ArticleInternational journal of cancer2008
COX-2 and p53 in human sinonasal cancer: COX-2 expression is associated with adenocarcinoma histology and wood-dust exposure.
Article in International journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Tumors of the Nose and Paranasal Sinuses: Promoting Factors and Molecular Mechanisms-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Immunohistochemical evaluation of cyclooxygenase-2 expression in feline nasal malignant epithelial tumours.Journal of feline medicine and surgery · 2025Article
- Genome-wide somatic mutation analysis of sinonasal adenocarcinoma with and without wood dust exposure.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024Article
- Article
- Next-generation sequencing for identification of actionable gene mutations in intestinal-type sinonasal adenocarcinoma.Scientific reports · 2021Article
- Sinonasal Squamous Cell Carcinoma: Etiology, Pathogenesis, and the Role of Human Papilloma Virus.Current otorhinolaryngology reports · 2020Article
- Prognostic Value of Accumulative Expression of COX-2 and p53 in Small and Diffuse Large B Cell Lymphoma.Pathology oncology research : POR · 2020Article
- Sinonasal carcinoma: clinical, pathological, genetic and therapeutic advances.Nature reviews. Clinical oncology · 2014Review
- Establishment and genetic characterization of six unique tumor cell lines as preclinical models for sinonasal squamous cell carcinoma.Scientific reports · 2014Article
- Benign lesions in mucosa adjacent to intestinal-type sinonasal adenocarcinoma.Pathology research international · 2011Article
- Establishment and genetic characterization of an immortal tumor cell line derived from intestinal-type sinonasal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2011Article
- Gene expression profiling in sinonasal adenocarcinoma.BMC medical genomics · 2009Article
- Genetic and clinical aspects of wood dust related intestinal-type sinonasal adenocarcinoma: a review.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2009Review
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Authors and funding
11 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The causal role of wood-dust exposure in sinonasal cancer (SNC) has been established in epidemiological studies, but the mechanisms of SNC carcinogenesis are still largely unknown. Increased amounts of COX-2 are found in both premalignant and malignant tissues, and experimental evidence link COX-2 to development of cancer. Many signals that activate COX-2 also induce tumor suppressor p53, a transcription factor central in cellular stress response. We investigated COX-2 and p53 expressions by immunohistochemistry in 50 SNCs (23 adenocarcinomas, and 27 squamous cell carcinomas (SCC); 48 analyzed for COX-2; 41 for p53). Occupational histories and smoking habits were available for majority of the cases. Most of the adenocarcinoma cases with exposure history data had been exposed to wood dust at work in the past (88%, 14/16). For smokers, 63% (12/19) presented with SSC, whereas 64% (7/11) of nonsmokers displayed adenocarcinoma. COX-2 was expressed at higher levels in adenocarcinoma as compared to SSC (p < 0.001). COX-2 expression showed significant association with occupational exposure to wood dust (p = 0.024), and with nonsmoking status (p = 0.001). No statistically significant associations between the exposures and p53 accumulation were found; however, the p53 accumulation pattern (p = 0.062 for wood dust exposure) resembled that of COX-2 expression. In summary, our findings show increased COX-2 expression in SNC adenocarcinoma with wood dust exposure, suggesting a role for inflammatory components in the carcinogenesis process. In contrast, SCCs predominated among smokers and expressed COX-2 rarely; this may suggest at least partially different molecular mechanisms.
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