口腔黏膜上皮癌变过程中内皮素Ⅰ表达的定量研究

目的 了解正常口腔黏膜,癌前病变及癌组织中内皮素I(ET-I)表达特点及其变化规律。方法采用免疫组化和图象分析技术,对人正常口腔黏膜(NOR)10例、口腔黏膜下纤维化(OSF)10例、鳞状细胞癌(SCC)15例上皮细胞的ET-I含量进行图像分析。结果 ①ET-I在OSF、OLK、SCC组织中的表达增强,阳性物质主要位于上皮棘细胞、基质细胞的胞浆胞膜上,且ET-I含量显著高于正常对照组(p<0.01)。②OLK、SCC上皮细胞ET-I含量呈显著增加趋势(p<0.05)。③OSF上皮细胞ET-I含量显著高于OLK(p<0.05),与SCC相比无显著性差异(p>0.05)。结论 ET-I含量在口腔癌前病变至癌变过程中可能存在一种量变关系,OSF中ET-I过量表达可能提示其上皮细胞的癌变潜能。     

Review of high‐risk features of cutaneous squamous cell carcinoma and discrepancies between the American Joint Committee on Cancer and NCCN Clinical Practice Guidelines In Oncology

Cutaneous squamous cell carcinoma (SCC) is a malignancy that arises from epidermal keratinocytes. Although the majority of cutaneous SCC cases are easily treated without further complication, some behave more aggressively and carry a poor prognosis. These “high‐risk” cutaneous SCCs commonly originate in the head and neck and have an increased tendency toward recurrence, local invasion, and distant metastasis. Factors for high‐risk cutaneous SCC include large size (>2 cm), a deeply invasive lesion (>2 mm), incomplete excision, high‐grade/desmoplastic lesions, perineural invasion (PNI), lymphovascular invasion, immunosuppression, and high‐risk anatomic locations. Both the National Comprehensive Cancer Network^® (NCCN^®) and the American Joint Committee on Cancer (AJCC) identify several of these high‐risk features of cutaneous SCC. The purpose of this article was to review the high‐risk features included in these guidelines, as well as their notable discrepancies and omissions. We also provide a brief overview of current prophylactic measures, surgical options, and adjuvant therapies for high‐risk cutaneous SCC. © 2016 Wiley Periodicals, Inc. Head Neck 39: 578–594, 2017     

鳞状上皮细胞癌抗原检测在宫颈鳞癌中的临床意义

目的：探讨血清鳞状上皮细胞癌相关抗原（SCC—Ag）检测在宫颈鳞癌中的临床意义。方法：用全自动化学发光分析仪检测107例不同临床分期宫颈鳞癌患者血清SCC—Ag的含量,并与对照组进行对比分析。结果：SCC-Ag阳性率随临床分期进展而增高,不同分组之间呈显著性差异（P〈0．01）。SCC—Ag在宫颈鳞癌的表达与临床分期有关（P〈0．01）。结论：SCC—Ag是宫颈鳞癌较特异的肿瘤标志物,对宫颈鳞癌的辅助诊断、治疗效果及预后的判断有较大的价值。     

Association between epstein barr virus and tongue squamous cell carcinoma in iranian patients

Detection of Epstein-Barr virus in oral squamous cell carcinoma suggests its involvement in the carcinogenesis of oral cavity. But, there are few studies on the incidence of EBV genome in squamous cell carcinomas at specific locations in the oral cavity like tongue and with different tumor progression. In this study the presence of EBV genome in tongue Squamous Cell Carcinoma (TSCC) in Iranian patients were investigated. Accordingly, a total of 94 cases with TSCC were firstly analyzed for the presence of viral genome through Nested PCR. Patients were divided into different groups based on their gender and the size, nodal involvement, grade and stage of their tumor. Results showed the presence of EBV genome in 72.3% of TSCCs with no significant difference between two genders, although slightly higher in females. Interestingly, PCR products of EBV genome showed a statistically significant higher distribution in TSCCs at IVa stage (p = 0.04), while a considerable low involvement of EBV genome was seen in T1-sized tumors. The result of this study further emphasizes the role of EBV in oral SCCs – mainly at tongue. This is the first investigation to clarify the association between EBV genome and different tumor size and stage in TSCCs; however, more studies in different regions and larger populations should be performed to be able to draw a firmed conclusion.     

