No Chemopreventive Effect of Nonsteroidal Anti-Inflammatory Drugs on Nonmelanoma Skin Cancer: Evidence from Meta-Analysis

Zhang, Bo; Liang, Xiangdang; Ye, Liaosha; Wang, Yungui

doi:10.1371/journal.pone.0096887

Cited by 23 publications

(34 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Whether an agent is a good chemoprophylactic candidate is determined by the risk : benefit ratio. Many agents, such as beta carotene, selenium, synthetic retinoids (tretinoin, isotretinoin) and nonsteroidal anti‐inflammatory drugs have been tested but showed no chemopreventive effect on BCC development . However, when retinoids were used in patients with genodermatoses (NBCCS, XP) a more promising protective effect was seen on BCC development .…”

Section: Preventionmentioning

confidence: 99%

Epidemiology of basal cell carcinoma: scholarly review

et al. 2017

View full text Add to dashboard Cite

Basal cell carcinoma (BCC) is the most common cancer in white-skinned individuals with increasing incidence rates worldwide. Patients with BCC place a large burden on healthcare systems, because of the high incidence and the increased risk of synchronous and metachronous BCCs and other ultraviolet radiation (UVR) related skin cancers (i.e. field cancerization). As a result, the disability-adjusted life years and healthcare costs have risen significantly in recent decades. BCC is a complex disease, in which the interplay between UVR, phenotype (UVR-sensitive) and genotype (somatic mutations and germline mutations/polymorphisms) fulfils a key role in the aetiopathogenesis. Prevention programmes with continual refinements and improvements could be of major importance in tackling the growing skin cancer problem. To provide the most appropriate BCC care, physicians should engage in shared decision-making and choose their treatments wisely.

show abstract

Section: Preventionmentioning

confidence: 99%

Epidemiology of basal cell carcinoma: scholarly review

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Systematic reviews, including observational studies and a randomized clinical trial, have assessed the association between aspirin and nonaspirin NSAID use and KC . Muranushi et al .…”

Section: Discussionmentioning

confidence: 99%

Aspirin and nonsteroidal anti‐inflammatory drug use and keratinocyte cancers: a large population‐based cohort study of skin cancer in Australia

Pandeya¹,

Olsen

Thompson³

et al. 2019

Br J Dermatol

View full text Add to dashboard Cite

Summary Background Nonsteroidal anti‐inflammatory drugs (NSAIDs) have been postulated as chemopreventive agents for basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), but findings from observational studies have been inconsistent, and clinical trial data are scant. Objectives To examine the association between aspirin and NSAID (nonaspirin) use and the risk of BCC and SCC in a large cohort specifically designed for skin cancer outcomes. Methods We used data from the QSkin Study, a prospective cohort of 43 764 residents of Queensland, Australia (34 630 were included in this study and 23 581 were used in our primary analyses). We used Cox proportional hazards models to estimate the hazard ratios (HRs) between self‐reported aspirin and NSAID use 1 year prior to study baseline and the first histologically confirmed BCC or SCC for high‐risk (history of skin cancer excisions or more than five actinic lesions treated) and average‐to‐low‐risk participants (no history of skin cancer excision and at most five actinic lesions treated). Results After a median of 3 years of follow‐up, 3421 participants developed BCC and 1470 SCC (2288 BCC and 932 SCC with complete covariate information). Among the high‐risk group (1826 BCC and 796 SCC), compared with never use, frequent (at least weekly) NSAID use was associated with reduced risk of BCC (HR 0·84, 95% confidence interval 0·71–0.99) but not SCC. Aspirin use was associated with reduced risk of SCC (HR 0·77, 95% confidence interval 0·64–0·93) only among infrequent (less than weekly) users and was not associated with BCC. We observed no association between NSAID or aspirin use and the risk of BCC or SCC among average‐to‐low‐risk participants. Conclusions While some weakly inverse associations were observed between prior use of aspirin or NSAIDs and skin cancer, the inconsistent patterns of associations do not provide convincing evidence that these medications reduce subsequent skin cancer risk. Further data on doses, duration and long‐term follow‐up may help us to comprehend the cumulative dose effect.

