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Actinic Keratoses (actinic + keratose)

Distribution by Scientific Domains

Medical Sciences	94%

Kinds of Actinic Keratoses

multiple actinic keratose

Selected Abstracts

Topical 3.0% diclofenac in 2.5% hyaluronan gel in the treatment of actinic keratoses

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 11 2001
John E. Wolf Jr MD
Background Actinic keratoses (AKs) are epidermal skin lesions with the potential to develop into invasive squamous cell carcinoma (SCC). Treatment at an early stage may prevent development of SCC. Current treatment options are highly destructive and associated with significant side-effects. Early studies with topical diclofenac were encouraging and led to its evaluation for the treatment of actininic keratosis. Previous studies have demonstrated that 3% diclofenac in 2.5% hyaluronan gel is effective and well tolerated in the treatment of AK. The present study was designed to further explore the therapeutic potential of this gel. Methods This randomized, double-blind, placebo-controlled trial involved outpatients with a diagnosis of five or more AK lesions contained in one to three 5 cm2 blocks. Patients received either active treatment (3% diclofenac gel in 2.5% hyaluronan gel) or inactive gel vehicle (hyaluronan) as placebo (0.5 g b.i.d. in each 5 cm2 treatment area for 90 days). Assessments included the Target Lesion Number Score (TLNS), Cumulative Lesion Number Score (CLNS), and Global Improvement Indices rated separately by both the investigator (IGII) and patient (PGII). Results Results obtained from 96 patients at follow up (30 days after end of treatment) indicated that a significantly higher proportion of patients who received active treatment had a TLNS = 0 compared to the placebo group (50% vs. 20%; P < 0.001). There was also a significant difference between the two groups in CLNS, with 47% of patients in the active treatment group having a CLNS = 0 compared with only 19% in the placebo group (P < 0.001). The proportion of patients with an IGII score of 4 (completely improved) at follow-up was 47% in the active treatment group compared with only 19% in the placebo group (P < 0.001); for PGII these values were 41% vs. 17%, P < 0.001. Both treatments were well tolerated, with most adverse events related to the skin. Conclusions Topical 3% diclofenac in 2.5% hyaluronan gel was effective and well tolerated for the treatment of AK. [source]

Actinic keratoses: a cosmetic nuisance or a mortal risk?

JOURNAL OF COSMETIC DERMATOLOGY, Issue 4 2004
R Cerio
[source]

Tenascin expression in actinic keratosis

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 11 2006
Maria Lentini
Background:, Tenascin is an extracellular matrix protein frequently expressed around neoplastic and non-neoplastic lesions of the skin. Actinic keratoses (AKs) are intraepidermal neoplastic lesions of the sun-exposed skin. They are classified according to the extension of dysplasia in four stages; they also present different histological varieties. Methods:, We performed an immunohistochemical study using tenascin monoclonal antibody diluted 1 : 50 on 150 cases of AKs classified, respectively, in histotypes (38 hypertrophic, 18 atrophic, 21 bowenoid, 19 acantolytic, and 40 mixed) and in stages (27 stage I, 46 stage II, 42 stage III, and 35 stage IV; 14 in tumoral progression). Results:, Tenascin positivity was observed in all cases at the dermal level close to the epithelial lesion. The intensity of reaction increased from stage I to stage IV and, of course, also in tumoral progression. Its expression was not related to the histotypes. In very few cases, the atypical keratinocytes were positive. Conclusions:, Tenascin expression in AKs is related to the stages of dysplasia. In fact, the immunostaining intensity corresponds to the degree of the dysplasia rather than the thickness of the involved epidermis. Tenascin plays a role in neoplastic progression working as an anti-adhesive factor. [source]

Topical 3.0% diclofenac in 2.5% hyaluronic acid gel induces regression of cancerous transformation in actinic keratoses

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 3 2010
T Dirschka
Abstract Background, Actinic keratoses (AKs) are frequently diagnosed in dermatological patients. As they represent in situ carcinomas, effective treatment is required. Objectives, We investigated the effect of topical 3.0% diclofenac in 2.5% hyaluronic acid gel on AK. Methods, Sixty-five patients with AKs were clinically evaluated before and after 3 months' treatment with topical 3.0% diclofenac in 2.5% hyaluronic gel. Biopsy specimens were taken and stained with haematoxylin-eosin and immunohistological markers. Specimens were evaluated for histological type of AKs using the AK classification scheme suggested by Röwert-Huber et al. [(early) in situ squamous cell carcinoma type AK Grade I,III], number of mitoses per high-power field and expression of immunohistological markers. Results, Complete clinical resolution was observed in 11 patients (16.9%). A significant (P < 0.001) downgrading of AK grade was observed. Complete histological resolution was achieved in 15 patients (23.1%). The number of mitoses per high-power field was reduced significantly (P < 0.001). The expression of anti-p53-antibody decreased significantly (P = 0.009), as did the expression of anti-MiB-1 antibody (P = 0.021). Conclusions, 3.0% diclofenac in 2.5% hyaluronic acid gel causes regression of signs of cancerous transformation after 3 months' therapy. [source]

Intraindividual, right,left comparison of topical 5-aminolevulinic acid photodynamic therapy vs.

