ArticleSurgical neurology international2011
The therapeutic potential of inhibitors of the signal transducer and activator of transcription 3 for central nervous system malignancies.
Article in Surgical neurology international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- STAT3 is a biologically relevant therapeutic target in H3K27M-mutant diffuse midline glioma.Neuro-oncology · 2022Article
- Role of the circulatory interleukin-6 in the pathogenesis of gliomas: A systematic review.World journal of methodology · 2022Article
- WP1066 induces cell death in a schwannomatosis patient-derived schwannoma cell line.Cold Spring Harbor molecular case studies · 2022Article
- Phospho-valproic acid (MDC-1112) suppresses glioblastoma growth in preclinical models through the inhibition of STAT3 phosphorylation.Carcinogenesis · 2019Article
- The role of interleukin-6-STAT3 signalling in glioblastoma.Oncology letters · 2018Review
- Cryptotanshinone inhibits human glioma cell proliferation in vitro and in vivo through SHP-2-dependent inhibition of STAT3 activation.Cell death & disease · 2017Article
- Inhibition of STAT3 enhances the radiosensitizing effect of temozolomide in glioblastoma cells in vitro and in vivo.Journal of neuro-oncology · 2016Article
- Microenvironmental clues for glioma immunotherapy.Current neurology and neuroscience reports · 2014Review
- Cryptotanshinone inhibits human glioma cell proliferation by suppressing STAT3 signaling.Molecular and cellular biochemistry · 2013Article
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
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh-grade primary and metastatic central nervous system (CNS) tumors are common, deadly, and refractory to conventional therapy and continue to be therapeutically challenging. A key nodal transcriptional factor, the signal transducer and activator of transcription 3 (STAT3), drives the fundamental components of tumor malignancy and metastases in the CNS by enhancing proliferation, angiogenesis, invasion, metastasis, and immunosuppression. The introduction of STAT3 inhibitors in clinical trials for this patient population is imminent.
methodsSTAT3 inhibitors have been extensively tested in a variety of preclinical murine models.
resultsThe STAT3 inhibitor, WP1066, has displayed marked efficacy with minimal toxicity against malignancy in murine models, including established intracerebral tumors. The mechanism of this in vivo efficacy of the STAT3 blockade agents is a combination of direct tumor cytotoxicity and immune cytotoxic clearance.
conclusionsGiven their direct antitumor cytotoxic effects, STAT3 inhibitors may exert therapeutic activity in the monotherapy setting but may also have compelling use as immunotherapeutic modulators or as a salvage therapy.
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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.