salicylates and Skin-Neoplasms

Chemical peeling is a common treatment in cosmetic dermatology. A peel that has been used for many years is trichloroacetic acid. Its adverse effects have for a long time been a major limitation. We present a practical review of the characteristics, mechanisms of action, indications, and complications of superficial chemical peels and of peeling with trichloroacetic acid.

Topics: Acids; Animals; Chemexfoliation; Collagen Type I; Drug Combinations; Elastin; Epidermis; Ethanol; Facial Dermatoses; Humans; Hyperpigmentation; Keratolytic Agents; Lactic Acid; Mice; Pigmentation Disorders; Precancerous Conditions; Resorcinols; Salicylates; Skin Aging; Skin Neoplasms; Trichloroacetic Acid

Today, topical application of sunscreens, containing ultraviolet-filters (UV-filters), is preferred protection against adverse effects of ultraviolet radiation. Evidently, use of sunscreens is effective in prevention of sunburns in various models. However, evidence for their protective effects against melanoma skin cancer is less conclusive. Three important observations prompted us to review the animal data and human studies on possible side effects of selected chemical UV-filters in cosmetics. (1) the utilization of sunscreens with UV-filters is increasing worldwide; (2) the incidence of the malignant disorder for which sunscreens should protect, malignant melanoma, is rapidly increasing and (3) an increasing number of experimental studies indicating that several UV-filters might have endocrine disruptive effects. The selected UV-filters we review in this article are benzophenone-3 (BP-3), 3-benzylidene camphor (3-BC), 3-(4-methyl-benzylidene) camphor (4-MBC), 2-ethylhexyl 4-methoxy cinnamate (OMC), Homosalate (HMS), 2-ethylhexyl 4-dimethylaminobenzoate (OD-PABA) and 4-aminobenzoic acid (PABA). The potential adverse effects induced by UV-filters in experimental animals include reproductive/developmental toxicity and disturbance of hypothalamic-pituitary-thyroid axis (HPT). Few human studies have investigated potential side effects of UV-filters, although human exposure is high as UV-filters in sunscreens are rapidly absorbed from the skin. One of the UV-filters, BP-3, has been found in 96% of urine samples in the US and several UV-filters in 85% of Swiss breast milk samples. It seems pertinent to evaluate whether exposure to UV-filters contribute to possible adverse effects on the developing organs of foetuses and children.

Topics: 4-Aminobenzoic Acid; Animals; Benzyl Compounds; Camphor; Cinnamates; Endocrine Disruptors; Humans; Hypothalamo-Hypophyseal System; Melanoma; para-Aminobenzoates; Receptors, Estrogen; Salicylates; Skin Neoplasms; Sunburn; Sunscreening Agents; Thyroid Gland; Ultraviolet Rays

Topics: Adrenal Cortex Hormones; Anti-Inflammatory Agents; Antimalarials; Azathioprine; Cushing Syndrome; Cyclophosphamide; Drug Eruptions; Gold; Humans; Lichen Planus; Nail Diseases; Pemphigus; Penicillamine; Pigmentation Disorders; Pruritus; Purpura; Salicylates; Skin Neoplasms; Urticaria

Basal cell carcinoma (BCC) is one of the commonest malignancies occurred on sun-exposed skin, mainly by UV-B radiation, of lighter-skinned individuals. The aim of the present study was to develop advanced drug delivery formulations used in BCC therapy that overcomes chemotherapy-induced side-effects of skin photosensitivity by an integrative approach of nanoencapsulation in conjunction with combination therapy that uses chemotherapeutic, chemoprotective and sunscreen agents. The combination of anticancer drug together with sunscreen agent is very useful in therapy, especially for individuals who are more exposed to the sun without using a sunscreen. Nanostructured lipid carriers (NLCs) employed as drug delivery systems were co-loaded with 5-fluorouracil (5-FU), a hydrophilic chemotherapeutic drug, and ethylhexyl salicylate (EHS), a lipophilic UV-B sunscreen agent. The NLCs were developed using bioactive squalene (50.8% w/w) from amaranth seed oil as chemoprotective agent. By varying the concentrations of 5-FU and EHS, the co-loaded NLCs presented particle sizes of about 100nm, acceptable physical stability with values smaller than -25mV and appropriate entrapment efficiency that reaches values over 65% for both types of drugs. The UV-B blocking ability of EHS loaded into NLCs were influenced by the concentration of 5-FU. The amaranth oil offered a capacity of 70% in scavenging the free radicals. In vitro drug release showed that NLCs presented sustained release of 5-FU that followed the Fick's law of diffusion.

