ArticleNeoplasia (New York, N.Y.)2015
JAK kinase inhibition abrogates STAT3 activation and head and neck squamous cell carcinoma tumor growth.
Article in Neoplasia (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Tumor growth suppression by inhibiting both autophagy and STAT3 signaling in HNSCC.Oncotarget · 2015Pooled it
- Distinct single-cell cellular states and ecosystems linked to HPV status distinguish therapeutic vulnerability of head and neck squamous cell carcinoma.Communications biology · 2026Article
- Loss of JAK1 Function Causes G2-M Cell-Cycle Defects Vulnerable to KIF18A Inhibition.Cancer research · 2026Article
- Characterizing the Head and Neck Cancer Microenvironment: Implications for Immunotherapy and Prognosis.Advances in experimental medicine and biology · 2026Review
- Current and Emerging Protein Biomarkers for the Diagnosis and Prognosis of Head and Neck Cancer.Genes · 2025Review
- Siramesine induced cell death of glioblastoma through inactivating the STAT3-MGMT signaling pathway.Journal of translational medicine · 2025Article
- Prevalence and biological impact of clinically relevant gene fusions in head and neck cancers.NPJ precision oncology · 2025Article
- Head and neck cancer: pathogenesis and targeted therapy.MedComm · 2024Review
- Crosstalk between CAFs and tumour cells in head and neck cancer.Cell death discovery · 2024Review
- Exploring Novel Frontiers: Leveraging STAT3 Signaling for Advanced Cancer Therapeutics.Cancers · 2024Review
- Molecular pathways and targeted therapies in head and neck cancers pathogenesis.Frontiers in oncology · 2024Review
- In-depth analysis of the interplay between oncogenic mutations and NK cell-mediated cancer surveillance in solid tumors.Oncoimmunology · 2024Review
- Understanding the role of nerves in head and neck cancers - a review.Oncology reviews · 2024Review
- Vortioxetine hydrobromide inhibits the growth of gastric cancer cells in vivo and in vitro by targeting JAK2 and SRC.Oncogenesis · 2023Article
- Heterogeneity of cancer-associated fibroblasts in head and neck squamous cell carcinoma: opportunities and challenges.Cell death discovery · 2023Review
- Malignancies in Patients with Celiac Disease: Diagnostic Challenges and Molecular Advances.Genes · 2023Review
- Targeted therapy for head and neck cancer: signaling pathways and clinical studies.Signal transduction and targeted therapy · 2023Review
- JAK/STAT pathway: Extracellular signals, diseases, immunity, and therapeutic regimens.Frontiers in bioengineering and biotechnology · 2023Review
- STAT3 Activation as a Predictive Biomarker for Ruxolitinib Response in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- STAT3 pathway in cancers: Past, present, and future.MedComm · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant activation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) 3 has been implicated in cell proliferation and survival of many cancers including head and neck squamous cell carcinoma (HNSCC). AZD1480, an orally active pharmacologic inhibitor of JAK1/JAK2, has been tested in several cancer models. In the present study, the in vitro and in vivo effects of AZD1480 were evaluated in HNSCC preclinical models to test the potential use of JAK kinase inhibition for HNSCC therapy. AZD1480 treatment decreased HNSCC proliferation in HNSCC cell lines with half maximal effective concentration (EC50) values ranging from 0.9 to 4 μM in conjunction with reduction of pSTAT3(Tyr705) expression. In vivo antitumor efficacy of AZD1480 was demonstrated in patient-derived xenograft (PDX) models derived from two independent HNSCC tumors. Oral administration of AZD1480 reduced tumor growth in conjunction with decreased pSTAT3(Tyr705) expression that was observed in both PDX models. These findings suggest that the JAK1/2 inhibitors abrogate STAT3 signaling and may be effective in HNSCC treatment approaches.
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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.