Arachidonic acid metabolites in cutaneous carcinomas. Evidence suggesting that elevated levels of prostaglandins in basal cell carcinomas are associated with an aggressive growth pattern

Vanderveen, Evelyn E.

doi:10.1001/archderm.122.4.407

Cited by 42 publications

(21 citation statements)

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“…The observed inverse associations of linoleic acid and total omega-6 concentrations with BCC in our study are consistent with our previous findings on dietary intake of PUFA in relation to skin cancer (12), but they are contrary to hypotheses generated from animal studies which indicate omega-6 PUFA increase carcinogenesis (1,5,7). Furthermore, the lower BCC tumor incidence with greater linolenic acid levels among persons with a history of skin cancer is a novel finding not previously reported (12,13).…”

Section: Discussionsupporting

confidence: 91%

“…Experimental studies have shown that although omega-3 PUFA affects early promotional stages by increasing tumor latency and decreasing tumor numbers, omega-6 PUFA has reverse effects (1,4,5). Elevated blood concentrations of omega-6 PUFA increase the levels of prostaglandin E2 (PGE-2), an immunoregulator associated with aggressive keratinocytic skin cancer growth (6,7). Conversely, omega-3 PUFA, particularly eicosapentaenoic acid (EPA), has anti-inflammatory effects in skin post-UVR exposure, reducing sunburn sensitivity and PGE-2 levels (3,8) and preventing DNA damage (9).…”

Section: Introductionmentioning

confidence: 99%

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Plasma Omega-3 and Omega-6 Concentrations and Risk of Cutaneous Basal and Squamous Cell Carcinomas in Australian Adults

Wallingford

Hughes

Green

et al. 2013

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Laboratory-based evidence suggests that omega-3 and omega-6 polyunsaturated fatty acids may affect skin photocarcinogenesis, but epidemiologic evidence is inconsistent. In 1,191 White Australian adults, we prospectively investigated associations between baseline plasma concentrations of omega-3 and omega-6 fatty acids and cutaneous basal cell carcinomas (BCC) and squamous cell carcinomas (SCC). Relative risks (RR) and 95% confidence intervals (CI) were estimated on the basis of number of histologically confirmed tumors diagnosed during follow-up (1997-2007). Plasma eicosapentaenoic acid (EPA) concentrations and omega-3/-6 ratio showed significant inverse associations with SCC tumors, comparing higher tertiles with the lowest, in age-and sex-adjusted models (P trend ¼ 0.02 and 0.03, respectively) which weakened after adjustment for past sun exposure. Associations between EPA and SCC were stronger among participants with a history of skin cancer at baseline (n ¼ 378; highest vs. lowest tertile: RR ¼ 0.50; 95% CI, 0.28-0.92; P trend ¼ 0.01). Total omega-6 was inversely associated with BCC tumors in multivariate models (P ¼ 0.04; highest vs. lowest tertile: RR ¼ 0.71; 95% CI, 0.51-0.99), and more strongly in the subgroup with past skin cancer. Linoleic and linolenic acids were also inversely associated with BCC occurrence in this subgroup. When fatty acids were analyzed as continuous variables, however, there was no evidence of any linear or nonlinear associations. This study provides some support for reduced skin cancer risk with high plasma concentrations of omega-3 and omega-6 fatty acids, but results depended on how fatty acid data were modeled. Further investigation of these associations in larger datasets is needed. Cancer Epidemiol Biomarkers Prev; 22(10); 1900-5. Ó2013 AACR.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Plasma Omega-3 and Omega-6 Concentrations and Risk of Cutaneous Basal and Squamous Cell Carcinomas in Australian Adults

Wallingford

Hughes

Green

et al. 2013

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Finally, EP 1 , EP 2 , EP 3 , DP 2 , FP, and to a lesser extent, EP 4 were found in the hair shaft cuticle whereas EP 4 , FP, DP 2 and TP were also detected in the cortex (mainly in the keratogenous zone). Discussion PGD 2 , PGE 2 , PGF 2a , PGI 2 and TXA 2 were detected in skin (30)(31)(32)(33)(34), whilst PGE 2 and PGF 2a production was revealed in hair and skin cells (5,9). Local prostanoid production was likely mirrored by some specific prostanoid receptor expression.…”

Section: Immunohistochemistrymentioning

confidence: 92%

Prostanoid receptors in anagen human hair follicles

Colombe

Michelet

Bernard

2007

Experimental Dermatology

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Prostanoid pathway in hair follicle gained closer attention since trichogenic side-effects on hair growth has been observed concomitantly with prostaglandin F 2a receptor (FP) agonist treatment of intraocular pressure. We thus investigated prostanoid receptor distribution in anagen hair follicle and different cell types from hair and skin. Using RT-PCR, Western blot and immunohistochemistry (IHC), we found that all receptors were present in hair follicle. This data shed new light on an underestimated complex network involved in hair growth control. Indeed most of these receptors showed a wide spectrum of expression in cultured cells and the whole hair follicle. Using IHC, we observed that expression of prostaglandin E 2 receptors (EP 2 , EP 3 , EP 4 ), prostaglandin D 2 receptor (DP 2 ), prostanoid thromboxane A 2 receptor (TP) and to a lesser extent EP 1 involved several hair follicle compartments. On the opposite, Prostaglandin I 2 receptor (IP) and DP 1 were more specifically expressed in hair cuticle layer and outer root sheath (ORS) basal layer, respectively. FP expression was essentially restricted to ORS companion layer and dermal papilla (DP). Although extracting a clear functional significance from this intricate network remains open challenge, FP labelling, i.e. could explain the biological effect of PGF 2a on hair regrowth, by directly modulating DP function.

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“…Additional studies have provided strong support for a role of COX-2 in cancer (DuBois, 2003). Of the PGH 2 -derived products, PGE 2 is of particular interest because PGE 2 levels are increased in a variety of human tumors (Jung et al, 1985;Vanderveen et al, 1986;McLemore et al, 1988;LeFever and Funahashi, 1990;Rigas et al, 1993). Moreover, PGE 2 stimulates tumor growth, mediates immune suppression, inhibits apoptosis, and stimulates angiogenesis (Plescia et al, 1975;Ben-Av et al, 1995;Sheng et al, 2001).…”

Section: Cancermentioning

confidence: 99%