Topics: Amaranthus; Antioxidants; Calorimetry, Differential Scanning; Carcinoma, Basal Cell; Drug Carriers; Fluorouracil; Humans; Lipids; Nanoparticles; Particle Size; Plant Oils; Salicylates; Skin Neoplasms; Squalene; Sunscreening Agents; Ultraviolet Rays

Previous studies found that repeated application of smoke condensate from tobacco-burning reference cigarettes to chemically initiated SENCAR mouse skin promoted the development of tumors in a statistically significant and dose-dependent manner, while condensate from prototype cigarettes that primarily heat tobacco promoted statistically fewer tumors. Based on the recognized correlation between sustained, potentiated epidermal hyperplasia and tumor promotion, we conducted tests to examine the utility of selected short-term analyses for discriminating between condensates exhibiting significantly different promotion activities. In vitro analyses assessing the potential for inducing cytotoxicity (ATP bioluminescence) or free radical production (cytochrome c reduction, salicylate trapping) demonstrated significant reductions when comparing condensate collected from prototype cigarettes to reference condensate. Short-term in vivo analyses conducted within the context of a mouse skin, tumor-promotion protocol (i.e., comparative measures of epidermal thickness, proliferative index, myeloperoxidase activity, leukocyte invasion, mutation of Ha-ras, and formation of modified DNA bases) provided similar results. Reference condensate induced statistically significant and dose-dependent increases (relative to vehicle control) for nearly all indices examined, while prototype condensate possessed a significantly reduced potential for inducing changes that we regarded as consistent with sustained epidermal hyperplasia and/or inflammation. Collectively, these data support the contention that selected short-term analyses associated with sustained hyperplasia and/or inflammation are capable of discriminating between smoke condensates with dissimilar tumor-promotion potentials. Moreover, our results suggest that comparative measures of proliferative index and myeloperoxidase activity, both possessing favorable correlation coefficients relative to tumor formation (i.e., > or = 0.95 after 8 or 12 weeks of promotion), may constitute reasonable end points for further investigation.

Topics: Adenosine Triphosphate; Animals; Body Weight; Carcinogenicity Tests; Carcinogens; Cell Proliferation; Cytochromes c; DNA Adducts; Genes, ras; Hydroxyl Radical; Hyperplasia; Inflammation; Leukocytes; Luminescent Measurements; Mice; Mice, Inbred SENCAR; Oxidation-Reduction; Oxidative Stress; Peroxidase; Salicylates; Skin; Skin Neoplasms; Smoke; Superoxides

The constitutive activity of a number of growth and cell survival pathways are thought to contribute to the inherent resistance of melanoma to chemotherapy and radiotherapy. Many of these pathways are driven through the small GTPase Ras. Novel drugs such as the farnesyl transferase inhibitors (FTIs) and farnesyl thiosalicylic acid (FTS) interfere with the signaling of oncogenic Ras. The aim of our study was to assess the anti-tumour activity of the FTI SCH66336 in melanoma and to assess whether SCH66336 and FTS could modulate chemoresistance in melanoma cells. SCH66336 had marked anti-proliferative activity in both human and mouse melanoma cell lines, but not in non-transformed NIH 3T3 cells. The anti-proliferative activity of SCH66336 was due to G1-phase cell cycle arrest and retinoblastoma protein inactivation, followed by apoptosis. Cisplatin, when administered alone, induced little apoptosis. In combination with cisplatin, both FTS and SCH66336 markedly enhanced the level of cisplatin-induced apoptosis, an effect that was associated with enhanced G2/M cell cycle arrest. Pharmacological inhibitors of either ERK or PI-3 kinase/Akt did not mimic the chemosensitising activity of either SCH66336 or FTS. In summary, our study demonstrates that SCH66336 has good in vitro anti-tumour activity in both human and mouse melanoma cell lines, and suggests that Ras antagonists could be useful in overcoming chemoresistance to cisplatin in melanoma.

