Disseminated superficial actinic porokeratosis: a clinical study

Disseminated superficial actinic porokeratosis is an autosomal dominant condition that requires sun exposure for full expression. It affects only sun-exposed areas, with relative sparing of the face. In sun-damaged skin of Australians disseminated superficial actinic porokeratosis is commonly mistaken for solar keratosis. Twenty-nine subjects with disseminated superficial actinic porokeratosis were involved in an extensive questionnaire and clinical study. The distribution of lesions was charted on all subjects, with a mean count of 268 lesions per subject. We found no evidence that skin cancer had arisen in disseminated superficial actinic porokeratosis lesions. A review of the etiologic and clinical features of disseminated superficial actinic porokeratosis also is presented.     

Microarray analysis of aberrant gene expression in actinic keratosis: effect of the Toll-like receptor-7 agonist imiquimod

BACKGROUND: The molecular events leading to actinic keratosis (AK) are not well understood. OBJECTIVE: To identify and compare gene expression changes in AK lesions and in sun-exposed nonlesional skin and to determine the effect of imiquimod 5% cream on these changes. METHOD: A double-blind, vehicle-controlled, randomized study was conducted to evaluate the molecular changes in AK treated with imiquimod. Seventeen male subjects with >/= 5 AK lesions on the scalp applied vehicle or imiquimod three times a week for 4 weeks. Gene expression analysis using Affymetrix oligonucleotide arrays was performed on shave biopsies of lesions taken before and after treatment. Confocal microscopy was performed on the study area as an adjunctive diagnostic procedure. RESULTS: We identified gene expression changes which occur in sun-exposed, nonlesional skin as well as in AK lesions. These changes include, but are not limited to, the overexpression of oncogenic and proliferative genes and diminished expression of tumour suppressor genes. The gene expression changes observed in AK lesions and in sun-exposed, nonlesional skin were consistent with the confocal microscopy observations, which showed abnormalities in the sun-exposed, nonlesional skin, similar in nature but less pronounced than abnormalities seen in AK. Imiquimod partially or totally reversed the aberrant expression of some of the genes observed in AK, consistent with clearing of lesions and normalization of confocal cellular images. CONCLUSIONS: The data show that profound gene expression changes occur in sun-exposed, nonlesional skin which progress further in AK lesions. The data also suggest that imiquimod may play a role in normalizing gene expression and cellular morphology in sun-damaged skin.     

光线性角化病159例与皮肤鳞状细胞癌51例临床病理特征分析

目的了解滇东地区光线性角化病与鳞状细胞癌的疾病构成比、一般情况和临床病理特征。方法采用回顾性研究方法对曲靖市第一人民医院皮肤科2014年1月-2018年12月共5年行病理检查确诊的光线性角化病和皮肤鳞状细胞癌患者的临床和病理检查资料进行分析。结果159例光线性角化病(AK)与51例(SCC)鳞状细胞癌患者中女性多于男性,光线性角化病和鳞状细胞癌的发病平均年龄分别为(66.32±14.63)岁和(65.00±16.26)岁。光线性角化病和鳞状细胞癌患者皮损发生于曝光部位的分别占98.11%和78.43%。51例鳞状细胞癌患者中,有3例均是光线性角化病继发鳞状细胞癌,均为女性,年龄均>70岁,发病部位均为曝光部位。5年确诊光线性角化病患者占总病检患者的构成比相对稳定,其中鳞状细胞癌有所波动。AK病理分型分为肥厚型98例(61.64%)、萎缩型26例(16.35%)、棘层松解型12例(7.55%)、色素型9例(5.66%)、苔藓样型9例(5.66%)、鲍温样型5例(3.14%);SCC病理分级Ⅰ级39例(76.47%)、Ⅱ级11例(21.57%)、Ⅲ级1例(1.96%)、Ⅳ级0例。光线性角化病与鳞状细胞癌中临床诊断与病理诊断符合率分别为61.00%和56.86%,易被误诊为其他疾病。结论滇东地区光线性角化病与鳞状细胞癌以中老年女性为主,主要位于头面颈部等曝光部位,与紫外线关系密切,其中发生于曝光部位、皮损多样、病程长的老年女性光线性角化病患者易继发鳞状细胞癌,但临床病理诊断符合率较低,需引起重视。     

Contribution to characterization of skin field cancerization activity: morphometric,chromatin texture,proliferation, and apoptosis aspects

