SGK1在日光性角化病、基底细胞癌及鳞状细胞癌中的表达

目的：检测SGK1在日光性角化病（AK）、基底细胞癌（BCC）及鳞状细胞癌（SCC）中的表达。方法：采用免疫组化SABC法检测SGK1在25例正常皮肤(NS)、25例AK、28例BCC、28例皮肤鳞状细胞癌标本中的表达。结果：NS、AK、BCC和SCC标本中,SGK1阳性细胞率分别为（40.03±14.42）%,（36.63±14.28）%,（52.82±18.73）%和（52.58±20.13）%。BCC组和SCC组分别与NS组比较,差异均有统计学意义（Ps<0.05）。各组SGK1染色阳性细胞率>50%的标本分别为6例（24%）,3例（12%）,16例（57.14%）和14例（50%）,BCC组和SCC组分别与NS组比较,差异均有统计学意义（Ps<0.05）。结论：SGK1的高表达可能与基底细胞癌及鳞状细胞癌的发病有关。     

日光性角化病合并鳞状细胞癌和皮角1例

日光性角化病合并鳞状细胞癌和皮角１例王爱民，成建新，刘超美，王秀清患者男，６５岁。渔民。５年前开始于右面部发生２个绿豆大小浅灰褐色斑，表面结干硬痂。近半年皮损增大明显，且表面破溃久不愈合。近２年又于右手背发生２个、左手虎口处发生１个类似的损害，尤其左...     

日光性角化病与鳞状细胞癌

日光性角化病是一种常见的皮肤癌前病变，部分病变可发展成鳞状细胞癌，而鳞状细胞癌是除恶性黑素瘤以外的最具侵袭性生长能力的皮肤恶性肿瘤。因此早期诊断和治疗甚为重要。综述日光性角化病的发病情况、可能发展为鳞状细胞癌的实验研究进展。     

Caveolin-1、Met蛋白在日光性角化病、鲍温病和皮肤鳞状细胞癌中的表达

目的：检测Caveolin-1、Met蛋白在肿瘤边缘正常皮肤、日光性角化病、鲍温病和皮肤鳞状细胞癌组织中的表达情况。方法：通过免疫组化SP法，对肿瘤边缘正常皮肤、日光性角化病(Actinic keratosis，AK)、鲍温病(Bowen's Disease，BD)、皮肤鳞状细胞癌(cutaneous squamous cell carcinoma，cSCC)标本中Caveolin-1、Met进行检测。结果：Caveolin-1在正常皮肤、AK、BD、SCC中阳性率依次为16.7%、36.8%、52.9%、78.9%，四组间采用Kruskal-wallis H秩和检验，差异具有统计学意义(P<0.05)。Met在正常皮肤、AK、BD、SCC中阳性率依次为8.3%、26.3%、58.8%、84.2%，四组间采用Kruskal-wallis H秩和检验，P<0.05，差异具有统计学意义。在cSCC组中，Caveolin-1、Met阳性表达之间呈现正相关(r=0.484,P=0.036)。结论：Caveolin-1、Met在AK、BD和cSCC细胞中表达强度与恶性程度相关，且Caveolin-1、Met可能在cSCC发生、发展中具有协同作用。     

沉默信息调节蛋白3在日光性角化病和皮肤鳞状细胞癌中的表达及意义

目的 比较沉默信息调节蛋白3(SIRT3)在正常皮肤（NS）、日光性角化病（AK）和皮肤鳞状细胞癌（cSCC）组织中的表达情况。方法 通过免疫组化SABC法检测30例NS、30例AK和28例cSCC组织标本中的SIRT3表达。结果 SIRT3在c SCC组中阳性细胞率为（60.27%±17.90）%,显著高于NS组（40.99%±14.98）%和AK组（45.31%±12.66）%。SIRT3的阳性细胞率在NS组和AK组之间的差异无统计学意义。SIRT3在NS、AK和cSCC组织中染色强阳性率分别为13.33%(4/30)、26.67%(8/12)和42.86%(12/28),cSCC组与NS组的差异有统计学意义（P<0.05）。结论 SIRT3的高表达可能与c SCC的发病机制相关。     

热休克蛋白60在鳞状细胞癌、鲍温丘疹病、日光性角化病中的表达

目的探讨热休克蛋白60(HSP60)在皮肤鳞状细胞癌(SCC)、鲍温丘疹病(BP)、日光性角化病(AK)中的表达水平,比较HSP60在SCC、BP、AK病中阳性率的表达异同,发现其相关性及意义。方法以瘤旁正常组织为对照,采用免疫组化EnVision两步法测定HSP60在皮肤SCC、BP、AK肿瘤组织中的表达情况并与正常组对照。同时将皮肤SCC组依据分化程度分为低分化和高分化两组,并进行组间的阳性率表达对照。结果 HSP60在AK、BP、SCC肿瘤组织中的阳性率均显著高于瘤旁正常组织(P0.05);三组间两两比较结果为AK=SCC=BP(P0.05),无统计学意义。SCC低分化和高分化组间无统计学意义。结论 HSP60在AK、BP、SCC中高表达。HSP60的高表达可能与SCC、AK和BP的生物行为有关。     

