ArticleInternational journal of immunopathology and pharmacology2017
MDSCs are involved in the protumorigenic potentials of GM-CSF in colitis-associated cancer.
Article in International journal of immunopathology and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- APX3330 reverses the immunosuppressive tumor microenvironment during colorectal carcinogenesis.Cancer cell international · 2026Article
- Unraveling the Complexities of Myeloid-Derived Suppressor Cells in Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- Neutrophils: From Inflammatory Bowel Disease to Colitis-Associated Colorectal Cancer.Journal of inflammation research · 2025Review
- The Dark Knight: Functional Reprogramming of Neutrophils in the Pathogenesis of Colitis-Associated Cancer.Cancer immunology research · 2024Review
- Immune landscape and response to oncolytic virus-based immunotherapy.Frontiers of medicine · 2024Review
- Gastrodin Attenuates Colitis and Prevents Tumorigenesis in Mice by Interrupting TLR4/MD2/NF-κB Signaling Transduction.Anti-cancer agents in medicinal chemistry · 2024Article
- Local radiotherapy for murine breast cancer increases risk of metastasis by promoting the recruitment of M-MDSCs in lung.Cancer cell international · 2023Article
- Targeting oral tumor microenvironment for effective therapy.Cancer cell international · 2023Review
- Endoplasmic reticulum stress mediates the myeloid-derived immune suppression associated with cancer and infectious disease.Journal of translational medicine · 2023Review
- Cancer immune exclusion: breaking the barricade for a successful immunotherapy.Frontiers in oncology · 2023Review
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Granulocyte-Macrophage Colony-Stimulating Factor Modulates Myeloid-Derived Suppressor Cells and Treg Activity in Decompensated Cirrhotic Patients With Sepsis.Frontiers in immunology · 2022Article
- Dendritic Cells Pulsed with Cytokine-Adjuvanted Tumor Membrane Vesicles Inhibit Tumor Growth in HER2-Positive and Triple Negative Breast Cancer Models.International journal of molecular sciences · 2021Article
- The role of myeloid-derived suppressor cells in gastrointestinal cancer.Cancer communications (London, England) · 2021Review
- Lgals3bp suppresses colon inflammation and tumorigenesis through the downregulation of TAK1-NF-κB signaling.Cell death discovery · 2021Article
- Therapeutic effects of dihydroartemisinin in multiple stages of colitis-associated colorectal cancer.Theranostics · 2021Article
- Urinary 8-iso PGF2α and 2,3-dinor-8-iso PGF2α can be indexes of colitis-associated colorectal cancer in mice.PloS one · 2021Article
- Ubiquitination of RIPK1 regulates its activation mediated by TNFR1 and TLRs signaling in distinct manners.Nature communications · 2020Article
- Anti-VEGF therapy resistance in ovarian cancer is caused by GM-CSF-induced myeloid-derived suppressor cell recruitment.British journal of cancer · 2020Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation is thought to be a major driving force for the development of colitis-associated colorectal cancer (CAC). As one member of proinflammatory cytokine family, granulocyte macrophage colony-stimulating factor (GM-CSF) has been identified to play a key role in CAC pathogenesis recently. The underlying mechanisms, however, remain largely unknown. In this study, we found that myeloid-derived suppressor cells (MDSCs) accumulated increasingly in the lesions during the progression from colitis to cancer, which was critical for CAC formation. Importantly, this MDSC accumulation was controlled by GM-CSF. MDSC number decreased significantly in GM-CSF-deficient mice suffering from CAC induction, and transfusion of MDSCs from wild-type CAC-bearing mice into GM-CSF-deficient counterparts led to recurrence of CAC. Furthermore, the supernatants of CAC lesions or GM-CSF alone was sufficient to differentiate hematopoietic precursors into MDSCs. Addition of neutralizing anti-GM-CSF antibody impaired the MDSC-differentiating effects of the supernatants of CAC lesions. Overall, these findings shed new insights into the mechanisms of GM-CSF underlying CAC development, by inducing/recruiting CAC-promoting MDSCs. Blocking GM-CSF activity or MDSC function may represent new therapeutic strategies for CAC in clinic.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.