BackgroundA skin field cancerization is a cutaneous area with subclinical changes resultant from chronic sun exposure, with a higher predisposition to development of pre-neoplastic and neoplastic lesions. So far, there are no well-defined objective parameters that can indicate their degree of activity.ObjectivesTo describe and compare morphometric aspects and expression of factors related to apoptosis and cell proliferation in actinic keratosis (AK), in both photoexposed and photoprotected epidermis.MethodsA cross-sectional study of patients with actinic keratosis in the forearms, biopsied at two points: the actinic keratosis and the axillary region. The biopsies of the actinic keratosis, perilesional area, and axilla were evaluated through keratinocyte intraepithelial neoplasia (KIN), and immunohistochemistry of p53, survivin, and Ki67. Nuclear morphometry of basal layer cells was performed through digital image analysis: entropy, area, perimeter, Ra, fractal dimension, circularity, color intensity, and largest diameter.ResultsThere were 13 patients included and 38 actinic keratosis biopsied. In morphometry, 1039 nuclei were analyzed, of which 228 represented axillary skin, 396 demonstrated actinic keratosis, and 415 represented the perilesional area to the actinic keratosis. There was a significant difference (p < 0.05) in all variables tested for the topographies evaluated. A significant correlation was identified between nucellar morphometric elements, KIN, proliferation markers, and apoptosis. Joint patterns of p53, Ki67, and KIN discriminated the topographies sampled.Study limitationsThis was a cross-sectional study with a small number of patients.ConclusionsThere are patterns of proliferation, resistance to apoptosis, and different cellular morphometrics between photoprotected skin and photoexposed skin. The joint expression of p53, Ki67, and KIN can characterize skin field cancerization activity.     

Lewandowsky and lutz dysplasia: report of two cases in a family

Lewandowsky and Lutz dysplasia, also known as epidermodysplasia verruciformis (EV), is an inherited disorder in which there is widespread and persistent infection with human papilloma virus, defect in cell-mediated immunity and propensity for malignant transformation. Differential clinical and histopathologic evolutions of lesions in two cases of familial EV are compared and discussed in detail. Cases were followed up for 7 years. Detailed history, clinical features and investigations, including skin biopsy from different sites at different times, were examined. Generalized pityriasis versicolor like hypopigmented lesions in both the cases, together with variable pigmented nodular actinic keratosis like lesions on sun-exposed areas, were present. Multiple skin biopsies done from various sites on different occasions revealed features typical of EV along with lesions, i.e., actinic keratosis, Bowen's disease, basal and squamous cell carcinoma, in the elder sibling. However, skin biopsy of the other sibling showed features of EV and seborrheic keratosis only till date. This study reveals that the disease progression is variable among two individuals of the same family. Malignant lesions were seen only on sun-exposed areas and may be associated with other skin lesions or infections such as angiokeratoma of Fordyce and tinea cruris, as seen in this report.     

Prevalence of solar damage and actinic keratosis in a Merseyside population

This study examines the prevalence of sun-related damage to the skin in a caucasian population in north-west England. The importance of constitutional factors (complexion, skin type and age) as well as environmental and occupational exposures for the development of actinic keratosis (AK) and skin cancers was assessed in people over 40 years of age attending outpatient clinics (non-dermatology) at four centres in north-west England (Mersey region). Nine hundred and sixty-eight volunteers (531 men and 437 women) were recruited. The overall prevalence of AK was 15.4% in men and 5.9% in women. The prevalence was strongly related to age in both sexes, being 34.1% and 18.2%, respectively, in men and women aged 70 years and above, and was most strongly related to two objective signs of sun exposure, namely degree of solar elastosis and presence of solar lentigines. The prevalence of AK was higher in subjects with red hair and freckles, particularly women. There was no evidence of an increased prevalence of AK in relation to any occupation. There was a high prevalence of seborrhoeic keratosis and viral warts in both sexes, which was age-related in the case of seborrhoeic keratosis. Ten cases of basal cell carcinoma, eight cases of Bowen's disease and one case of malignant melanoma were identified. This study shows that the sun exposure received in 'normal' life in England is sufficient to cause potentially malignant skin damage in a significant proportion of the population.     

