ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2013
Hope and fear for interferon: the receptor-centric outlook on the future of interferon therapy.
Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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
57 citing papers in PubMed, 75 citations in OpenAlex.
- Review
- Therapeutic efficacy of oncolytic adenovirus YSCH-01 in osteosarcoma evaluated in PDX and CDX mouse models.Scientific reports · 2025Article
- PARP11 inhibition inactivates tumor-infiltrating regulatory T cells and improves the efficacy of immunotherapies.Cell reports. Medicine · 2024Article
- Cloning of human Type I interferon cDNAs.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2024Article
- Regulation of cellular senescence by innate immunity.Biophysics reports · 2023Article
- Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Review
- Protection of Regulatory T Cells from Fragility and Inactivation in the Tumor Microenvironment.Cancer immunology research · 2022Article
- CK1α upregulates the IFNAR1 expression to prompt the anti-HBV effect of type I IFN in hepatoma carcinoma cells.Virologica Sinica · 2022Article
- Mechanisms regulating transitory suppressive activity of neutrophils in newborns: PMNs-MDSCs in newborns.Journal of leukocyte biology · 2022Article
- Targeting PARP11 to avert immunosuppression and improve CAR T therapy in solid tumors.Nature cancer · 2022Article
- Novel Treatment Strategies Utilizing Immune Reactions against Chronic Myelogenous Leukemia Stem Cells.Cancers · 2021Review
- A small-molecule SUMOylation inhibitor activates antitumor immune responses and potentiates immune therapies in preclinical models.Science translational medicine · 2021Article
- Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer.Cancer immunology, immunotherapy : CII · 2021Article
- Immune suppressive activity of myeloid-derived suppressor cells in cancer requires inactivation of the type I interferon pathway.Nature communications · 2021Article
- Review
- Type I interferons and related pathways in cell senescence.Aging cell · 2020Review
- Cancer-associated fibroblasts downregulate type I interferon receptor to stimulate intratumoral stromagenesis.Oncogene · 2020Article
- Malignant cell-specific pro-tumorigenic role of type I interferon receptor in breast cancers.Cancer biology & therapy · 2020Article
- PARP1 Enhances Influenza A Virus Propagation by Facilitating Degradation of Host Type I Interferon Receptor.Journal of virology · 2020Article
- Cellular Caspase-3 Contributes to EV-A71 2AVirologica Sinica · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
After several decades of intense clinical research, the great promise of Type I interferons (IFN1) as the anticancer wonder drugs that could cure or, at the very least, curb the progression of various oncological diseases has regrettably failed to deliver. Severe side effects and low efficacy of IFN1-based pharmaceutics greatly limited use of these drugs and further reduced the enthusiasm of clinical oncologists for future optimization of IFN1-based therapeutic modalities. Incredibly, extensive clinical studies to assess the efficacy of IFN1 alone or in combination with other anticancer drugs have not been paralleled by an equal scope in defining the determinants that confer cell sensitivity or refractoriness to IFN1. Given that all effects of IFN1 on malignant and benign cells alike are mediated by its receptor, the mechanisms regulating these receptor cell surface levels should play a paramount role in shaping the magnitude and duration of IFN1-elicited effects. These mechanisms and their role in controlling IFN1 responses, as well as an ability of a growing tumor to commandeer these events, are the focus of our review. We postulate that activation of numerous signaling pathways leading to elimination of IFN1 receptor occurs in cancer cells and benign cells that contribute to tumor tissue. We further hypothesize that activation of these eliminative pathways enables the escape from IFN1-driven suppression of tumorigenesis and elicits the primary refractoriness of tumor to the pharmaceutical IFN1.
Indexed as
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.