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 9 2009
5% imiquimod cream for actinic keratoses on the upper extremities
Abstract Backround, Actinic keratoses (AKs) are considered as in situ squamous cell carcinoma. Early and effective treatment is important. Objective, To compare the efficacy, cosmetic outcome and patient preference of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) with that of 5% imiquimod (IMIQ) cream in patients with AKs on the dorsa of hands and forearms. Methods, Subjects received two ALA-PDT treatment sessions and one or two courses of imiquimod (three times per week for 4 weeks each). Treatments were randomly allocated to alternate upper extremities. Assessments included lesion response one and six months after treatment, cosmetic outcome evaluated by the investigators and patients' preference 6 months after treatment. Efficacy end point included the individual AK lesion clearance rate. Results, Thirty patients with 256 lesions were included in the study. At the first follow-up, treatment with ALA-PDT resulted in significantly larger rate of cured lesions relative to 5% IMIQ cream (70.16% vs. 18.26%). At the second follow-up both treatments showed a high rate of cured lesions (65.32% for PDT vs. 55.65% for IMIQ cream). Response rates obtained in grade I lesions were higher for both treatments (71.64% for PDT vs. 72.13% for IMIQ), while treatment with PDT resulted in a significant larger rate of cured grade II lesions (57.89% for PDT vs. 37.03 for IMIQ). Difference in cosmetic outcome was not statistically significant. Results for subject preference favoured ALA-PDT. Conclusions, Our study shows that ALA-PDT and 5% IMIQ cream are both attractive treatment options for upper extremities AKs with comparable efficacy and cosmetic outcomes. Conflicts of interest None declared. [source]

Gene expression in actinic keratoses: pharmacological modulation by imiquimod

BRITISH JOURNAL OF DERMATOLOGY, Issue 6 2004
B. Lysa
Summary Background, Actinic keratoses (AKs) are premalignant lesions that can progress into squamous cell carcinoma. Imiquimod, which belongs to the new class of immune-response modifiers, was recently shown to be effective in the treatment of AKs. The underlying mechanisms are not fully understood. Objectives, To study the expression of individual genes in uninvolved skin and AKs before therapy and to elucidate the way in which the expression of these genes is influenced by imiquimod therapy. Methods, We treated 13 patients with AK with imiquimod and compared gene expression before, during (five patients) and after (eight patients) therapy with that in uninvolved skin. We analysed genes coding for inflammatory cytokines or their receptors, adhesion molecules, anti-apoptotic proteins, p53 and toll-like receptors (TLRs) by reverse-transcriptase polymerase chain reaction. Results, Comparing uninvolved skin and untreated AK, we found significant differences in the expression of interleukin (IL)-6, hurpin, TLR7 and TLR8. During imiquimod therapy, we detected a further upregulation of interferon-,, IL-6, IL-10 receptor 1 and TLR7. In contrast, two anti-apoptotic genes, hurpin and HAX-1, were downregulated. We did not detect significant differences in gene expression for p53, tumour necrosis factor-, and ,- and ,-catenins. Clinically, the upregulated expression of the proinflammatory cytokines correlated with the local inflammation induced by imiquimod. Conclusions, Our results indicate that specific differences in gene expression are detectable between AK and uninvolved skin. Imiquimod influenced the expression of most genes analysed in this study. This work extends previous findings on the effects of imiquimod on gene regulation in AKs. [source]

Actinic keratoses in renal transplant recipients do not improve with calcipotriol cream and all- trans retinoic acid cream as monotherapies or in combination during a 6-week treatment period

BRITISH JOURNAL OF DERMATOLOGY, Issue 4 2002
J.V. Smit
No abstract is available for this article. [source]

Actinic keratosis treated with an immune response modifier: a case report of six patients

CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 2003
L. Bianchi
Summary Actinic keratoses (AKs) are intraepidermal tumours, which result from the proliferation of transformed neoplastic keratinocytes. They are typically induced by chronic exposure to ultraviolet radiation, and can often develop into squamous cell carcinoma (SCC). Six patients, who presented with AKs located on the head, face and chest, were treated with the immune response modifier, imiquimod, as a 5% cream five times per week for up to 8 weeks. The majority of patients experienced mild to moderate side-effects, consisting of erythema, itching and burning. Topical application of imiquimod for 4,8 weeks resulted in complete clearance in all patients. No new or recurrent lesions were observed during a 6,8 month follow-up period. [source]

Photoallergic contact dermatitis from topical diclofenac in Solaraze® gel

CONTACT DERMATITIS, Issue 6 2006
L. Kowalzick
Solaraze® gel (Shire Deutschland GmbH & Co. KG, Cologne, Germany) containing 3% diclofenac has been licensed in 2001 as a topical treatment for actinic keratoses. It is commonly used in dermatological practice. Undesirable effects are believed to be rare but include pruritus, paresthesia and application-site reactions (dry skin, rash, erythema, contact dermatitis and vesicobullous eruptions). Recently, a few cases of contact dermatitis due to three different allergens including diclofenac have been reported (1,2). [source]

Photodynamic Therapy for the Treatment of Cutaneous Neoplasia, Inflammatory Disorders, and Photoaging

DERMATOLOGIC SURGERY, Issue 5 2009
EMILY TIERNEY MD
BACKGROUND Photodynamic therapy (PDT) has demonstrated high efficacy, minimal side effects, and improved cosmetic outcome when used for the treatment of actinic keratoses (AK), basal cell carcinoma (BCC), squamous cell carcinoma, and photoaging. METHODS To review the literature on the use of PDT in dermatologic surgery using MEDLINE. RESULTS Published clinical studies using PDT in the treatment of AKs yield overall efficacy rates ranging from 50% to 71% with one treatment to as high as 88% to 90% with two or more treatments. For superficial BCC, initial clearance rates were 76% to 97%, and for Bowen's disease, initial clearance rates ranged from 72% to 94% overall. The use of PDT for photorejuvenation is a relatively new application of this technology, which has shown promise in improving the appearance of fine lines, pigmentary variation, and telangiectasias. CONCLUSIONS The advantages of photodynamic therapy include the capacity for noninvasive targeted therapy through topical application of aminolevulinic acid and methyl aminolevulinic acid, with outstanding cosmetic results. Although the theory behind the use of chemical photosensitizers and ultraviolet light to treat a wide variety of skin disorders is straightforward, the practical application of this technology is evolving. Additional research into the precise mechanisms of action for specific photosensitizers and optimal light sources will be highly beneficial to the advancement of this technology. [source]

Does Imiquimod Histologically Rejuvenate Ultraviolet Radiation,Damaged Skin?

DERMATOLOGIC SURGERY, Issue 12 2007
KATHLEEN SMITH MD
BACKGROUND Imiquimod (IMI) 5% is believed by some to result in an improved cosmetic appearance of chronically ultraviolet radiation (UV)-damaged skin. OBJECTIVE The objective was to determine what histologic and immunohistologic changes were present in actinically damaged skin after treatment with IMI. METHODS AND MATERIALS Pre- and posttherapy biopsies of 12 patients with histories of actinic keratoses were evaluated with routine histology and immunohistochemical stains including p53, p63, proliferating cell nuclear antigen (PCNA), c-kit, and Factor XIIIa. RESULTS After IMI therapy there was less compact hyperkeratosis, a more uniform rete ridge pattern with a more ordered proliferation of the epidermis, and a decrease in sun-damaged melanocytes. The papillary dermis showed a more uniform cellularity, and there was increased cellularity within the area of solar elastosis. After therapy, staining for p53, p63, and PCNA was decreased within the epidermis; staining for c-kit was decreased but more uniform in the basal cell; and Factor XIIIa expression was increased within the papillary dermis with a more ordered pattern of staining. CONCLUSION These morphologic and immunohistochemical patterns may explain some of the improvement in overall skin appearance after IMI therapy and may be related to the spectrum of signaling pathways induced by the imidazoquinolines. [source]

5-Aminolevulinic Acid Photodynamic Therapy: Where We Have Been and Where We Are Going