HSP10在皮肤鳞状细胞癌、鲍温样丘疹病和日光性角化病中的表达

目的: 检测热休克蛋白10(HSP10)在皮肤鳞状细胞癌(SCC)、鲍温样丘疹病(BP)和日光性角化病(AK)中的表达。方法:采用免疫组化EnVision法检测HSP10在皮肤SCC、BP、AK中的表达。结果: 与其周围正常皮肤表达相比,BP组有统计学意义,AK和SCC组无统计学意义。AK与BP,AK与SCC阳性率比较有统计学意义(P0.05)。结论:HSP10在BP高表达,与BP的生物学行为可能有相关性。     

Raptor、Rictor和磷酸化Akt在日光性角化病、Bowen病及鳞状细胞癌中的表达

目的:检测Raptor、Rictor和磷酸化Akt(p-Akt)在日光性角化病、Bowen病和鳞状细胞癌中的表达。方法:采用免疫组化法检测Raptor、Rictor及p-Akt(Ser473)在20例正常皮肤、20例日光性角化病、20例Bowen病及40例鳞状细胞癌中的表达。结果:Raptor在鳞状细胞癌、Bowen病和日光性角化病中的阳性表达率分别为87.50%、70.00%和60.00%,均高于正常皮肤的25.00%(均P0.05);其中低分化鳞状细胞癌中Raptor的阳性表达率为100%,高于高分化鳞状细胞癌的阳性表达率75%(P0.05)。Rictor在鳞状细胞癌、Bowen病和日光性角化病中的阳性表达率分别为80.00%、70.00%及55.00%,均高于正常皮肤阳性表达率的20%(均P0.05);p-Akt(Ser473)在鳞状细胞癌、Bowen病和日光性角化病中的阳性表达率分别为77.50%、65.00%及50.00%,而正常皮肤阳性表达率为0。鳞状细胞癌、Bowen病和日光性角化病中Rictor的阳性表达水平和p-Akt(Ser473)的阳性表达水平均呈正相关(均P0.05)。结论:Raptor、Rictor和p-Akt(Ser473)的高表达可能与日光性角化病、Bowen病和鳞状细胞癌的发生发展有关。     

Smad7在脂溢性角化病、日光性角化病及基底细胞癌中的表达

目的： 检测Smad7在脂溢性角化病、日光性角化病以及基底细胞癌中的表达。方法：对脂溢性角化病、日光性角化病及基底细胞癌标本（各30例）和30例正常标本进行免疫组化染色。结果：23例脂溢性角化病标本、23例日光性角化病标本和28例基底细胞癌标本中Smad7染色阳性,阳性细胞率分别为（31.0±23.0）%,（32.7±26.3）%和（62.6±32.1）%,均显著高于正常组织的（6.7±5.0%）。结论： Samd7可能与脂溢性角化病、日光性角化病以及基底细胞癌的发病有关。     

日光性角化病继发鲍恩病和梭形细胞鳞状细胞癌1例

患者男,59岁,农民.患者于2年前不明原因面部左颧骨处出现一带状斑疹,有瘙痒感,未诊治.近1年因反复挠抓局部形成隆起性暗红斑,并在暗红斑上出现一红色半球形肿块,局部有少量渗液及痂皮,于2009年4月8日来我院诊治.     

Caspase-3在皮肤鳞状细胞癌及光线性角化病中的表达

目的：检测Caspase-3在皮肤鳞状细胞癌及光线性角化病组织中的表达。方法： 应用免疫组化法检测16例皮肤鳞状细胞癌皮损、27例光线性角化病皮损及24例正常皮肤组织中Caspase-3蛋白的表达。结果：Caspase-3在皮肤鳞状细胞癌、光线性角化病及正常皮肤组织的表达率分别为37.50%,51.85%,79.17%,其表达含量在皮肤鳞状细胞癌、光线性角化病、正常皮肤组织逐渐增加。结论：Caspase-3蛋白表达下调可能参与皮肤鳞状细胞癌及光线性角化病的发病过程。     

Expression of p53 and p16 in actinic keratosis,bowenoid actinic keratosis and Bowen's disease