show abstract

“…In the development of skin cancer, there has been conflicting evidence regarding the chemopreventive role of NSAIDs (Asgari, Chren, Warton, Friedman, & White, ; Elmets, Ledet, & Athar, ; Muranushi, Olsen, Pandeya, & Green, ; Zhang, Liang, Ye, & Wang, ). A case‐control study of 415 patients (43–85 years of age) diagnosed with SCC in the Kaiser Permanente Northern California population matched on age, gender, and race with 415 control subjects found no associations between the use of aspirin or other NSAIDs (self‐reported regular use or pharmacy data) and SCC risk (Asgari et al, ).…”

Section: Nsaids As Chemopreventive Agentsmentioning

confidence: 99%

“…A case‐control study of 415 patients (43–85 years of age) diagnosed with SCC in the Kaiser Permanente Northern California population matched on age, gender, and race with 415 control subjects found no associations between the use of aspirin or other NSAIDs (self‐reported regular use or pharmacy data) and SCC risk (Asgari et al, ). A subsequent meta‐analysis of data from eight studies (seven observational studies and one randomized controlled trial) investigating the effects of NSAIDs on nonmelanoma skin cancers (NMSCs) found no significant differences between users and nonusers of NSAIDs in their risk of developing SCC (relative risk [RR] = 0.86 [95% CI 0.73–1.02], p = .085) or basal cell carcinoma (BCC) (RR = 0.94 [95% CI 0.85–1.04], p = .266) (Zhang et al, ). In contrast, evidence from several preclinical, epidemiological, and translational studies has suggested that COX‐2 inhibitors could have potential in preventing NMSC development (Elmets et al, ).…”

Section: Nsaids As Chemopreventive Agentsmentioning

confidence: 99%

Treatment of actinic keratosis through inhibition of cyclooxygenase‐2: Potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5%

Thomas

Pinto

Cruz

et al. 2019

Dermatologic Therapy

View full text Add to dashboard Cite

Cyclooxygenase‐2 (COX‐2) and its metabolic product prostaglandin E2 (PGE2) are induced in response to growth factors, inflammatory cytokines, tumor promoters, activated oncogenes, and, in the skin, ultraviolet (UV) radiation. Accumulating evidence suggests a role for the COX‐2/PGE2 pathway in tumorigenesis in various tissue types including cutaneous squamous cell carcinoma. There is also strong evidence for a role in the development of actinic keratoses (AKs) — common dysplastic lesions of the skin associated with UV radiation overexposure — considered as part of a continuum with skin cancer. Non‐steroidal anti‐inflammatory drugs (NSAIDs) exert their anti‐inflammatory, analgesic, and antipyretic effects by reversibly or irreversibly acetylating COX isoforms, inhibiting downstream prostaglandins, and may have a chemopreventive role in malignancies, including skin cancer. Topical treatment of AK lesions with the NSAID diclofenac sodium 3% in combination with hyaluronic acid 2.5% has been shown to be effective and well tolerated, although the mechanism of action remains to be elucidated.

show abstract

No Chemopreventive Effect of Nonsteroidal Anti-Inflammatory Drugs on Nonmelanoma Skin Cancer: Evidence from Meta-Analysis

Cited by 23 publications

References 23 publications

Epidemiology of basal cell carcinoma: scholarly review

Epidemiology of basal cell carcinoma: scholarly review

Aspirin and nonsteroidal anti‐inflammatory drug use and keratinocyte cancers: a large population‐based cohort study of skin cancer in Australia

Treatment of actinic keratosis through inhibition of cyclooxygenase‐2: Potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5%

Contact Info

Product

Resources

About