Topics: 3T3 Cells; Actins; Alkyl and Aryl Transferases; Animals; Apoptosis; Blotting, Western; Cell Cycle; Cell Division; Cisplatin; Colony-Forming Units Assay; Drug Synergism; Enzyme Inhibitors; Farnesol; Farnesyltranstransferase; Humans; In Situ Nick-End Labeling; In Vitro Techniques; Melanoma; Mice; Microscopy, Confocal; Mitogen-Activated Protein Kinases; Piperidines; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Pyridines; Retinoblastoma Protein; Salicylates; Skin Neoplasms; Tumor Cells, Cultured

Topical application of alpha-tocopherol (alphaTH), the most prominent naturally occurring form of vitamin E, inhibits ultraviolet (UV) B-induced photocarcinogenesis and DNA photodamage in C3H mice in vivo. In this study, we compared alphaTH with other vitamin E compounds and with three commercial sunscreen compounds for their ability to inhibit DNA photodamage in C3H mouse skin in vivo. When applied in a 5% dispersion in a neutral cream vehicle, alpha-tocopherol (alphaTH), gamma-tocopherol (gammaTH), and delta-tocopherol (deltaTH) each produced a statistically significant inhibition of thymine dimer formation, whereas alpha-tocopherol acetate (alphaTAc) and alpha-tocopherol methyl ether (alphaTOMe) did not. Application of 5% dispersions of the commercial sunscreen agent octylmethoxycinnamate also inhibited dimer formation, whereas ethylhexyl salicylate and oxybenzone did not, despite their considerably greater UVB absorbances than alphaTH. To test the hypothesis that cellular uptake and distribution are necessary for optimal photoprotection by tocopherols, photoprotection was studied in mouse 308 keratinocyte cells in vitro. Preincubation of 308 cells with 1 microM alphaTH for at least 2 h before exposure to 2.5 J/m2/s UVB for 10 min significantly (P < 0.05) attenuated thymine dimer formation. Pre-incubation with 1 microM gammaTH, deltaTH, alphaTAc, or alphaTOMe for 2 h did not inhibit thymine dimer formation significantly. Uptake of alphaTH was measured after incubation with 1 microM [2H3]alphaTH (d3-alphaTH) and resulted in a time-dependent increase in alphaTH levels. Use of d3-alphaTH allowed separate, simultaneous measurement of added d3-alphaTH and unlabeled endogenous alphaTH by gas chromatography-mass spectrometry. Accumulation of 167 +/- 62 pmol d3-alphaTH/mg protein was measured within 1 h in whole-cell fractions. d3-AlphaTH in the nuclear fraction reached levels of 15 +/- 4 pmol d3-alphaTH/mg protein at 2 h. Accumulation of alphaTH in the whole cell and nuclei corresponded temporally with significant protection against DNA photodamage. The kinetics of accumulation of the three tocopherols in whole cells and in nuclei were similar. Although only alphaTH conferred significant protection compared with irradiated controls at 2 h, the differences between individual tocopherols were not statistically significant. This work suggests that incorporation of tocopherol compounds into sunscreen products confers protection against procarcinogenic DNA photoda

Topics: Administration, Cutaneous; alpha-Tocopherol; Animals; Anticarcinogenic Agents; Benzophenones; Biological Transport; Cell Nucleus; Cells, Cultured; Cinnamates; DNA Damage; Ethers; Female; Keratinocytes; Mice; Mice, Inbred C3H; Neoplasms, Radiation-Induced; Photochemistry; Pyrimidine Dimers; Radiation Tolerance; Radiation-Protective Agents; Salicylates; Skin; Skin Neoplasms; Sunscreening Agents; Tocopherols; Ultraviolet Rays; Vitamin E

Merkel cell carcinoma (MCC) is a neuroendocrine malignancy showing poor response to a variety of therapeutic strategies. We evaluated the antitumor activity of S-trans, trans-farnesylthiosalicylic acid (FTS), a new inhibitor of Ras signal transduction, in a newly established SCID mouse xenotransplantation model for human MCC (seven animals per group). FTS injected intraperitoneally at 5 mg/kg per day for 2 weeks up-regulated the tumor suppressor p53 and induced tumor cell apoptosis in established MCCs growing subcutaneously in SCID mice. These effects led to a statistically significant inhibition of MCC growth (P<0.002). The mean tumor weights following FTS or control treatment were 0.32+/-0.15 g and 1.08+/-0.29 g, respectively. There was no evidence of FTS related toxicity at the effective dose used. Our findings stress the notion that FTS may qualify as a novel and rational treatment approach for MCC and possibly for other tumors that rely on tyrosine kinase signaling.

