ArticleCancer gene therapy2025
Regulation of nucleotide excision repair by wild-type HRAS signaling in head and neck cancer.
Article in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- DNA Repair, Epigenetic Dysregulation, and Cytokine Network Crosstalk in Head and Neck Cancer: Emerging Therapeutic Opportunities and Clinical Trials.Current oncology reports · 2026Review
- Review
- Molecular Mechanisms in Oral Squamous Cell Carcinoma: Integrative Roles of Cancer-Associated Fibroblasts, Immune Microenvironment, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Novel Therapeutic Strategies for Squamous Cell Carcinoma of the Head and Neck: Beyond EGFR and Checkpoint Blockade.Biomedicines · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Head and neck squamous cell carcinoma (HNSCC) is characterized by a high rate of locoregional or distant relapse among patients. It is well established that resistance to chemotherapeutic drugs has an important role in the emergence of the recurrent and/or metastatic type of this malignancy which is associated with poor prognosis. Therefore, understanding the molecular basis of chemoresistance in head and neck cancer is required for the development of effective therapeutic strategies. Activating mutations in the HRAS gene are driver events in human cancer. Although numerous studies have demonstrated that oncogenic HRAS mutations promote chemoresistance in HNSCC, the molecular profile of HNSCC tumors that overexpress wild-type HRAS (wtHRAS
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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.