六个基因与缺乏和熟练的DNA修复个体的临床表型相关。

Translational oncogenomics Pub Date : 2008-02-10
Tobias Gremmel, Susanne Wild, Winfried Schuller, Viola Kürten, Klaus Dietz, Jean Krutmann, Mark Berneburg
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引用次数: 0

摘要

着色性干皮病(XP)是一种遗传性疾病,其特征是色素沉着不足/过度,对紫外线(UV)辐射的敏感性增加,皮肤癌风险增加2000倍。xp患者的细胞在负责修复紫外线诱导的DNA损伤的核苷酸切除修复(NER)中存在缺陷。这种缺陷解释了他们的突变表型,但并不能预测他们患皮肤癌的风险增加。因此,我们对来自三个不同临床严重程度的互补组(XP- a、XP- d、XP- f)的XP细胞以及DNA修复正常但皮肤癌风险增加(年龄≥2例基底细胞癌或鳞状细胞癌)的患者进行了阵列分析,测量了1000多个基因在uvb照射后的表达
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Six genes associated with the clinical phenotypes of individuals with deficient and proficient DNA repair.

Xeroderma pigmentosum (XP) is a genetic disorder characterised by hypo-/hyperpigmentation, increased sensitivity to ultraviolet (UV)-radiation and an up to 2000-fold increased skin cancer risk. Cells from XP-patients are defective in nucleotide excision repair (NER) responsible for repair of UV-induced DNA damage. This defect accounts for their mutator phenotype but does not predict their increased skin cancer risk. Therefore, we carried out array analysis to measure the expression of more than 1000 genes after UVB-irradiation in XP cells from three complementation groups with different clinical severity (XP-A, XP-D, XP-F) as well as from patients with normal DNA repair but increased skin cancer risk (≥2 basal or squamous cell carcinoma at age <40yrs). Of 144 genes investigated, 20 showed differential expression with p < 0.05 after irradiation of cells with 100 mJ/cm(2) of UVB. A subset of six genes showed a direct association of expression levels with clinical severity of XP in genes affecting carcinogenesis relevant pathways. Genes identified in XP cells could be confirmed in cells from patients with no known DNA repair defects but increased skin cancer risk. Thus, it is possible to identify a small gene subset associated with clinical severity of XP patients also applicable to individuals with no known DNA repair defects.

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