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Sci Transl Med:避无可避!炎症竟成皮肤癌“真凶”,该重视起来了!

2018-08-26 Paris,Zoe 转化医学网

有研究表明,皮肤癌发病与日光照射、电离辐射损伤、接触化学制品、病毒和灼伤等因素相关,其中长期暴露在太阳紫外线下会导致DNA突变,进而发展为皮肤癌。

导  读

有研究表明,皮肤癌发病与日光照射、电离辐射损伤、接触化学制品、病毒和灼伤等因素相关,其中长期暴露在太阳紫外线下会导致DNA突变,进而发展为皮肤癌。而在最近,由加州大学旧金山分校(UC San Francisco)和费城托马斯·杰斐逊大学(Thomas Jefferson University)的科学家领导的研究人员发现,慢性皮肤损伤慢可以通过新发现的机制触发癌症,他们的新研究发表在2018年8月22日的《科学转化医学》(Science Translational Medicine)杂志上。

以往对头颈部癌症患者的研究表明,组织炎症和癌症之间存在千丝万缕的联系,但这种联系背后的具体机制仍然不明确。为了彻底了解这种机制,Raymond Cho博士研究了一种罕见的皮肤病——隐性营养不良型大疱性表皮松解症(RDEB)。

患有RDEB的患者有时被称为“蝴蝶儿童”,他们的皮肤极其脆弱,因其缺乏结缔蛋白胶原,便使得他们的皮肤容易起水泡和疤痕,哪怕是最轻微的接触。除了以上表现外,患者还经常在生命早期在经常受伤的部位发生侵袭性鳞状细胞癌。

侵袭性鳞状细胞癌

RDEB是一种及其可怕的疼痛状态,但统计学表明,往往癌症才是导致这些患者过早死亡的关键原因。“这些患者得癌症的原因还不完全清楚,但我们发现,癌症与慢性组织损伤的相关性非常明显,因为皮肤的脆弱性是这种疾病的根源。”Raymond Cho博士在接受采访时表示。

由于RDEB非常罕见–在美国每1000万活产中大约有5个病例发生,Cho和South需要来自世界各地的研究人员组成一个联盟,从患病儿童中收集足够数量的组织样本,用于这项新的研究,包括癌变、炎症和正常组织的样本。

研究人员没有把重点放在几个与癌症相关的基因上,而是在这些样本中对基因组的整个蛋白质编码部分进行测序,从而使他们能够在发炎和癌变组织中发现基因组中明显不同于紫外线辐射引起的突变特征类型的细微DNA变异模式。

研究人员表明,这种突变模式是由一种叫做APOBEC的蛋白质引起的,这种蛋白质通常在增加细胞蛋白质的多样性方面发挥着作用,而且其抵御病毒的意义重大。在RDEB患者中,由于慢性组织炎症的发生,APOBEC似乎变得异常活跃,这导致它在整个基因组引入了突变,其中一些最终更是导致了癌症的发生。

为了验证这种解释,他们利用UCSF的Cho实验室开发的一种计算方法,排除了DNA修复的问题,因为它是许多癌症中变异水平增加的常见原因。而RDEB组织样本基因组中的突变密度模式同样表明正常的DNA修复机制在癌症发生发展中运作正常,这更加证实了RDEB患者的致癌突变仅仅是炎症和功能失调的APOBEC所致的说法。

在许多方面,癌症就像无法愈合的伤口。而新的机制解释了慢性组织损伤引起的炎症是如何导致癌症的。这将为医学界提供新的机会,以制定预防由炎症引起的癌症的措施,正如科学家们已经成功地处理了紫外线照射造成的癌症一样。

原始出处:Cho RJ1, Alexandrov LB2, den Breems NY3, et al. APOBEC mutation drives early-onset squamous cell carcinomas in recessive dystrophic epidermolysis bullosa. Sci Transl Med. 2018 Aug 22;10(455).

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    2018-09-10 bsmagic9140
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    2018-08-27 kafei

    学习了谢谢

    0

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    2018-08-26 liumin1987

    炎症和皮肤癌有关。

    0

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    2018-08-26 王秀

    学习了,涨知识了!

    0

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