Clinical, histopathological and immunohistochemical assessment of human skin field cancerization before and after photodynamic therapy

Summary Background The field cancerization concept in photodamaged patients suggests that the entire sun‐exposed surface of the skin has an increased risk for the development of (pre)‐malignant lesions, mainly epithelial tumours. Topical photodynamic therapy (PDT) is a noninvasive therapeutic method for multiple actinic keratosis (AK) with excellent outcome. Objectives To evaluate the clinical, histological and immunohistochemical changes in human skin with field cancerization after multiple sessions of PDT with methylaminolaevulinate (MAL). Methods Twenty‐six patients with photodamaged skin and multiple AK on the face received three consecutive sessions of MAL‐PDT with red light (37 J cm^?2), 1 month apart. Biopsies before and 3 months after the last treatment session were taken from normal‐appearing skin on the field‐cancerized area. Immunohistochemical stainings were performed for TP‐53, procollagen‐I, metalloproteinase‐1 (MMP‐1) and tenascin‐C (Tn‐C). Results All 26 patients completed the study. The global score for photodamage improved considerably in all patients (P < 0·001). The AK clearance rate was 89·5% at the end of the study. Two treatment sessions were as effective as three MAL‐PDT sessions. A significant decrease in atypia grade and extent of keratinocyte atypia was observed histologically (P < 0·001). Also, a significant increase in collagen deposition (P = 0·001) and improvement of solar elastosis (P = 0·002) were noticed after PDT. However, immunohistochemistry showed only a trend for decreased TP‐53 expression (not significant), increased procollagen‐I and MMP‐1 expressions (not significant) and an increased expression of Tn‐C (P = 0·024). Conclusions Clinical and histological improvement in field cancerization after multiple sessions of MAL‐PDT is proven. The decrease in severity and extent of keratinocyte atypia associated with a decreased expression of TP‐53 suggest a reduced carcinogenic potential of the sun‐damaged area. The significant increase of new collagen deposition and the reduction of solar elastosis explain the clinical improvement of photodamaged skin.     

Environmental and occupational skin diseases in Taiwan.

This presentation focuses on the four most important skin diseases in Taiwan thought to be of environmental and/or occupational origin. The majority of work-related dermatoses are contact dermatitis patients. Among occupational contact dermatitis patients, 58.5% involved irritant and 41.5%, allergic dermatitis. Electronics, hairdressing, medical practice, and construction were the most important occupations causing contact dermatitis. An endemic occurrence of chronic arsenism causing hyperpigmentation, keratosis, and cancer has been reported in Taiwan. Arsenical skin cancers present as multiple lesions at different disease stages. The skin cancers are usually found in non-sun-exposed areas. UVB exerts an inhibitory effect on the proliferation of arsenical cancers; this may explain its non-sun-exposed nature. An outbreak of premalignant and malignant skin lesions was reported among paraquat manufacturers in 1985. The skin lesions were mainly distributed over the sun-exposed areas. Photodamage and photocarcinogenesis revealed a strong association with exposure to bipyridines among paraquat manufacturers. In 1979, a mass poisoning occurred in Taiwan from cooking oil contaminated by polychlorinated biphenyls (PCBs). Over 60% of patients were in grades O-II by the Japanese classification. The blood PCB levels of the Taiwanese patients were found to be higher than those of the Yusho subjects.     

Increased expression of an epidermal stem cell marker, cytokeratin 19, in cutaneous squamous cell carcinoma

Background Cytokeratin 19 (CK19) has been considered to be a putative marker for epidermal stem cells in the hair follicle bulge. Cumulative reports have shown that epidermal stem cells play an important role in skin carcinogenesis. However, to date there has been no report on the clinical alteration of the stem cells in squamous cell carcinoma (SCC). Objectives To investigate alteration of the stem cells and proliferating cells and to assess their relationship and potential contribution to SCC. Methods Thirty paraffin‐embedded neoplastic skin lesions, consisting of 10 cases each of actinic keratosis (AK), Bowen disease (BD) and SCC, were examined immunohistologically for CK19 and Ki‐67. Results Positive reactivity for CK19 was seen in 30% of AK, 50% of BD and 80% of SCC lesions. There was significantly higher expression levels of CK19 in SCC than in AK and BD (P < 0·05). In addition, BD lesions harboured a significantly higher number of CK19‐positive cells than did AK lesions (P < 0·05). There were significant differences in Ki‐67 labelling indices between AK and BD and between AK and SCC (P < 0·001), but not between BD and SCC (P > 0·05). Furthermore, a serial section comparison study showed that there was a minor population of cells co‐expressing CK19 and Ki‐67 in a subset of the tumour cells of SCC samples. The percentage of CK19+ cells significantly correlated with that of Ki67+ cells in all examined neoplastic skin lesions. Conclusions These results suggest that CK19 expression may be associated with the retention of stem cell characteristics or a state that is uncommitted to terminal squamous differentiation.     

