ArticleInternational journal of clinical and experimental pathology2018
c-Jun and Camk2a contribute to the drug resistance of induction docetaxel/cisplatin/5-fluorouracil in hypopharyngeal carcinoma.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanisms of Resistance to Chemotherapy in Hypopharyngeal Carcinoma.Biomedicines · 2025Review
- HNCDrugResDb: a platform for deciphering drug resistance in head and neck cancers.Scientific reports · 2024Article
- FBXW7 attenuates tumor drug resistance and enhances the efficacy of immunotherapy.Frontiers in oncology · 2023Review
- Acryl-3,5-bis(2,4-difluorobenzylidene)-4-piperidone targeting cellular JUN proto-oncogene, AP-1 transcription factor subunit inhibits head and neck squamous cell carcinoma progression.Exploration of targeted anti-tumor therapy · 2023Article
- Article
- Article
- The dysregulated expression and functional effect of CaMK2 in cancer.Cancer cell international · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypopharyngeal carcinoma (HPC) is a subtype of head and neck squamous cell carcinoma, and prognosis has improved significantly over the past three decades. Induction docetaxel/cisplatin/5 fluorouracil (TPF) chemotherapy is regarded as the standard of treatment for locoregionally advanced HPC. However, patients who do not respond to cisplatin suffer, rather than benefit, from chemotherapy treatment. The goal of this study was to identify molecules involved in TPF resistance and to clarify their molecular mechanisms. Using the FaDu cell line as the cell model, the TPF IC50 was identified, and c-Jun, IL6, Camk2a, c-fos knockdown using siRNAs resulted in a significant declined TPF IC50. Retrospective analysis of the expression status of c-Jun, IL6, Camk2a, and c-fos by immunohistochemistry staining in sectioned HPC tissues from TPF-sensitive and TPF-insensitive patients shows that Camk2a and c-Jun were associated with the clinical pathogenesic features in HPC. The
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Identifiers
31949859PMC6962968W3008780258What 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.