Topics: Aged; Aged, 80 and over; Animals; Antineoplastic Agents; Apoptosis; Carcinoma, Merkel Cell; Cell Division; Farnesol; Female; Humans; Injections, Intraperitoneal; Male; Mice; Mice, SCID; Proto-Oncogene Proteins p21(ras); Salicylates; Skin Neoplasms; Statistics, Nonparametric; Transplantation, Heterologous; Tumor Cells, Cultured; Tumor Suppressor Protein p53

The petroleum ether extract of cashewnut shell (Anacardium occidentale) was tested for its mutagenic, carcinogenic and cocarcinogenic potency. Mutagenicity tests using Salmonella typhimurium (Ame's test) Strains TA 1535, TA 100 and TA 98 showed that cashewnut shell liquid is non-mutagenic up to a concentration of 0.003% (in 0.1 ml DMSO) with and without metabolic activation (S 9 mixture). Carcinogenicity testing using murine (female Swiss albino mice) two stage skin tumourigenesis model revealed that cashewnut shell liquid has no tumour initiating potency at a concentration of 10% (in 0.2 ml acetone) while it may act as weak promoter (P < 0.05) at a concentration of 5% (in 0.2 ml acetone). Testing for cocarcinogenic potency of cashewnut shell liquid (2% and 5% in 0.2 ml acetone) demonstrated that it has no cocarcinogenic potency on mouse skin tumour model when applied along with 2 x 10(-6)% benzo(a)pyrene in acetone up to a period of 20 weeks.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Anacardic Acids; Animals; Carcinogenicity Tests; Carcinogens; Cocarcinogenesis; Female; Mice; Mutagenicity Tests; Neoplasms, Experimental; Plant Extracts; Plants, Toxic; Resorcinols; Salicylates; Salmonella typhimurium; Skin Neoplasms

The ability of a biomimetic superoxide dismutase agent, copper(II)(3,5-diisopropylsalicylate)2 (CuDIPS), to modulate benzoyl peroxide (BzPo)-induced tumor promotion and progression in mouse skin multistage carcinogenesis was evaluated. The results showed a significant inhibition of tumor incidence by CuDIPS pretreatment during promotion-progression. Different types of tumors were developed: papillomas, keratoacanthomas and squamous cell carcinomas. There was a significant increase in the keratoacanthoma-papilloma ratio when the period of treatment with BzPo was prolonged, which was inhibited by CuDIPS pretreatment. CuDIPS induced a significant inhibition of malignant conversion. Our results suggest that reactive oxygen species could be important in BzPo-induced promotion and progression.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Antineoplastic Agents; Benzoyl Peroxide; Carcinoma, Squamous Cell; Cocarcinogenesis; Female; Incidence; Keratoacanthoma; Mice; Papilloma; Salicylates; Skin Neoplasms

A keratinocyte-mediated mutagenesis assay, and the murine skin multistage carcinogenesis tumor model were used to survey the chemopreventive properties of Cu(II)(3,5-diisopropylsalicylate)2 [CuDIPS] and its analogs. Supplementation of cocultures of newborn SENCAR keratinocytes and Chinese hamster lung fibroblasts (V79 cells) with CuDIPS, 3,5-diisopropylsalicylate (DIPS), and CuSO4 resulted in dose-dependent killings of V79 cells (LD50 of 34, 75, 960 microM, respectively), and inhibitions of benzo[a]pyrene (BP) and 7,12-dimethylbenz[a]anthracene (DMBA) mutagenesis (ED50 of 13, 95, 80 microM, and 40, 125, 110 microM, respectively). Analyses of dose-response curves suggest (i) CuDIPS preferentially inhibits BP mutagenesis; (ii) the antimutagenic activity of CuDIPS towards DMBA and the cytotoxicity of the copper complex are derived from the DIPS component of the chelate; (iii) the antimutagenic activity of CuDIPS towards BP requires both copper and DIPS; and (iv) DIPS and CuDIPS induced cytotoxicity is required for inhibition of mutagenesis. Inhibition of mutagenesis by CuDIPS was not mediated by modulation of promutagen metabolism because antimutagenic concentrations of the chelate had no significant effects on DMBA- and BP-dependent cytotoxicities. Topical pretreatment of SENCAR mice with CuDIPS (100-4000 nmol) 15 min prior to initiation with DMBA or BP resulted in small (38% maximum) non-dose-responsive reductions of papillomas/mouse following 20 weeks of promotion.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Antineoplastic Agents; Benzo(a)pyrene; Cell Line; Cell Survival; Cells, Cultured; Copper; Copper Sulfate; Epidermal Cells; Epidermis; Mice; Mice, Inbred Strains; Mutation; Papilloma; Salicylates; Skin Neoplasms