Clinical comparison of actinic changes preceding squamous cell carcinoma vs. intraepidermal carcinoma in renal transplant recipients

Intraepidermal carcinoma (IEC) is a type of in situ squamous cell carcinoma (SCC), although progression of IEC is rare. We sought to investigate differences between the actinic skin changes preceding the development of both SCC and IEC. Photographs of 63 skin sites at which either SCC or IEC subsequently developed in 37 renal transplant recipients (RTRs) were examined for features of actinic change. We found that areas of skin with an actinic keratosis (AK) > 1 cm² in size were four times more likely to develop SCC as opposed to IEC (OR = 4.42; 95% CI 1.25–15.60). Skin sites with ≥ 25% of the area affected by AK were again four times more likely to develop SCC than IEC. These results highlight the scale of visible actinic damage required for development of SCC compared with IEC, emphasizing the importance of treating areas of skin with marked visible actinic change to reduce SCC risk in RTRs.     

Reduction in lesions from Lmax: a new concept for assessing efficacy of field-directed therapy for actinic keratosis. Results with imiquimod 3.75%

Background

Current parameters for assessing the efficacy of actinic keratosis (AK) treatments compare clinical lesions at the start and end of a study. However, the sun-exposed field also contains subclinical lesions which may become detectable during treatment. Lmax, the maximum lesion count during treatment, is a new concept to better assess the efficacy of field-directed AK therapies. Measuring efficacy using the reduction in lesions from Lmax includes for the first time the clearance of both subclinical and clinical lesions.

Objectives

To evaluate the reduction of lesions from Lmax to study end and compare the results with traditional efficacy endpoints using imiquimod 3.75% (IQ3.75%) as an example of field-directed AK therapy.

Materials & Methods

Pooled analysis of data from two 14-week, vehicle-controlled, double-blind studies of IQ3.75%.

Results

With IQ3.75%, the median number of lesions increased from 10 at baseline to an Lmax of 22. The median absolute reduction in lesions to study end was 18 from Lmax versus 7 from baseline. The median percentage reduction in AK lesions to study end was 92.2% from Lmax compared with 81.8% from baseline.

Conclusions

The reduction in lesion count from Lmax is a novel efficacy parameter that should become the new way of evaluating field-directed AK therapies since it enables their efficacy against both clinical and subclinical lesions to be accurately determined. Together, the Lmax concept and IQ3.75% represent a newapproach for the management ofAKacross a large sun-exposed field.

     

Differential expression of ezrin in epithelial skin tumors: cytoplasmic ezrin immunoreactivity in squamous cell carcinoma

Background Ezrin is a cytoskeleton linker protein that is actively involved in regulating the growth and metastatic capacity of cancer cells. The purpose of the study was to assess the expression pattern of ezrin in normal skin and various epithelial neoplasms. Methods We used immunohistochemical techniques to examine the expression of ezrin in paraffin‐embedded tissues of squamous cell carcinoma (n = 23), basal cell carcinoma (n = 10), Bowen’s disease (n = 10), actinic keratosis (n = 10), keratoacanthoma (n = 9), seborrheic keratosis (n = 5), psoriasis vulgaris (n = 5), and normal control skin (n = 5). Results In Bowen’s disease, actinic keratosis, keratoacanthoma, and seborrheic keratosis, ezrin was dominantly expressed in the cell membrane except for the cornified layer. In squamous cell carcinoma (SCC) specimens, the percentage of ezrin‐positive cells was increased compared with Bowen’s disease, actinic keratosis, keratoacanthoma, and seborrheic keratosis. Especially in SCC samples, ezrin expression was markedly expressed in the cytoplasm. In addition, there was a correlation between the pattern of ezrin expression and tumor differentiation in SCC. Basal cell carcinoma showed intense and diffuse staining especially in the solid growth pattern. Conclusions Our findings suggest that dysregulation of ezrin may be important in the development of cutaneous epithelial malignancies and tumor grade. We suggest that the cytoplasmic localization of ezrin may be useful in the diagnosis of skin SCC.     