DERMATOLOGIC SURGERY, Issue 8 2004
Michael H. Gold MD
Background. Photodynamic therapy, utilizing the topical administration of 20% 5-aminolevulinic acid, has generated a great deal of interest in the dermatology community over the past several years. Objective. The purpose of this article is to review the history of photodynamic therapy in dermatology and to review recent new advances with this technology that will increase its appeal to all dermatologists. Methods. A literature review and results of new clinical trials with regards to photorejuvenation and acne vulgaris treatments with 5-aminolevulinic acid photodynamic therapy are presented. Results. Short-contact, full-face 5-aminolevulinic acid photodynamic therapy treatments with a variety of lasers and light sources have shown to be successful in treating all facets of photorejuvenation and the associated actinic keratoses as well as disorders of sebaceous glands, including acne vulgaris. The treatments are relatively pain-free, efficacious, and safe. They are also making already available laser/light source therapies work better for acne vulgaris and photorejuvenation. Conclusions. The use of 5-aminolevulinic acid photodynamic therapy with short-contact, full-face broad-application therapy is now able to bridge the world of medical and cosmetic dermatologic surgery. This therapy is available for all dermatologists to utilize in the care of their patients. [source]

Human Papillomavirus and Overexpression of P16INK4a in Nonmelanoma Skin Cancer

DERMATOLOGIC SURGERY, Issue 3 2004
Ingo Nindl PhD
Background. P16INK4a overexpression has been identified as a specific biomarker in high-risk human papillomavirus (HPV),infected cervical (pre)cancer lesions. Objective. To evaluate the overexpression of this cyclin-dependent kinase inhibitor in skin tumors depending on HPV infections, we analyzed normal skin, benign skin disease, and skin cancer specimens. Methods. Biopsies of 23 patients with normal histology (3), psoriasis (2), verrucae vulgaris (2), actinic keratoses (5), squamous cell carcinoma (SCC) in situ (3), Bowen's carcinoma (1), and SCC (7) were analyzed. Specimens of 23 patients were immunostained using the monoclonal antibody E6H4 specific for p16INK4a. HPV status was assessed by a polymerase chain reaction (PCR) system to detect all currently known HPV types. MY (MY09/MY11 and MYN9/MYN10)-, CP (CP65/CP70 and CP66/CP69)-nested PCR, and three single PCR methods CN1, CN3, and CN4 were used in a first step, and HPV typing was performed by restriction fragment length polymorphism analysis. Only ,-globin,positive patients were included in this study. Results. HPV DNA was detected in all actinic keratoses, SCC in situ, Bowen's carcinoma, and SCC, in 50% (one of two) of verrucae vulgaris, in 66% (two of three) of normal skin, and in none of two psoriasis. P16INK4a expression was not detected in normal skin, psoriasis, and verrucae vulgares. Overexpression of p16INK4a was detected in a subset of dysplastic cells (10% to 80%) of all skin (pre)cancer lesions such as actinic keratoses, SCC in situ, Bowen's carcinoma, and SCC infected with HPV independent of sun exposure. Conclusion. P16INK4a appears to be overexpressed in a portion of dysplastic cells from actinic keratoses and SCC. Further studies to examine the association of HPV infection and the overexpression of p16INK4a are warranted. [source]

Rapid Development of Keratoacanthomas After a Body Peel

DERMATOLOGIC SURGERY, Issue 2 2003
SueEllen Cox MD
Resurfacing techniques have been traditionally limited to the face because of a lack of predictability and standardization for peeling nonfacial skin. There is a need for medical and surgical intervention for treating nonfacial skin that is actinically damaged. Medium-depth chemical peels (Jessner +35% trichloroacetic acid) remove the photodamaged epidermis to stimulate the production of new collagen in the dermis and remove lesions associated with facial actinic damage, including lentigines and actinic keratoses. Widespread actinic damage is common on the arms and chest. A 70% glycolic acid gel plus 40% trichloroacetic acid peel (Cook Body Peel) is a controlled peel that predictably enables peeling of nonfacial skin in a uniform and safe fashion with specific clinical endpoints. An unusual complication of this body peel is reported. [source]

Topical diclofenac in the treatment of actinic keratoses

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2007
Hans F. Merk Prof. Dr. Med.
First page of article [source]

Xeroderma pigmentosum with limited involvement of the UV-exposed areas: a case report