The present study was designed to compare the skin tumor promoting and epidermal ornithine decarboxylase (ODC) inducing activities of various structural analogs of anthralin (1,8-dihydroxy-9-anthrone) and chrysarobin (1,8-dihydroxy-3-methyl-9-anthrone). Groups of 30 SENCAR mice each were initiated with 7,12-dimethylbenz[a]anthracene and 2 weeks later promoted with once- or twice-weekly applications of various doses of these anthrone derivatives. Carbon-10 (C10)-acyl derivatives of anthralin were active skin tumor promoters in the range of 25-440 nmol per mouse. 10-Acetylanthralin was significantly more active than 10-myristoyl-anthralin at low doses (e.g. 25 and 50 nmol per mouse) and nearly as potent as the unsubstituted compound. Higher doses (greater than or equal to 100 nmol per mouse) of this derivative were toxic, hence, reducing the final papilloma response. On a relative activity scale where anthralin is 1.0, these derivatives had activities that were approximately 0.7 and 0.2, respectively. 10,10-Dipropylanthralin was totally inactive at the doses tested. C6-Substituted derivatives of chrysarobin demonstrated diverse tumor promoting activities when tested in the range of 25-440 nmol per mouse. On a relative activity scale where chrysarobin is 1.0, 6-methoxychrysarobin (physcion anthrone) was approximately 0.9, whereas 6-hydroxychrysarobin (emodin anthrone) had no activity. Chrysophanic acid (1,8-dihydroxy-3-methyl-9,10-anthraquinone) was also inactive as a tumor promoter at the doses tested. In general, the tumor promoting activities of these anthrone derivatives correlated very well with their ability to induce epidermal ODC after a single topical application indicating an important role for this enzyme in skin tumor promotion by anthones. The ability of C10-substituted derivatives of anthralin to undergo base catalyzed oxidation in vitro correlated with both ODC inducing and tumor promoting activities. In addition, copper(II)bis(diisopropylsalicylate) was found to inhibit both ODC induction and skin tumor promotion by chrysarobin. These latter data, when taken together, suggest a role for oxidation at C10 in skin tumor promotion by anthrone derivatives.

Topics: Animals; Anthracenes; Anthralin; Enzyme Induction; Female; Free Radicals; Mice; Ornithine Decarboxylase; Salicylates; Skin; Skin Neoplasms; Structure-Activity Relationship

Currently, 25 different types of human papillomavirus (HPV) are recognized, each responsible for a characteristic clinical manifestation of warts or wart-like lesions. Increasingly, evidence supports a close relationship between certain types of HPVs--5, 8, 14, 16, 18, and perhaps 6 and 11--and malignant transformation. Before therapy is initiated, the probability of spontaneous resolution must be considered. The discomfort and possible risks of treatment must be balanced against the patient's discomfort and pain. Possible modes of treatment include topical therapy, cryotherapy and surgery, intralesional injections, and immunotherapy.

