Prostaglandin‐H‐synthase isozyme expression in normal and neoplastic human skin

Müller‐Decker, Karin; Reinerth, Günther; Krieg, Peter; Zimmermann, R.; Heise, H; Bayerl, Christiane; Marks, Friedrich; Fürstenberger, Gerhard

doi:10.1002/(sici)1097-0215(19990827)82:5<648::aid-ijc6>3.3.co;2-4

Cited by 27 publications

(40 citation statements)

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“…In our study, the precancerous lesions and SCCs expressed COX-2 at a similar level. Although some authors have reported stronger COX-2 staining in SCCs compared to KA [35,36] more groups have described similar (or only slightly higher) COX-2 expression in SCCs compared to precancerous lesions like AK, KA and BD [37][38][39][40][41].…”

Section: Discussionmentioning

confidence: 98%

“…Literature data on COX-2 expression in normal skin varies from reports of nondetectable expression levels [41], to the expression observed only in some cells of the granular and spinous layers of the epidermis [34,35,37] or restricted exclusively to the epidermal basal layer [39,40,42,43]. Leong et al [34] described an association between differentiation of human keratinocytes in vitro and expression of COX-2.…”

Section: Discussionmentioning

confidence: 99%

“…Nijsten et al [38] described comparable levels of COX-2 expression in SCCs and actinic keratoses (AK), stronger than in BDs, while in normal skin they were able to detect COX-2 in only two of 35 cases investigated with the staining limited to cells of the granular layer. Interestingly, several authors did not detect COX-2 expression in keratinocytes of granular and spinous layers and instead reported the staining of cells within the basal layer [39][40][41][42][43]. Müller-Decker et al [39] observed COX-2 staining of some cells of the epidermal basal layer in only two of nine samples of normal skin.…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

“…Interestingly, several authors did not detect COX-2 expression in keratinocytes of granular and spinous layers and instead reported the staining of cells within the basal layer [39][40][41][42][43]. Müller-Decker et al [39] observed COX-2 staining of some cells of the epidermal basal layer in only two of nine samples of normal skin. In the same study, clear COX-2 expression was detected in all examined cases of AK, KA, SCC and in one case described as skin cancer in situ.…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

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Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

Kuźbicki¹,

Lange²,

Stanek-Widera³

et al. 2011

Folia Histochem Cytobiol.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

See 2 more Smart Citations

Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

Kuźbicki¹,

Lange²,

Stanek-Widera³

et al. 2011

Folia Histochem Cytobiol.

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“…It is likely that the nicotine infusion activated nicotinic receptors located on endothelial cells of the cutaneous blood vessels (Hagforsen et al 2002), which subsequently activated COX also located in the endothelial cells (Muller-Decker et al 1999). The activation of COX by nicotine may increase superoxide production from COX itself (Egan et al 1976), or NADPH oxidase (Zhang et al 2011).…”

Section: Cutaneous Vasodilationmentioning

confidence: 99%

Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for K_Ca, K_ATP, and K_Vchannels, nitric oxide, and prostanoids

Fujii

Louie

McNeely

et al. 2017

Appl. Physiol. Nutr. Metab.

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Effect of NSAIDs on the recurrence of nonmelanoma skin cancer

Grau¹,

Baron²,

Langholz³

et al. 2006

Intl Journal of Cancer

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Experimental studies have consistently shown a protective effect of nonsteroidal antiinflammatory drugs (NSAIDs) against nonmelanoma skin cancers (NMSC). However, little human epidemiological research has been done in this regard. We used data from the Skin Cancer Chemoprevention Study to explore the association of NSAID use and with the risk of basal-cell carcinoma (BCC) and squamous-cell carcinoma (SCC). 1,805 subjects with a recent history of NMSC were randomized to placebo or 50 mg of daily b-cartene. Participants were asked about their use of over-the-counter and prescription medications at baseline and every 4 months during the trial. Skin follow-up examinations were scheduled annually with a study dermatologist; confirmed lesions were the endpoints in the study. We used a risk set approach to the analysis of grouped times survival data and unconditional logistic regression to compute odds ratios [ORs] for various exposures to NSAIDs. The use of NSAIDs was reported in over 50% of questionnaires. For BCC, NSAIDs exhibited a weak protective effect in crude analyses, which attenuated markedly after adjustment. For SCC, the use of NSAIDs in the year previous to diagnosis reduced the odds by almost 30% (adjusted OR5 0.71, 95% CI 0.48-1.04). When we accounted for frequency of use, results for BCC were not striking, and there were inconsistent suggestions of an inverse association with SCC. There were some indications of a modest, nonsignificant reduction on the number of BCCs and SCCs with NSAID use. Our data suggest a weak and inconsistent chemopreventive effect of NSAIDs on BCC and SCC. ' 2006 Wiley-Liss, Inc.The chemopreventive effect of nonsteroidal antiinflammatory drugs (NSAIDs), particularly aspirin, on nonmelanoma skin cancer (NMSC) has been repeatedly shown in animal [1][2][3][4][5] and in in vitro studies. 6,7 In humans, some experimental studies have reported that topical or oral NSAIDs may lead to regression of skin neoplasms. [8][9][10] Findings from both observational studies [11][12][13][14][15][16][17] and clinical trials 18-20 are consistent with a protective effect of NSAIDs against colorectal neoplasia, but few epidemiological studies have investigated the preventive effects of NSAIDs on risk of nonmelanoma skin cancer, 21,22 the most commonly occurring cancer in the Caucasian population. 23,24 However, results from 1 single-arm, unblinded study and from a randomized trial of topical diclofenac for treatment of actinic keratoses, a well-known precursor of SCC, have been encouraging. 25,26 In the present analysis, we used data from a skin cancer chemoprevention trial, 27 to explore the relationship between NSAID use and the occurrence of nonmelanoma skin cancer, both basal-cell carcinomas (BCC) and squamous-cell carcinomas (SCC). Material and methodsThe Skin Cancer Prevention Study was a randomized, double blind trial of oral b-carotene for the prevention of nonmelanoma skin cancer in patients with a recent history of these tumors. Details of the study design and methods have been described el...

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Prostaglandin‐H‐synthase isozyme expression in normal and neoplastic human skin

Cited by 27 publications

References 0 publications

Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for K_Ca, K_ATP, and K_Vchannels, nitric oxide, and prostanoids

Effect of NSAIDs on the recurrence of nonmelanoma skin cancer

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Prostaglandin‐H‐synthase isozyme expression in normal and neoplastic human skin

Cited by 27 publications

References 0 publications

Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for KCa, KATP, and KVchannels, nitric oxide, and prostanoids

Effect of NSAIDs on the recurrence of nonmelanoma skin cancer

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Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for K_Ca, K_ATP, and K_Vchannels, nitric oxide, and prostanoids