组织学克隆变化——诊断发育不良的一个特征

Lewei Zhang, Tarinee Lubpairee, D. Laronde, M. Guillaud, C. MacAulay, M. Rosin
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The following histological conditions were used to defi ne such change: (1) hyperorthokeratosis; (2) hyperchromatism but no other features of dysplasia; (3) sharp margin demarcation from adjacent area by both the hyperorthokeratosis and hyperchromasia (clonal change), and (4) no prominent rete ridges, marked acanthosis or heavy infl ammation. Lesions fi tting these criteria were termed orthokeratotic lesions with no dysplasia. Methods: Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 214 patients with primary oral premalignant lesions, 194 had mild or moderate dysplasia (dysplasia group) and 20 fi t the criteria for orthokeratotic lesions without dysplasia (orthokeratotic with no dysplasia group). The two groups were compared for their cancer risks using clinical (site and toluidine blue), histological (nuclear phenotype score), and molecular criteria (loss of heterozygosity) and by outcome (progression). 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引用次数: 0

摘要

目的:组织学诊断标准用于评估发育不良的程度,从而评估癌前病变癌症进展的风险。与邻近区域明显区分的高骨质增生症和高增生症形式的克隆性变化目前不是发育不良诊断标准的一部分。本研究的目的是确定这种克隆变化是否应被视为发育不良的诊断特征。以下组织学条件用于定义这种变化:(1)高骨再生病;(2) 深染,但没有其他发育不良特征;(3) 高骨质增生症和高增生症(克隆性改变)与邻近区域的边界清晰,(4)没有突出的网嵴、明显的棘皮病或严重炎症。符合这些标准的病变称为无发育不良的角膜塑形性病变。方法:对一项基于人群的纵向研究中随访超过10年的患者进行分析。在214名原发性口腔癌前病变患者中,194名患者患有轻度或中度发育不良(发育不良组),20名患者符合无发育不良的角膜塑形病变标准(无发育不良角膜塑形组)。使用临床(部位和甲苯胺蓝)、组织学(核表型评分)和分子标准(杂合性缺失)以及结果(进展)比较两组的癌症风险。结果和结论:无发育不良的角膜矫正术组病变与发育不良病变具有相似的癌症风险(临床、组织学和分子风险)和进展时间。我们建议将克隆性改变作为诊断发育不良的标准。研究文章组织学克隆变化发育不良诊断的特征Lewei Zhang1-3*,Tarinee Lubbairee1,3,Denise M Laronde1,3,4,Martial Guillaud3,4,Calum E MacAulay3,4和Miriam P Rosin3-51不列颠哥伦比亚大学牙科学院口腔生物与医学科学系,加拿大温哥华2BC口腔活检服务,温哥华总医院,温哥华,加拿大3BC口腔癌症预防计划,BC癌症机构,加拿大温哥华4BC癌症研究中心,加拿大温哥华5生物医学生理学和运动学学院,西蒙·弗雷泽大学,加拿大伯纳比*通讯地址:Lewei Zhang,不列颠哥伦比亚大学口腔生物与医学科学系,温哥华综合医院,不列颠哥伦比亚省口腔癌症预防计划,不列颠哥伦比亚癌症机构,加拿大不列颠哥伦比亚省温哥华威斯布鲁克购物中心2199号,V6T 1Z3,电话:+1-604-875-4318/778-387-3885;电子邮件:leweizhang888@gmail.com提交:2017年9月23日批准:2018年8月27日发布:2018年08月28日版权所有:©2018张L等。这是一篇根据知识共享署名许可证分发的开放获取文章,该许可证允许在任何媒体上不受限制地使用、分发和复制,前提是正确引用原作
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Histological clonal change - A feature for dysplasia diagnosis
Aims: Histological diagnostic criteria are used for the assessment of the degree of dysplasia and hence the risk of cancer progression for premalignant lesions. Clonal changes in the form of hyperorthokeratosis and hyperchromasia that are sharply demarcated from adjacent areas are not currently part of the criterion for dysplasia diagnosis. The objective of this study was to determine whether such clonal change should be regarded as a diagnostic feature for dysplasia. The following histological conditions were used to defi ne such change: (1) hyperorthokeratosis; (2) hyperchromatism but no other features of dysplasia; (3) sharp margin demarcation from adjacent area by both the hyperorthokeratosis and hyperchromasia (clonal change), and (4) no prominent rete ridges, marked acanthosis or heavy infl ammation. Lesions fi tting these criteria were termed orthokeratotic lesions with no dysplasia. Methods: Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 214 patients with primary oral premalignant lesions, 194 had mild or moderate dysplasia (dysplasia group) and 20 fi t the criteria for orthokeratotic lesions without dysplasia (orthokeratotic with no dysplasia group). The two groups were compared for their cancer risks using clinical (site and toluidine blue), histological (nuclear phenotype score), and molecular criteria (loss of heterozygosity) and by outcome (progression). Results and conclusions: The lesions from orthokeratotic with no dysplasia group showed a similar cancer risk (clinical, histological and molecular risk) and time to progression as the dysplastic lesions. We recommend that the clonal change should be included as a criterion for dysplasia diagnosis. Research Article Histological clonal change A feature for dysplasia diagnosis Lewei Zhang1-3*, Tarinee Lubpairee1,3, Denise M Laronde1,3,4, Martial Guillaud3,4, Calum E MacAulay3,4 and Miriam P Rosin3-5 1Department of Oral Biological and Medical Sciences, Faculty of Dentistry, the University of British Columbia (BC), Vancouver, Canada 2BC Oral Biopsy Service, Vancouver General Hospital, Vancouver, Canada 3BC Oral Cancer Prevention Program, BC Cancer Agency, Vancouver, Canada 4BC Cancer Research Centre, Vancouver, Canada 5School of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, Canada *Address for Correspondence: Lewei Zhang, Department of Oral Biological and Medical Sciences, Faculty of Dentistry, University of British Columbia, BC Oral Biopsy Service, Vancouver General Hospital, BC Oral Cancer Prevention Program, BC Cancer Agency, 2199 Wesbrook Mall, Vancouver BC, Canada, V6T 1Z3, Tel: +1-604-875-4318 / 778-387-3885; Email: leweizhang888@gmail.com Submitted: 23 September 2017 Approved: 27 August 2018 Published: 28 August 2018 Copyright: © 2018 Zhang L, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
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