Expression of cyclooxygenase‐1 and cyclooxygenase‐2 in bronchial epithelium and nonsmall cell lung carcinoma

Hastürk, Serap; Kemp, Bonnie L.; Kalapurakal, Shyla K.; Kurie, Jonathan M.; Hong, Waun Ki; Lee, Jin S.

doi:10.1002/cncr.10262.abs

Cited by 16 publications

(23 citation statements)

References 13 publications

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“…It is possible that smoking might induce COX‐2 expression. In 101 lung carcinoma samples, a greater percent of COX‐2 expression was reported for smokers than for nonsmokers (32% vs. 10%) 17. Similarly, cigarette tar extracts increased COX activity in rat pulmonary alveolar macrophages 18.…”

Section: Discussionmentioning

confidence: 96%

“…In 101 lung carcinoma samples, a greater percent of COX-2 expression was reported for smokers than for nonsmokers (32% vs. 10%). 17 Similarly, cigarette tar extracts increased COX activity in rat pulmonary alveolar macrophages. 18 Because lung carcinoma is the leading cause of cancer deaths, the possibility that commonly used pain medication can reduce the rates should be explored further.…”

Section: Discussionmentioning

confidence: 97%

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Risk of lung carcinoma among users of nonsteroidal antiinflammatory drugs

Muscat¹,

Chen²,

Richie³

et al. 2003

Cancer

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BACKGROUNDNonsteroidal antiinflammatory drugs (NSAIDs) inhibit the development of lung tumors in experimental animals. To the authors' knowledge there are little data regarding whether regular use of NSAIDs reduces the risk of developing lung carcinoma in humans.METHODSThe association between lung carcinoma risk and regular use of NSAIDs, including aspirin, was evaluated in a hospital‐based case–control study of 1038 patients and 1002 controls.RESULTSThe relative risk estimate of lung carcinoma associated with using NSAIDs 3 times a week or more for 1 or more years demonstrated an odds ratio (OR) of 0.68 (95% confidence interval [95% CI], 0.53–0.89). Results were similar when separated by lung histologic type. The association varied by smoking status. The OR was1.28 (95% CI, 0.73–2.25) in never‐smokers and 0.60 (95% CI 0.45–0.80) in ever‐smokers. The smoking‐specific risk estimates for aspirin were similar to those for all NSAIDs.CONCLUSIONSThe results of the current study suggest a possible chemoprotective benefit with the use of NSAIDs among individuals who are former or current smokers. Cancer 2003;97:1732–6. © 2003 American Cancer Society.DOI 10.1002/cncr.11242

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 97%

Risk of lung carcinoma among users of nonsteroidal antiinflammatory drugs

Muscat¹,

Chen²,

Richie³

et al. 2003

Cancer

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“…41,42 Chronic inflammation drives the metaplastic change from respiratory epithelium to squamous epithelium, increases cell turnover and promotes angiogenesis within invasive tumours. 41,42 Chronic inflammation drives the metaplastic change from respiratory epithelium to squamous epithelium, increases cell turnover and promotes angiogenesis within invasive tumours.…”

Section: The Role Of Inflammationmentioning

confidence: 99%

“…41,42 Chronic inflammation drives the metaplastic change from respiratory epithelium to squamous epithelium, increases cell turnover and promotes angiogenesis within invasive tumours. 42,44 SPECIFIC CONSIDERATIONS 43 Amongst other changes, there is up-regulation of the cyclo-oxygenase COX-2, which catalyses the synthesis of pro-inflammatory prostaglandins, in squamous dysplasias and invasive carcinomas alike (and for invasive tumours, this applies to both SCCs and adenocarcinomas).…”

Section: The Role Of Inflammationmentioning

confidence: 99%

Facts and fiction: premalignant lesions of lung tissues

Klebe

Henderson

2013

Pathology

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“…The high level of COX-2 expression was an independent prognostic factor for survival in the multivariate analysis. TABLE 2 summarizes the preclinical studies of COX-2 expression in human lung cancers [46][47][48][49]57,58,[60][61][62][63]. In this study, high COX-2 expression was associated with inferior survival and was an independent prognostic factor for patient outcome.…”

Section: Cox-2 In Lung Cancer Progressionmentioning

confidence: 81%

COX-2 and its inhibition as a molecular target in the prevention and treatment of lung cancer

Liao

Milas²

2004

Expert Review of Anticancer Therapy

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Lung cancer is the leading cause of cancer death in the USA. Conventional therapy using chemotherapy, radiation therapy, and a combination of the two, has yielded modest improvement in patient outcome. Dysfunction and dysregulation of many molecular processes and signaling pathways are involved in the development and growth of malignant lung tumors, and in conferring resistance to standard cancer treatments. Cyclooxygenase (COX)-2, an enzyme involved in prostaglandin production in pathologic states, is often overexpressed in premalignant and malignant lesions. Overexpression of COX-2 in lung cancer is associated with more aggressive biologic tumor behavior and adverse patient outcome. In preclinical studies, inhibition of this enzyme with selective COX-2 inhibitors enhances tumor response to radiation and chemotherapeutic agents. These findings quickly led to clinical studies. Phase I and II clinical trials of the combination of selective COX-2 inhibitors with radiotherapy, chemotherapy, or both in patients with lung cancer have been initiated and some preliminary results are available. In this review, the relationship between overexpression of COX-2 and lung cancer, the antitumor effect of selective COX-2 inhibitors, and the rationale for using selective COX-2 inhibitors combined with radiotherapy and chemotherapy, will be described. Current clinical protocols and preliminary findings will also be summarized.

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Expression of cyclooxygenase‐1 and cyclooxygenase‐2 in bronchial epithelium and nonsmall cell lung carcinoma

Cited by 16 publications

References 13 publications

Risk of lung carcinoma among users of nonsteroidal antiinflammatory drugs

Risk of lung carcinoma among users of nonsteroidal antiinflammatory drugs

Facts and fiction: premalignant lesions of lung tissues

COX-2 and its inhibition as a molecular target in the prevention and treatment of lung cancer

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