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2003
Mostafa Mirshams-Shahshahani MD
A 21-year-old woman with skin type IV, who had developed photophobia and brown, spotty, hyperpigmented lesions on her face from early childhood, presented to our center for treatment of her facial lesions. Examination on admission revealed numerous, freckle-like, hyperpigmented macules and actinic keratoses over the central part of the face, with sparing of the forehead, chin, and peripheral area (Fig. 1). The area involved was approximated to be around 2% of the total body surface. The dorsal parts of the hands showed no lesions (Fig. 2), but guttate hypomelanotic lesions were apparent on both forearms. Figure 1. Limitation of xeroderma pigmentosum lesions to the center of the face Figure 2. Hands are devoid of any lesions Histologic examination of biopsies from four different facial lesions revealed them to be keratoacanthoma (1.5 × 2.5 cm ulcerative nodule on the right cheek), sclerosing basal cell epithelioma (nasal lesion), lentigo simplex, and hypertrophic actinic keratosis. Corneal clouding, conjunctival injection, loss of lashes, and atrophy of the lids were apparent on ophthalmologic examination. Other parts of the physical examination, including examination of the oral cavity, were nonsignificant. In addition, except for the presence of mild eczema in a sibling, the patient's family history regarding the presence of any similar problem and also any other important dermatologic or general disorder was negative. [source]

Topical 3.0% diclofenac in 2.5% hyaluronan gel in the treatment of actinic keratoses

Treatment of actinic keratoses with birch bark extract: a pilot study

JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, Issue 2 2006
Constance Huyke
aktinische Keratosen; Betulinsäure; Betulin; Oleanolsäure Summary Background: Birch bark contains a variety of apoptosis-inducing and anti-inflammatory substances such as betulinic acid, betulin, oleanolic acid and lupeol. Therefore, birch bark extract may be effective in the treatment of actinic keratoses. To address this issue, a pilot study using a standardized birch bark ointment was performed. Methods: Twenty-eight patients with actinic keratoses were enrolled in this prospective, non-randomized pilot study. Fourteen patients were treated with birch bark ointment only; fourteen patients received a combination therapy with cryotherapy and birch bark ointment. Treatment response was assessed clinically after two months. Results: Clearing of more than 75 % of the lesions was seen in 79 % of the patients treated with birch bark ointment monotherapy. The response rate of the combined treatment modality was 93 %. Therapy with birch bark ointment was well tolerated. Conclusion: In this pilot study, a standardized birch bark extract was effective in the treatment of actinic keratoses. This therapy is easy to perform and it has no side effects. Birch bark ointment may be a new therapeutic option for actinic keratoses. Zusammenfassung Hintergrund: Birkenkork ist reich an Triterpenen (Betulin, Betulinsäure, Oleanolsäure, Lupeol, Erythrodiol), für die Apoptose induzierende und antientzündliche Wirkungen beschrieben sind. Deshalb könnte sich ein Extrakt aus Birkenkork für die Therapie von aktinischen Keratosen eignen. Mit der hier untersuchten Birkenkork-Creme liegt erstmals eine galenische Formulierung vor (Birkenkorkextrakt, pflanzliche Öle, Wasser), in der die Wirkstoffe des Birkenkorks in therapeutisch ausreichender Menge vorhanden sind. Methoden: Im Rahmen der prospektiven, nicht randomisierten Pilotstudie wurden 28 Patienten mit aktinischen Keratosen behandelt. 14 Patienten erhielten eine Creme mit Birkenkorkextrakt als Monotherapie, 14 Patienten wurden zusätzlich kryotherapeutisch behandelt. Die Birkenkork-Creme wurde von den Patienten zweimal täglich aufgetragen. Das klinische Ansprechen wurde nach zwei Monaten erfasst. Ergebnisse: Bei Behandlung mit Birkenkorkextrakt als Monotherapie zeigten 79 % der Patienten nach einem Beobachtungszeitraum von zwei Monaten eine klinische Abheilung von über 75 % der Läsionen. Bei der Kombinationsbehandlung mit Kryotherapie kam es bei 93 % der Patienten zu einem Ansprechen auf die Behandlung. Die Verträglichkeit der Birkenkork-Creme war in allen Fällen sehr gut. Schlussfolgerung: Im Rahmen dieser Pilotstudie zeigte die lokale Anwendung eines standardisierten Birkenkorkextraktes eine gute Wirksamkeit bei der Behandlung aktinischer Keratosen. Die Anwendung ist einfach und die Verträglichkeit sehr gut. Deshalb stellt Birkenkorkextrakt eine interessante neue Therapieoption für aktinische Keratosen dar. [source]

Behandlung aktinischer Keratosen mit Birkenkorkextrakt: Eine Pilotstudie

Activation of Src-family tyrosine kinases in hyperproliferative epidermal disorders