Topics: Administration, Topical; Bleomycin; Carcinoma, Squamous Cell; Cell Transformation, Neoplastic; Cryosurgery; Female; Humans; Immunotherapy; Injections; Male; Papillomaviridae; Salicylates; Salicylic Acid; Skin Neoplasms; Tumor Virus Infections; Uterine Neoplasms; Warts

The effect of phorbol ester tumour promoters on the release of superoxide anion radicals .O2- by human peripheral leukocytes and the role of such radicals in tumour promotion of mouse skin was studied. No significant difference was found between complete [12-O-tetradecanoylphorbol-13-acetate (TPA)] as compared with incomplete [12-O-retinoylphorbol-13-acetate (RPA), 12-O-(2Z,4E,6,8)tetradecatetraenoylphorbol-13-acetate (Ti8), mezerein] tumour promoters upon induction of .O2- when measured by the reduction of ferricytochrome c. The semisynthetic phorbol esters 12-O-ethacrynylphorbol-13-acetate (EPA) and 4-O-methyl-TPA were less active, and phorbol diacetate, phorbol and ionophore A 23187 were found to be inactive in stimulating superoxide anion radicals. TPA-induced .O2- release from leukocytes was strongly inhibited by Cu(II)-(diisopropylsalicylate)2 (CuDIPS), and, to a lesser extent, by ethacrynic acid, nordihydroguaiaretic acid and quercetin. Retinoic acid exhibited only a moderate inhibitory effect. No .O2- release was observed in epidermal cell cultures upon TPA treatment. When analysed by the alkaline elution technique, TPA-induced .O2- release from leukocytes did not lead to measurable DNA damage in co-cultivated keratinocytes even in the presence of DNA repair inhibitors. In multi-stage-tumourigenesis experiments including two-stage promotion, retinoic acid, ethacrynic acid and CuDIPS were unable to inhibit tumour promotion in mouse skin when applied in combination with TPA in first stage promotion. gamma-Irradiation at a dose level shown to cause DNA damage in vitro could not replace TPA as a stage I-promoting agent. It is concluded that superoxide anion radicals--if related to promotion at all--may play a role in stage II rather than in stage I of mouse skin tumour promotion.

Topics: Animals; Cells, Cultured; Chromosome Aberrations; DNA; Female; Free Radicals; Leukocytes; Mice; Mice, Inbred Strains; Salicylates; Skin Neoplasms; Superoxides; Tetradecanoylphorbol Acetate

Cu(II) (3,5-diisopropyl salicylate)2 (CuDIPS) which is an anti-inflammatory copper coordination compound (mol. wt. 503) possessing superoxide dismutase (SOD) activity was tested to determine its effect on 7,12-dimethylbenz[a]anthracene (DMBA)-induced initiation of tumors in mouse skin and on mutagenicity to 6-thioguanine resistance in a mouse keratinocyte mediated Chinese hamster V-79 cell system. A single application of CuDIPS (0.4 mg/mouse) administered at a short interval before DMBA application when followed by 20 weeks of promotion by TPA reduced the mouse skin tumor yield by 55%. When DMBA-induced cell-mediated mutagenesis was tested in the presence of CuDIPS a significant reduction in the number of V-79 6-thioguanine resistant mutants was observed.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Benz(a)Anthracenes; Biotransformation; Cocarcinogenesis; Cricetinae; Female; Mice; Salicylates; Skin Neoplasms

A low molecular weight, lipophilic, copper coordination complex with superoxide dismutase-mimetic activity inhibited biochemical and biological actions of a tumor promoter in mouse epidermis. Such inhibitory effects implicate reactive oxygen species in the tumor promotion process.

Topics: Animals; Antineoplastic Agents; Carcinogens; Female; Mice; Ornithine Decarboxylase; Papilloma; Salicylates; Skin Neoplasms; Superoxide Dismutase; Tetradecanoylphorbol Acetate

Topics: Adrenocorticotropic Hormone; Alopecia; Betamethasone; Dermatitis, Seborrheic; Detergents; Eczema; Female; Hair; Hexachlorophene; Humans; Impetigo; Lice Infestations; Lichen Planus; Male; Psoriasis; Pyridinium Compounds; Salicylates; Scalp Dermatoses; Selenium; Skin Neoplasms; Sulfur; Tinea Capitis

Topics: Adolescent; Adult; Antineoplastic Agents; Clioquinol; Drug Combinations; Female; Flumethasone; Humans; Male; Middle Aged; Neomycin; Ointments; Salicylates; Skin Diseases; Skin Neoplasms

Topics: Aged; Carcinoma, Basal Cell; Female; Humans; Petrolatum; Photosensitivity Disorders; Psoriasis; Salicylates; Skin Neoplasms; Time Factors; Xeroderma Pigmentosum