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COX-2 and p53 in human sinonasal cancer: COX-2 expression is associated with adenocarcinoma histology and wood-dust exposure

Holmila, Reetta; Cyr, Diane; Luce, Danile; Heikkila, Pirjo; Dictor, Michael LU ; Steiniche, Torben; Stjernvall, Tuula; Bornholdt, Jette; Wallin, Hakan and Wolff, Henrik, et al. (2008) In International Journal of Cancer 122(9). p.2154-2159
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... (More)
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. (Less)
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published
subject
keywords
wood dust exposure, p53 expression, sinonasal cancer, COX-2 expression, smoking
in
International Journal of Cancer
volume
122
issue
9
pages
2154 - 2159
publisher
John Wiley & Sons
external identifiers
  • wos:000254224100032
  • scopus:40749154944
ISSN
0020-7136
DOI
10.1002/ijc.23360
language
English
LU publication?
yes
id
a2a5f546-420b-4369-96b8-ffa76b9047ec (old id 1185036)
date added to LUP
2008-09-02 15:31:33
date last changed
2017-02-26 03:33:41
@article{a2a5f546-420b-4369-96b8-ffa76b9047ec,
  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 &lt; 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.},
  author       = {Holmila, Reetta and Cyr, Diane and Luce, Danile and Heikkila, Pirjo and Dictor, Michael and Steiniche, Torben and Stjernvall, Tuula and Bornholdt, Jette and Wallin, Hakan and Wolff, Henrik and Husgafvel-Pursiainen, Kirsti},
  issn         = {0020-7136},
  keyword      = {wood dust exposure,p53 expression,sinonasal cancer,COX-2 expression,smoking},
  language     = {eng},
  number       = {9},
  pages        = {2154--2159},
  publisher    = {John Wiley & Sons},
  series       = {International Journal of Cancer},
  title        = {COX-2 and p53 in human sinonasal cancer: COX-2 expression is associated with adenocarcinoma histology and wood-dust exposure},
  url          = {http://dx.doi.org/10.1002/ijc.23360},
  volume       = {122},
  year         = {2008},
}