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 3 2008
Elias E. Ayli
Background:, Src-family tyrosine kinases (SFKs) are important regulators of keratinocyte growth and differentiation. In a broad range of cell types, persistent activation of SFKs correlates with increased cell proliferation. In this study, we determined if SFK activity is increased in cutaneous neoplasia and psoriasis, common hyperproliferative epidermal disorders. Methods:, Formalin-fixed tissue sections of unremarkable epidermis, psoriasis, actinic keratoses (AKs), squamous cell carcinoma in situ (SCIS) and squamous cell carcinoma (SCC) were subjected to immunohistochemical staining for activated SFKs. Results:, All psoriasis specimens displayed significantly greater staining for activated SFKs than sections of unremarkable skin. In the psoriasis biopsies, the degree of epidermal hyperplasia was proportional to the level of activated SFK staining. All AKs, SCISs and SCCs exhibited more prominent staining than sections of unremarkable epidermis. No discernable difference in activated SFK staining was seen between AKs, SCIS and SCC specimens. Conclusions:, This study shows increased staining of activated SFKs in human biopsy specimens of psoriasis and cutaneous neoplasia. These data provide direct evidence for increased activation of SFKs in the pathogenesis of hyperproliferative epidermal disorders. [source]

Atypical Response of Xeroderma Pigmentosum to 5-Fluorouracil: A Histopathological Image Analysis Study Reveals New Insight into Etiopathogenesis

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005
S.A. Centurion
Xeroderma pigmentosum (XP) is a recessively inherited genodermatosis associated with extreme sun sensitivity, defective repair of several types of sunlight induced adducts in cellular DNA, and numerous, early-onset skin cancers. The dry, rough skin corresponds to progressive cytologic atypia and loss of polarity in the underlying epidermis. Associated with these changes are immune deficiencies against ultraviolet radiation-induced skin cancer. 5-Fluorouracil (5-FU) is a DNA synthesis antimetabolite used against several types of cancers. Applied topically in normal subjects it is associated with moderate to severe inflammation in areas where actinic keratoses have arisen followed by ablation of the actinic keratoses which is dependent on the inflammation. We applied 5-FU to the sun-exposed skin of two patients with XP, a 14 year-old light complected black male and a 14 year-old Caucasian female. No inflammation was observed, but marked improvement in the clinical presentation of the skin was seen, as well as an absence of new malignancies. This change was confirmed histopathologically and correlated with normalization of polarity and cytologic changes in the epidermal cells. These histologic findings were quantitated using computerized image analysis. These results may be due to activation of alternative DNA repair pathways in these nucleotide excision repair deficient cells. [source]

Activation of P44/42 Map Kinases within Human Epidermal Neoplasia.

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005
Bryon Jackson
Squamous cell carcinoma (SCC) arises from a series of genetic changes that form a clone of keratinocytes with enhanced growth characteristics. The p44/42 Map kinase pathway is a highly conserved growth regulatory pathway that helps relay critical signals from the cell membrane to the nucleus. Evidence demonstrating activation of the p44/42 pathway in the human cutaneous SCC has not been established. This study examined if p44/42 MAP kinase is activated in lesions of keratinocytic neoplasia. Lesions from the defined stages of keratinocytic neoplasia, normal skin, actinic keratoses, squamous cell carcinoma in situ, and squamous cell carcinoma, were randomly selected from archived material and studied. Antibodies that detect human p44/42 (phosphorylated and unphosphorylated) and only phosphorylated, activated, human p44/42 were used. The intensity and prevalence of cytoplasmic and nuclear staining was evaluated in the lesional cells. The results suggest that there is a not a simple linear relationship between the amount of nuclear staining and the type of lesion. The results show that there was a significant increase in the level of nuclear phosphorylated p44/42 staining progressing from an actinic keratoses to a sqaumous cell carcinoma in situ. These findings suggest that p44/42 MAP kinases are activated in keratinocytic neoplasia. [source]

Guidelines for practical use of MAL-PDT in non-melanoma skin cancer

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 5 2010
E Christensen
Abstract Methyl aminolaevulinate photodynamic therapy is increasingly practiced in the treatment of actinic keratoses, Bowen's disease and basal cell carcinomas. This method is particularly suitable for treating multiple lesions, field cancerization and lesions in areas where a good cosmetic outcome is of importance. Good treatment routines will contribute to a favourable result. The Norwegian photodynamic therapy (PDT) group consists of medical specialists with long and extensive PDT experience. With support in the literature, this group presents guidelines for the practical use of topical PDT in non-melanoma skin cancer. [source]

Topical 3.0% diclofenac in 2.5% hyaluronic acid gel induces regression of cancerous transformation in actinic keratoses

Smoking, sun exposure, number of nevi and previous neoplasias are risk factors for melanoma in older patients (60 years and over)