XERODERMA PIGMENTOSUM VARIANT: DNA PLOIDY ANALYSIS OF VARIOUS SKIN TUMORS AND NORMAL-APPEARING SKIN IN A PATIENT

Background. The patient with xeroderma pigmentosum provides an appropriate human model for the evaluation of tumor development and progression. Methods. We describe a patient with variant-type xeroderma pigmentosum who developed actinic keratoses, a squamous cell carcinoma, and its metastasis into a lymph node. DNA ploidy was measured and analyzed in cells of these tumors and the patient's sun-exposed as well as sun-shielded skin. Results. The sun-shielded skin showed a normal diploid dna distribution pattern, while the sun-exposed skin had an increased number of hyperdiploid cells. The actinic keratosis showed further increased hyperdiploid cells. The squamous cell carcinoma showed a large number of hyperdiploid cells and formed an aneuploid cell fraction. Histographically, the aneuploid cell fraction became more apparent and was revealed to be a major fraction in the metastatic squamous cell carcinoma. Conclusions. The changes in the DNA ploidy pattern well reflect the clinical and histologic characteristics of the respective skin conditions and likely provide the cellular basis for the sequential or stepwise carcinogenic process in the patient's xeroderma pigmentosum skin. Further studies are necessary to determine whether the present results explain the similar carcinogenic process in sun-damaged skin of the nonpredisposed general population.     

Case-based experience in the use of 5-fluorouracil cream 0.5% as monotherapy and in conjunction with glycolic acid peels for the treatment of actinic keratosis

Abstract

Actinic keratosis, commonly indicative of photodamage, requires treatment secondary to the risk of progression to squamous cell carcinoma. A number of effective treatments for actinic keratosis are available, including topical and lesion-directed therapies. While lesion-directed therapies such as cryotherapy are appropriate for isolated lesions, topical 5-fluorouracil is an effective modality for the treatment of multiple facial actinic keratoses. 5-Fluorouracil, available in a number of formulations, offers patients the benefit of treating subclinical lesions and may help to improve the overall appearance of the skin. In many cases, combination therapy is a better treatment option than monotherapy. The cases presented here demonstrate the use of topical 5-fluorouracil cream 0.5% as monotherapy and in conjunction with glycolic acid peels to treat facial actinic keratoses in two patients with extensive histories of prior actinic keratosis and skin cancer.     

Comparative study for the effect of photodynamic therapy,imiquimod immunotherapy and combination of both therapies on 40 lesions of actinic keratosis in Japanese patients

We treated 12, 15 and 13 Japanese actinic keratosis (AK) lesions with 5‐aminolevulinic acid photodynamic therapy (PDT), 5% imiquimod cream and combination of both therapies, respectively, and compared the effects. Patients underwent the second course, when AK lesions remained after the first course. Efficacy was evaluated 1 month after each treatment. Combination therapy cleared all AK lesions only after the first course, while PDT and imiquimod therapy cleared 41.7% and 66.7% of AK lesions after the first course, respectively. All residual AK lesions after the first course were cleared by the second courses of PDT or imiquimod therapy. During the course, erosion and crust developed significantly more frequently in combination therapy (P < 0.001). Most Japanese AK lesions can be satisfactorily treated with either PDT or imiquimod monotherapy. However, only severe cases may better be treated with combination therapy, which show higher efficacy even though adverse events occur frequently.     

Viral DNA detection and RAS mutations in actinic keratosis and nonmelanoma skin cancers

Background Actinic keratosis (AK) is a well‐established precancerous skin lesion that has the potential to progress to squamous cell carcinoma (SCC). Basal cell carcinoma (BCC) is a locally aggressive slowly growing tumour that rarely metastasizes. A number of viruses have been proposed to play a role in the development of nonmelanoma skin cancers (NMSC), but the most plausible evidence to date suggests that cutaneous human papillomavirus (HPV) is the key instigating factor. Objectives To evaluate the prevalence of HPV, cytomegalovirus (CMV), herpes simplex virus (HSV) and Epstein–Barr virus (EBV) and investigate their relationship with the presence of RAS gene mutations in cutaneous lesions obtained from nonimmunosuppressed patients. Methods HPV, CMV, HSV and EBV detection was performed using polymerase chain reaction (PCR) in skin biopsies (26 AK, 12 SCC and 15 BCC samples) that were collected from immunocompetent patients. The RAS mutation incidence was also investigated in all cutaneous lesions by use of PCR/restriction fragment length polymorphism and direct DNA sequencing. Results Seventeen out of 53 (32%) skin lesions were found to be positive for HPV DNA. The highest incidences of HPV infection were five of 15 (33%) in BCC and four of 12 (33%) in SCC specimens. The HPV incidence was eight of 26 (31%) in AK and eight of 53 (15%) in normal skin tissue. Twelve out of 53 (23%) skin lesions were CMV‐positive. The highest incidence of CMV infection was six of 15 (40%), observed in BCC specimens. The CMV incidence was two of 26 (8%) in AK and four of 12 (33%) in SCC. No normal skin biopsy was found to be positive for CMV. All cutaneous samples were negative for HSV and EBV DNA, as assessed by our PCR‐based assays. Only three samples, one AK (4%), one BCC (6%) and one SCC (8%), were found to carry a G>T transversion at the second position of HRAS codon 12. Both HRAS mutant SCC and BCC biopsies were HPV‐ and CMV‐positive, as well. Conclusions HPV DNA is detected in NMSC, AK and normal skin biopsies. Our results also indicate that CMV is involved in NMSC at higher levels than in premalignant lesions, whereas the virus was not detected in normal skin biopsies. HSV and EBV do not appear to be involved in the pathogenesis of cutaneous lesions. Moreover, we suggest that the HRAS codon 12 mutation is not a very common event in AK or NMSC. Finally, both viral infection and HRAS activation appear to represent independent factors in the aetiology of NMSC, samples of which were obtained from immunocompetent patients.     

