...
首页> 外文期刊>The Journal of investigative dermatology. >Communications: high dermal mast cell prevalence is a predisposing factor for basal cell carcinoma in humans.
【24h】

Communications: high dermal mast cell prevalence is a predisposing factor for basal cell carcinoma in humans.

机译:交流:皮肤上肥大细胞的高患病率是人类基底细胞癌的诱因。

获取原文
获取原文并翻译 | 示例

摘要

Ultraviolet B radiation (280-320 nm) can initiate skin cancer as well as suppress the immune system, thereby preventing the rejection of ultraviolet-B-induced tumors. Recently we reported that there was not only a correlation but also a functional link between dermal mast cell prevalence and susceptibility to ultraviolet-B-induced systemic immunosuppression in multiple strains of mice. In this study, we investigated whether increased dermal mast cell prevalence is a significant predisposing factor for basal cell carcinoma development in humans. In 21 Danes with a history of basal cell carcinoma and 20 control subjects of similar age, sex, skin phototype, and recreational sun exposure over the past 12 mo, dermal mast cell prevalence was quantified on non-sun-exposed buttock skin. We investigated this skin site in order to avoid any changes in mast cell prevalence caused by sun exposure and assumed that the prevalence of mast cells in buttock skin correlated with that at sun-exposed sites at critical times in the development of basal cell carcinomas. Patients with a history of basal cell carcinoma had a significantly higher median dermal mast cell prevalence than control subjects (p = 0.01, Mann-Whitney U ). No correlation was observed between dermal mast cell prevalence and age of basal cell carcinoma patients and control subjects. These results suggest that increased dermal mast cell prevalence is a predisposing factor for basal cell carcinoma development in humans. We hypothesize that mast cells function in humans, as in mice, by initiating immunosuppression and thereby allowing a permissive environment for basal cell carcinoma development.
机译:紫外线B辐射(280-320 nm)可以引发皮肤癌并抑制免疫系统,从而防止紫外线B诱导的肿瘤被排斥。最近我们报道,在多种小鼠品系中,皮肤肥大细胞患病率与对紫外线-B诱导的全身免疫抑制的敏感性之间不仅存在关联,而且存在功能联系。在这项研究中,我们调查了增加的皮肤肥大细胞患病率是否是人类基底细胞癌发展的重要诱因。在过去12个月内有21名具有基底细胞癌病史的丹麦人和20名年龄,性别,皮肤照片类型和休闲性阳光照射类似的对照受试者中,未受阳光照射的臀部皮肤的皮肤肥大细胞患病率得到了定量。我们调查了这个皮肤部位,以避免由日光照射引起的肥大细胞患病率发生任何变化,并假设臀部皮肤中肥大细胞的患病率与基础细胞癌发展过程中关键时刻阳光照射部位的患病率相关。有基底细胞癌病史的患者的皮肤肥大细胞中位数患病率明显高于对照组(p = 0.01,Mann-Whitney U)。真皮肥大细胞患病率与基底细胞癌患者和对照组年龄之间没有相关性。这些结果表明增加的皮肤肥大细胞患病率是人类基底细胞癌发展的诱因。我们假设肥大细胞通过启动免疫抑制在人类中发挥作用,就像在小鼠中一样,从而为基底细胞癌的发展提供了一个宽松的环境。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号