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 1 2010
E Nagore
Abstract Background, Malignant melanoma risk factors have been studied in different geographical area populations. However, no study has focused on risk factors which are more frequently associated to the over 60's age group. Methods, A case-control study was performed that included 160 patients age , 60 years diagnosed of cutaneous melanoma and 318 controls matched for age and sex. Both groups were assessed, by personal interview and physical examination, for different phenotype characteristics (hair and eye color, phototype), the presence of other cutaneous lesions (solar lentigines, actinic keratoses and nevi), degree and type of solar exposure and personal and family past history of cutaneous or non-cutaneous cancer. Differences were evaluated by contingency tables and univariate and multivariate logistic regression. Results, Of 17 factors, those risk factors with a strong effect on the development of melanoma in the elderly were: fair eyes, severe sunburns, years of occupational sun exposure, smoking, > 50 melanocytic nevi and personal history of NMSC and other non-cutaneous neoplasias. Conclusions, Tobacco smoking is an independent risk factor for cutaneous melanoma in the elderly. Intense (both acute and chronic) sun exposure and constitutional features, such as tumor susceptibility (NMSC, non-cutaneous neoplasias, and multiple nevi) are also associated with melanoma risk. All these factors should help to better design educational campaigns in older people. [source]

UV-induced Immunosuppression in the Balance,

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2008
Frank R. De Gruijl
Around 1980, experiments with hairless mice showed us that UV-induced actinic keratoses (AK) and ensuing skin carcinomas did not arise independently: the rate of occurrence in one skin area was increased considerably if AKs had already been induced separately in another distant skin area, i.e. a systemic effect. The ground laying work of Margaret Kripke in the 1970s provided a fitting explanation: UV-induced immunosuppression and tolerance toward the UV-induced tumors. From Kripke's work a new discipline arose: "Photoimmunology." Enormous strides were made in exploring and expanding the effects from UV carcinogenesis to infectious diseases, and in elucidating the mechanisms involved. Stemming from concerns about a depletion of the ozone layer and the general impact of ambient UV radiation, the groups I worked in and closely collaborated with explored the anticipated adverse effects of UV-induced immunosuppression on healthy individuals. An important turning point was brought about in 1992 when the group of Kevin Cooper reported that immunosuppression could be induced by UV exposure in virtually all human subjects tested, suggesting that this is a normal and sound physiological reaction to UV exposure. This reaction could actually protect us from illicit immune responses against our UV-exposed skin, such as observed in idiopathic polymorphic light eruption. This premise has fruitfully rekindled the research on this common "sun allergy," affecting to widely varying degrees about one in five Europeans with indoor professions. [source]

Cyclooxygenase-2 Expression in Murine and Human Nonmelanoma Skin Cancers: Implications for Therapeutic Approaches,

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2002
Kathy P. An
ABSTRACT Inflammatory stimuli result in the production of cutaneous eicosanoids, which are known to contribute to the process of tumor promotion. Cyclooxygenase (COX), the rate-limiting enzyme for the production of prostaglandins (PG) from arachidonic acid, exists in at least two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and plays various physiological roles, whereas increased COX-2 expression is known to occur in several types of epithelial neoplasms. Enhanced PG synthesis is a potential contributing factor in UVB-induced nonmelanoma skin cancers (NMSC). Increased COX-2 staining occurs in murine skin neoplasms after chronic exposure to carcinogenic doses of UVB. In this study, immunohistochemical and Western blot analyses were employed to assess longitudinally COX-2 expression in a standard mouse UVB complete carcinogenesis protocol and in human basal cell carcinomas (BCC) and squamous cell carcinomas (SCC). During UVB irradiation of mice, COX-2 expression consistently increased in the hyperplastic skin, the benign papillomas and the SCC. COX-2 expression was also increased in human actinic keratoses, SCC and BCC as well as in murine SCC and BCC. The pattern of COX-2 expression was quite variable, occurring in a patchy distribution in some lesions with staining confined mainly to suprabasal cell layers. In general, COX-2 expression progressively became more extensive in benign papillomas and well-differentiated murine SCC. The staining was predominantly cytoplasmic and perinuclear in some focal areas in tissue stroma around both murine and human tumors. Western blot analysis confirmed negative COX-2 expression in normal skin, whereas acute UVB exposure resulted in increased enzyme expression, which continued to increase in developing papillomas and SCC. Because of the evidence indicating a pathogenic role for eicosanoids in murine and human skin neoplasms, we performed studies to assess the anti-inflammatory and anticarcinogenic effects of green tea extracts, which are potent antioxidants. Acute exposure of the human skin to UVB (minimum erythema dose × 4) caused a transient enhancement of the COX-2 expression, which reverted to baseline within hours; however, in murine skin the expression persisted for several days. Pretreatment with the topically applied green tea extract (1 mg/cm2) largely abrogated the acute COX-2 response to UVB in mice or humans. In summary, enhanced COX-2 expression serves as a marker of epidermal UVB exposure for murine and human NMSC. These results suggest that COX-2 inhibitors could have potent anticarcinogenic effects in UVB-induced skin cancer. [source]