The influence of the location of the lesion on the absolute risk of the development of skin cancer in a patient with actinic keratosis

The objective of this paper is to answer the clinical question whether the location of the lesion in an individual patient with actinic keratosis (AK) influences the absolute risk of the development of skin cancer. Between 0.025% and 16% of AK lesions advance towards squamous cell carcinoma per year. It is not well known whether this risk differs between locations on the body. A systematic search of available literature resulted in seven articles of which the two highest scoring on relevance and validity were selected. These two studies indicate that the absolute risk on the development of skin cancer in patients with AK differs between locations of the lesion and that time to progression from AK to squamous cell carcinoma is not different among the locations of the lesions. However, both studies have very limited sample sizes.     

Imaging actinic keratosis by high‐definition optical coherence tomography. Histomorphologic correlation: a pilot study

With the continued development of non‐invasive therapies for actinic keratosis such as PDT and immune therapies, the non‐invasive diagnosis and monitoring become increasingly relevant. High‐definition optical coherence tomography is a high‐resolution imaging tool, with micrometre resolution in both transversal and axial directions, enable to visualize individual cells up to a depth of around 570 μm filling the imaging gap between conventional optical coherence tomography and reflectance confocal microscopy. We sought to determine the feasibility of detecting and grading of actinic keratosis by this technique using criteria defined for reflectance confocal microscopy compared to histology. In this pilot study, skin lesions of 17 patients with a histologically proven actinic keratosis were imaged by high‐definition optical coherence tomography just before excision and images analysed qualitatively. The surrounding normal looking skin has been used as control group. In lesional skin, dyskeratotic and atypical keratinocytes could be noticed with this new technique. An atypical honeycomb pattern in variable degree or a disarranged epidermal pattern could be observed. A good correlation between the dimension of atypia and/or disarrangement of the spinous–granular layer on en face images and the histopathological grading could be demonstrated. Relevant cross‐sectional imaging criteria could be defined for the different histopathological variants of actinic keratoses. The surrounding skin displayed features of photodamage. Using features already suggested by reflectance confocal microscopy, the study implies that high‐definition optical coherence tomography facilitates in vivo diagnosis of actinic keratosis and allows the grading of different actinic keratosis lesions for increased clinical utility.     

紧密连接蛋白Claudin-1、7在日光性角化病和皮肤鳞状细胞癌中的表达

目的：检测紧密连接蛋白Claudin-1、7在日光性角化病(AK)和皮肤鳞状细胞癌（SCC）中的表达水平。方法：收集2014年11月至2016年11月我院病理科AK和SCC组织标本各30例,选取癌旁正常皮肤组织30例作为对照组,采用免疫组化方法检测癌旁正常表皮、AK和SCC组织中Claudin-1、7蛋白的表达。结果：对照组、AK和SCC组织中Claudin-1蛋白细胞阳性率分别为100%,53.33%和13.33%,三组两两比较,差异均有统计学意义(Ps<0.05)。Claudin-7在癌旁正常表皮、AK和SCC组织中均呈阴性表达。结论：Claudin-1蛋白在癌旁正常表皮、AK和SCC组织中表达水平逐渐下降,Claudin-1蛋白表达下调可能与表皮肿瘤的恶性转化有关。