Introduction Bowen's disease (BD) and bowenoid actinic keratosis (bAK) have traditionally been differentiated according to the presence or absence of dysplasia in the follicular epithelium. p16 has been suggested to be a useful tool to make the differential diagnosis between BD and AK and as a marker of bad prognosis. Materials Five biopsies of BD, five of AK and five of bAK where stained for p53 and p16. Results All lesions showed positive immunostaining of p53, affecting to the lower two thirdss of the epidermis in BD and bAK, and only the basal layer in non‐bAK. All the BD and bAK cases were positive for p16, showing a similar immunostaining pattern, whereas no staining was observed in non‐bAK. Discussion and conclusion These findings suggest a common pathogenic mechanism for BD and bAK. bAK might have worse prognosis than AK. p16 might not be useful as a tool for differential diagnosis between AK and BD because bAK and BD show an extremely similar immunohistochemical pattern.     

Sebaceous carcinoma in association with actinic keratosis: A report of two cases with an immunohistochemical study

We report two cases of sebaceous carcinoma associated with actinic keratosis (AK) with an immunohistochemical study, which suggests the possibility that sebaceous carcinoma really does develop within AK. Case 1 had sebaceous carcinoma arising within the atrophic type AK and case 2 had sebaceous carcinoma associated with bowenoid AK in the periphery and some parts of the overlying epidermis of the lesion.     

Dermoscopic features of actinic keratosis

Actinic keratosis (AK) is a keratinocytic neoplasm that typically develops on sun‐damaged skin of elderly individuals. Only a few reports so far have described the dermoscopic diagnostic features of AK, mainly focusing on facial non‐pigmented AKs. A typical feature of facial non‐pigmented AK is a composite pattern named “strawberry pattern”, characterized by a background erythema/red pseudonetwork consisting of unfocused, large vessels located between the hair follicles, associated with prominent follicular openings surrounded by a white halo. Dermoscopic characteristics of pigmented AK on the face include multiple slate‐gray to dark‐brown dots and globules around the follicular ostia, annular‐granular pattern and brown to gray pseudonetwork. Recognizing specific dermoscopic features of AK can be useful in guiding the clinician in the differential diagnosis of AK with melanocytic skin lesions such as LM and non‐melanocytic lesions. Histopathologic examination should be performed whenever clinical and/or dermoscopic differential diagnosis is inconclusive.     

Fluorescence diagnosis in actinic keratosis and squamous cell carcinoma

Background: As different tissue types have distinct capabilities to accumulate protoporphyrin IX, fluorescence diagnosis with aminolevulinic acid‐induced porphyrins (FDAP) could be used to discriminate between different types of tissue. Previous results demonstrated higher fluorescence ratios in squamous cell carcinoma (SCC) compared with actinic keratoses (AKs). Objectives: The lesional : non‐lesional fluorescence ratio of AKs was compared with the ratio of SCC. Other factors influencing macroscopic fluorescence were also assessed, including stratum corneum thickness, which has been demonstrated to account for heterogeneous fluorescence in psoriasis and in AKs. Methods: After 1 week of keratolytic pretreatment, FDAP was performed in 13 patients with 36 lesions suspected for AK or SCC. Biopsies were taken for histopathological diagnosis and measurement of stratum corneum thickness. Results: No significant differences were found in the fluorescence ratio (lesional : non‐lesional skin) between AKs and SCCs, although macroscopic fluorescence was significantly higher in Bowen's disease and micro‐invasive SCCs. Conclusions: There could be a potential applicability of FDAP to differentiate premalignant lesions with a tendency to progress into SCC and squamous cutaneous lesions already progressing into early invasive cancer from other squamous cutaneous (pre)malignancies. The amount of hyperkeratosis, invasiveness and degree of differentiation seem to be responsible for variations in fluorescence intensity.     

From actinic keratosis to squamous cell carcinoma

Summary The development of actinic keratosis (AK) and squamous cell carcinoma (SCC) is the result of a complex sequence of events initiated by exposure to ultraviolet (UV) light. The application of sunscreens prior to sun exposure has been reported to reduce the incidence of AK. The initial damage takes place in the DNA and most of the UV-induced lesions in the DNA are repaired. However, mutations may occur as a result of base mispairing of the cell and its DNA replicate before the DNA lesion is repaired. The genes involved in the repair process are also potential UV targets. Mutations in the tumour suppressor gene p53 are a common feature of AK and SCC. The hairless mouse is the best available animal model, in which lesions resembling human AK (papillomas), keratoacanthomas and SCCs may be induced. This model of multistage carcinogenesis offers an excellent tool for mechanistic studies. The relative efficacy of UV wavelengths (action spectrum) that induce SCC has been determined using the hairless mouse as a model. The action spectrum has been extrapolated to humans skin and is recognised worldwide.