ArticleMolecular oncology2014
COX-2 inhibition prevents the appearance of cutaneous squamous cell carcinomas accelerated by BRAF inhibitors.
Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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
26 citing papers in PubMed, 42 citations in OpenAlex.
- CAR-T cell therapy targeting surface expression of TYRP1 to treat cutaneous and rare melanoma subtypes.Nature communications · 2024Article
- Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies.Signal transduction and targeted therapy · 2023Review
- Neutrophil-Derived COX-2 has a Key Role during Inflammatory Hyperalgesia.Inflammation · 2022Article
- Reducing Skin Toxicities from EGFR Inhibitors with Topical BRAF Inhibitor Therapy.Cancer discovery · 2021Article
- Celecoxib as a Valuable Adjuvant in Cutaneous Melanoma Treated with Trametinib.International journal of molecular sciences · 2021Article
- miR-146a-5p impairs melanoma resistance to kinase inhibitors by targeting COX2 and regulating NFkB-mediated inflammatory mediators.Cell communication and signaling : CCS · 2020Article
- Overcoming Genetically Based Resistance Mechanisms to PD-1 Blockade.Cancer discovery · 2020Article
- Cutaneous Squamous Cell Carcinoma: From Biology to Therapy.International journal of molecular sciences · 2020Review
- Deep Functional and Molecular Characterization of a High-Risk Undifferentiated Pleomorphic Sarcoma.Sarcoma · 2020Article
- PAK4 inhibition improves PD-1 blockade immunotherapy.Nature cancer · 2020Article
- Overcoming Resistance to Therapies Targeting the MAPK Pathway in BRAF-Mutated Tumours.Journal of oncology · 2020Review
- Essential Oil ofMolecules (Basel, Switzerland) · 2019Article
- miR-26b Mimic Inhibits Glioma Proliferation In Vitro and In Vivo Suppressing COX-2 Expression.Oncology research · 2019Article
- Synergy from gene expression and network mining (SynGeNet) method predicts synergistic drug combinations for diverse melanoma genomic subtypes.NPJ systems biology and applications · 2019Article
- Voriconazole-induced photocarcinogenesis is promoted by aryl hydrocarbon receptor-dependent COX-2 upregulation.Scientific reports · 2018Article
- Preventive effect ofJournal of clinical biochemistry and nutrition · 2018Article
- Combination therapy of PKCζ and COX-2 inhibitors synergistically suppress melanoma metastasis.Journal of experimental & clinical cancer research : CR · 2017Article
- Article
- Primary Resistance to PD-1 Blockade Mediated by JAK1/2 Mutations.Cancer discovery · 2017Article
- Cutaneous wound healing through paradoxical MAPK activation by BRAF inhibitors.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Keratoacanthomas (KAs) and cutaneous squamous cell carcinomas (cuSCCs) develop in 15-30% of patients with BRAF(V600E) metastatic melanoma treated with BRAF inhibitors (BRAFi). These lesions resemble mouse skin tumors induced by the two-stage DMBA/TPA skin carcinogenesis protocol; in this protocol BRAFi accelerates tumor induction. Since prior studies demonstrated cyclooxygenase 2 (COX-2) is necessary for DMBA/TPA tumor induction, we hypothesized that COX-2 inhibition might prevent BRAFi-accelerated skin tumors. Celecoxib, a COX-2 inhibitor, significantly delayed tumor acceleration by the BRAFi inhibitor PLX7420 and decreased tumor number by 90%. Tumor gene expression profiling demonstrated that celecoxib partially reversed the PLX4720-induced gene signature. In PDV cuSCC cells, vemurafenib (a clinically approved BRAFi) increased ERK phosphorylation and soft agar colony formation; both responses were greatly decreased by celecoxib. In clinical trials trametinib, a MEK inhibitor (MEKi) increases BRAFi therapy efficacy in BRAF(V600E) melanomas and reduces BRAFi-induced KA and cuSCC frequency. Trametinib also reduced vemurafenib-induced PDV soft agar colonies, but less efficiently than celecoxib. The trametinb/celecoxib combination was more effective than either inhibitor alone. In conclusion, celecoxib suppressed both BRAFi-accelerated skin tumors and soft-agar colonies, warranting its testing as a chemopreventive agent for non-melanoma skin lesions in patients treated with BRAFi alone or in combination with MEKi.
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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.