ReviewImmunological investigations2012
Myeloid-derived suppressor cells adhere to physiologic STAT3- vs STAT5-dependent hematopoietic programming, establishing diverse tumor-mediated mechanisms of immunologic escape.
Review in Immunological investigations, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- Beyond cold to hot: oncolytic virotherapy as the next cornerstone of immuno-oncology.Nature reviews. Clinical oncology · 2026Review
- The recent progress of myeloid-derived suppressor cell and its targeted therapies in cancers.MedComm · 2023Review
- Selective activation of STAT3 and STAT5 dictates the fate of myeloid progenitor cells.Cell death discovery · 2023Article
- Targeting myeloid-derived suppressor cells in tumor immunotherapy: Current, future and beyond.Frontiers in immunology · 2023Review
- Myeloid-Derived Suppressive Cell Expansion Promotes Melanoma Growth and Autoimmunity by Inhibiting CD40/IL27 Regulation in Macrophages.Cancer research · 2021Article
- Suppressive myeloid cells are expanded by biliary tract cancer-derived cytokines in vitro and associate with aggressive disease.British journal of cancer · 2020Article
- Myeloid-derived suppressor cells (MDSCs) in patients with solid tumors: considerations for granulocyte colony-stimulating factor treatment.Cancer immunology, immunotherapy : CII · 2018Review
- Definitive activation of endogenous antitumor immunity by repetitive cycles of cyclophosphamide with interspersed Toll-like receptor agonists.Oncotarget · 2016Article
- Expansion of myeloid derived suppressor cells correlates with number of T regulatory cells and disease progression in myelodysplastic syndrome.Oncoimmunology · 2016Article
- Highlights on mechanisms of drugs targeting MDSCs: providing a novel perspective on cancer treatment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Myeloid derived suppressor cell infiltration of murine and human gliomas is associated with reduction of tumor infiltrating lymphocytes.Journal of neuro-oncology · 2015Article
- Immune tolerance in liver disease.Hepatology (Baltimore, Md.) · 2014Article
- Interactome analysis of myeloid-derived suppressor cells in murine models of colon and breast cancer.Oncotarget · 2014Article
- Dasatinib promotes the expansion of a therapeutically superior T-cell repertoire in response to dendritic cell vaccination against melanoma.Oncoimmunology · 2014Article
- Immunosuppressive therapy in allograft transplantation: from novel insights and strategies to tolerance and challenges.Central-European journal of immunology · 2014Review
- Modification of the tumor microenvironment as a novel target of renal cell carcinoma therapeutics.Cancer journal (Sudbury, Mass.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
The receptor tyrosine kinase inhibitor, sunitinib, is astonishingly effective in its capacity to reduce MDSCs in peripheral tissues such as blood (human) and spleen (mouse), restoring responsiveness of bystander T lymphocytes to TcR stimulation. Sunitinib blocks proliferation of undifferentiated MDSCs and decreases survival of more differentiated neutrophilic MDSC (n-MDSC) progeny. Ironically, sunitinib's profound effects are observed even in a total absence of detectable anti-tumor therapeutic response. This is best explained by the presence of disparate MDSC-conditioning stimuli within individual body compartments, allowing sensitivity and resistance to sunitinib to coexist within the same mouse or patient. The presence or absence of GM-CSF is likely the major determinant in each compartment, given that GM-CSF's capacity to preempt STAT3-dependent with dominant STAT5-dependent hematopoietic programming confers sunitinib resistance and redirects differentiation from the n-MDSC lineage to the more versatile monocytoid (m-MDSC) lineage. The clinical sunitinib experience underscores that strategies for MDSC and Treg depletions must be mindful of disparities among body compartments to avoid sanctuary effects. Ironically, m-MDSCs manifesting resistance to sunitinib also have the greatest potential to differentiate into tumoricidal accessory cells, by virtue of their capacity to respond to T cell-secreted IFN-γ or to TLR agonists with nitric oxide and peroxynitrate production.
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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.