Current thinking in management of the neck (including contralateral neck) in ipsilateral recurrent or second primary oral squamous cell carcinoma

Metastasis to the neck in patients with oral squamous cell carcinoma (SCC) has a huge impact on long-term survival and prognosis, and its incidence varies. Due consideration therefore should be given to management of the neck in each individual case. The pathways in patients with primary oral SCC are well-established, but there is a paucity of published papers on management of the neck in those with ipsilateral recurrent or second primary oral SCC whose necks have previously been operated on with or without radiotherapy or chemoradiotherapy, or treated with radiotherapy or chemoradiotherapy alone. These patients may be under treated because of failure to stage the most likely drainage site, and are likely to have a worse outcome if there is macroscopic recurrence in the neck after independent treatment of the recurrent or second primary tumour. Based on the current review, we think there is a need for a multicentre, collaborative, retrospective review of the outcomes of patients with ipsilateral second primaries or recurrent oral SCC in the previously treated neck. Our recommendations include consideration of positron emission tomography-computed tomography in all patients with recurrent or second primary oral SCC (if “hot” – neck dissection, if “cold” - sentinel node biopsy); consideration of sentinel node biopsy in all patients with recurrent or second primary oral SCC who have previously had treatment to the neck; and finally, consideration of definitive management of the sentinel biopsy zone or region if the node is invaded.     

Photodynamic therapy with topical methyl‐ and hexylaminolevulinate for prophylaxis and treatment of UV‐induced SCC in hairless mice

Please cite this paper as: Photodynamic therapy with topical methyl‐ and hexylaminolevulinate for prophylaxis and treatment of UV‐induced SCC in hairless mice. Experimental Dermatology 2010; 19 : e166–e172. Abstract Background: Hexyl aminolevulinate (HAL) is a long‐chained 5‐aminolevulinic acid‐ester that has been proposed as a novel photosensitizing agent to methyl aminolevulinate (MAL) in topical photodynamic therapy (PDT). The more lipophilic HAL, may improve treatment outcome for non‐melanoma skin cancer. Objective: To compare the prophylactic and therapeutic effects of HAL‐ and MAL‐PDT for ultraviolet‐induced squamous cell carcinomas (SCCs) in hairless mice. Methods: Mice (n = 249) were irradiated with solar UV‐radiation (UVR) until SCC occurred. Before any skin changes developed, two prophylactic PDT treatments were given, using creams of HAL (2%, 6%, 20%) or MAL (20%) followed by illumination (632 nm, Aktilite, Photocure). Two therapeutic PDT‐treatments were given by randomization to the first developed SCC of 1 mm. Primary end‐points were time to first SCC of 1 mm and complete SCC clearance. Secondary end‐points were time to SCC‐recurrence, PpIX fluorescence and skin reactions to PDT. Results: The median time to first SCC was significantly longer for mice treated with prophylactic HAL‐PDT (2%, 6% and 20% HAL, 264 days) and MAL‐PDT (20% MAL, 269 days) than mice exposed to UVR (186 days) and UVR + placebo‐PDT (199 days) (P < 0.0001). The therapeutic efficacy of HAL‐ and MAL‐PDT showed cure rates of 23–61.5% (P = 0.11). Similar PpIX fluorescence intensity and severity of clinical reactions were seen for HAL‐ and MAL‐groups, although mice developed more intense hyper‐pigmentation when treated with 20% MAL‐PDT compared with 2% HAL‐PDT. Conclusions: PDT with HAL (2%, 6% and 20%) and MAL (20%) is equally effective to prevent and treat UV‐induced SCC in hairless mice.     

HPV-16 viral load in oropharyngeal squamous cell carcinoma using digital PCR

Conclusions: We did not identify any strong associations between HPV-16 viral load and any of the clinical or lifestyle factors.

Objective: The epidemiology of oropharyngeal SCC is changing, with an increasing proportion of HPV-positive cases seen in the last decade. It is known that a high viral load is linked to the development of cervical cancer, the relation between viral load and oropharyngeal SCC is less clear. We sought to determine HPV-16 viral load in HPV-positive oropharyngeal SCCs using highly sensitive digital PCR and to identify clinical and lifestyle factors associated with viral load.

Subjects and methods: We analysed 45 HPV-16 positive oropharyngeal SCCs diagnosed between 2013 and 2015. All patients completed a lifestyle questionnaire and clinical data were extracted from medical charts. Viral load was determined using digital PCR assays for HPV-L1 and RNAseP.

Results: We found large variations in HPV-16 viral load from 1 to 930 copies per cell (median 34 copies per cell).