UV-induced immune suppression and sunscreen

PHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 3 2000
E. M. Gil
Sun protection factor (SPF) that measures sunscreen protection against erythema and edema may not be enough to measure a sunscreen's activity against many other biologic reactions induced by ultraviolet radiation (UV). It may be better to evaluate sunscreen efficacy using various tools including immune protection factor (IPF), mutation protection factor (MPF) and protection against photocarcinogenesis. In terms of immune protection, sunscreens protected against UV-induced immune suppression significantly. But protection in some cases was partial and often the IPF of sunscreens were less than the SPF. IPF may differ with various immunological endpoints, and it may be better to use a couple of different assays to measure sunscreen protection more objectively. Sunscreen use protects against most UV-induced non-melanoma skin cancers and actinic keratoses but its activity against melanoma is not clear. More studies with broad-spectrum stable sunscreens and better models for the investigation of malignant melanoma are required. [source]

Aggressive Cutaneous Squamous Cell Carcinoma Associated with Prolonged Voriconazole Therapy in a Renal Transplant Patient

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2008
A. Vanacker
A 69-year-old man, with a history of end-stage renal disease due to polyarteritis nodosa, followed by invasive pulmonary aspergillosis secondary to cyclophosphamide and corticosteroids, received a renal transplant 2 years ago under prophylactic treatment with voriconazole. Because of the severity of the aspergillosis, it was decided to continue voriconazole for a prolonged period. Eighteen months after transplantation, the patient developed a severe facial phototoxic reaction. A few months later, he developed multiple actinic keratoses and a large, rapidly expanding, poorly differentiated squamous cell carcinoma (SCC) with perineural invasion and metastatic lymph nodes, necessitating radical surgery and radiotherapy. Voriconazole therapy has been suggested to be involved in the development of multi-focal invasive SCC when complicated by a phototoxic reaction. Therefore, an alternative antifungal prophylaxis regimen (for instance with posaconazole) should be considered when evaluating patients for solid organ transplantation who are at high risk for the development of cutaneous malignancies. [source]

Photodynamic therapy of multiple actinic keratoses: reduced pain through use of visible light plus water-filtered infrared A compared with light from light-emitting diodes

BRITISH JOURNAL OF DERMATOLOGY, Issue 3 2010
V. Von Felbert
Summary Background, Photodynamic therapy (PDT) with methyl aminolaevulinate (MAL) is an effective treatment for multiple actinic keratoses (AKs). Pain, however, is a major side-effect. Objectives, To compare pain intensity, efficacy, safety and cosmetic outcome of MAL PDT with two different light sources in an investigator-initiated, randomized, double-blind study. Methods, Eighty patients with multiple AKs grade I,II were assigned to two groups: group 1, MAL PDT with visible light and water-filtered infrared A (VIS + wIRA); group 2, MAL PDT with light from light-emitting diodes (LEDs), with a further division into two subgroups: A, no spray cooling; B, spray cooling on demand. MAL was applied 3 h before light treatment. Pain was assessed before, during and after PDT. Efficacy, side-effects, cosmetic outcome and patient satisfaction were documented after 2 weeks and 3, 6 and 12 months. Where necessary, treatment was repeated after 3 months. Results, Seventy-six of the 80 patients receiving MAL PDT completed the study. Patient assessment showed high efficacy, very good cosmetic outcome and high patient satisfaction. The efficacy of treatment was better in the group of patients without spray cooling (P = 0·00022 at 3 months, P = 0·0068 at 6 months) and showed no significant differences between VIS + wIRA and LED. VIS + wIRA was significantly less painful than LED: the median of maximum pain was lower in the VIS + wIRA group than in the LED group for PDT without spray cooling. Pain duration and severity assessed retrospectively were less with VIS + wIRA than with LED, irrespective of cooling. Conclusions, All treatments showed high efficacy with good cosmetic outcome and high patient satisfaction. Efficacy of treatment was better without spray cooling. VIS + wIRA PDT was less painful than LED PDT for PDT without spray cooling. [source]