ArticlePloS one2013
IFN-γ Rα is a key determinant of CD8+ T cell-mediated tumor elimination or tumor escape and relapse in FVB mouse.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Bridging Radiotherapy to Immunotherapy: The IFN-JAK-STAT Axis.International journal of molecular sciences · 2021Pooled it
- Trial
- Cytokine Regulation of the Bone Pre- and Metastatic Niches: Implications for Breast Cancer Dormancy.Cells · 2026Review
- A cell cycle centric view of tumour dormancy.British journal of cancer · 2023Review
- Tumor-intrinsic sensitivity to the pro-apoptotic effects of IFN-γ is a major determinant of CD4Nature cancer · 2023Article
- Interferon-gamma inhibits aldehyde dehydrogenasebright cancer stem cells in the 4T1 mouse model of breast cancer.Chinese medical journal · 2021Article
- The tumor-promoting effects of the adaptive immune system: a cause of hyperprogressive disease in cancer?Cellular and molecular life sciences : CMLS · 2021Review
- Targeting Innate Immunity in Breast Cancer Therapy: A Narrative Review.Frontiers in immunology · 2021Review
- Tumor dormancy as an alternative step in the development of chemoresistance and metastasis - clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- The force awakens: metastatic dormant cancer cells.Experimental & molecular medicine · 2020Review
- The Interactions Between Cancer Stem Cells and the Innate Interferon Signaling Pathway.Frontiers in immunology · 2020Review
- IFN-γ orchestrates tumor elimination, tumor dormancy, tumor escape, and progression.Journal of leukocyte biology · 2018Review
- The STAT3 inhibitor pyrimethamine displays anti-cancer and immune stimulatory effects in murine models of breast cancer.Cancer immunology, immunotherapy : CII · 2018Article
- Immunotherapy of cancer: targeting cancer during active disease or during dormancy?Immunotherapy · 2017Review
- Tumor Dormancy and Relapse: From a Natural Byproduct of Evolution to a Disease State.Cancer research · 2017Review
- Mismatch Repair Deficiency and Response to Immune Checkpoint Blockade.The oncologist · 2016Review
- Adaptive Immune Regulation of Mammary Postnatal Organogenesis.Developmental cell · 2015Article
- Cancer Dormancy: A Regulatory Role for Endogenous Immunity in Establishing and Maintaining the Tumor Dormant State.Vaccines · 2015Review
- microRNAs function in CD8+T cell biology.Journal of leukocyte biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During the past decade, the dual function of the immune system in tumor inhibition and tumor progression has become appreciated. We have previously reported that neu-specific T cells can induce rejection of neu positive mouse mammary carcinoma (MMC) and also facilitate tumor relapse by inducing neu antigen loss and epithelial to mesenchymal transition (EMT). Here, we sought to determine the mechanism by which CD8+ T cells either eliminate the tumor, or maintain tumor cells in a dormant state and eventually facilitate tumor relapse. We show that tumor cells that express high levels of IFN-γ Rα are eliminated by CD8+ T cells. In contrast, tumor cells that express low levels of IFN-γ Rα do not die but remain dormant and quiescent in the presence of IFN-γ producing CD8+ T cells until they hide themselves from the adaptive immune system by losing the tumor antigen, neu. Relapsed tumor cells show CD44+CD24- phenotype with higher rates of tumorigenesis, in vivo. Acquisition of CD44+CD24- phenotype in relapsed tumors was not solely due to Darwinian selection. Our data suggest that tumor cells control the outcome of tumor immune surveillance through modulation of the expression of IFN-γ Rα.
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Identifiers
What OpenQuestion holds
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.