Human T-Cell Lymphoma.International journal of molecular sciences · 2022Article
- Histamine in cancer immunology and immunotherapy. Current status and new perspectives.Pharmacology research & perspectives · 2021Review
- Steering Mast Cells or Their Mediators as a Prospective Novel Therapeutic Approach for the Treatment of Hematological Malignancies.Frontiers in oncology · 2021Review
- LncRNAs Target Ferroptosis-Related Genes and Impair Activation of CD4Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer microenvironment is complex and consists of various immune cells. There is evidence for mast cell (MC) infiltration of tumors, but their role thereof is poorly understood. In this study, we explored the effects of mast cell and their mediators on the growth of hematological cancer cells. The affect is demonstrated using RBL-2H3 MCs, and YAC-1, EL4 and L1210 as hematological cancer cell lines. Direct contact with MCs or stimulation by their mediators caused growth inhibition of YAC-1 cells, growth enhancement of EL4 cells and no change in growth of L1210 cells. This effect was confirmed by cancer cell recovery, cell viability, mitochondrial health, and cell cycle analysis. MCs showed mediator release in direct contact with tumor cells. MC mediators' treatment to YAC-1 and EL4 yielded exactly opposite modulations of survival markers,
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