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DNA修复与基底细胞癌的流行病学

DNA repair and epidemiology of basal cell carcinoma.

作者信息

Grossman L, Wei Q

机构信息

Department of Biochemistry, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205, USA.

出版信息

Clin Chem. 1995 Dec;41(12 Pt 2):1854-63.

PMID:7497645
Abstract

In a molecular epidemiological study of DNA repair, host reactivation assay was used to measure the DNA repair capacity of cryopreserved lymphocytes from 88 primary basal cell carcinoma (BCC) patients and 135 cancer-free controls. In this study population, reduced repair of ultraviolet radiation-induced DNA damage contributed to the risk of sunlight-induced BCC. A family history of BCC is associated with low DNA repair. Repair of ultraviolet radiation-damaged DNA declines at a rate of approximately 1%/year in noncancerous controls. Reduced DNA repair is more likely seen in young BCC patients, indicating that BCC is a premature aging disease of the skin. The persistence of photochemical damage because of reduced repair results in point mutations in the p53 gene and allelic loss of the nevoid BCC gene located on chromosome 9q. Xeroderma pigmentosum appears to be a valid paradigm for the role of DNA repair in BCC in the general population.

摘要

在一项DNA修复的分子流行病学研究中,采用宿主细胞复活试验来检测88例原发性基底细胞癌(BCC)患者和135例无癌对照者冻存淋巴细胞的DNA修复能力。在该研究人群中,紫外线诱导的DNA损伤修复能力降低会增加日光性BCC的发病风险。BCC家族史与低DNA修复能力相关。在非癌对照者中,紫外线损伤DNA的修复能力以每年约1%的速率下降。DNA修复能力降低在年轻BCC患者中更为常见,这表明BCC是一种皮肤过早老化疾病。由于修复能力降低导致的光化学损伤持续存在,会引起p53基因的点突变以及位于9号染色体q臂上的痣样基底细胞癌基因的等位基因缺失。着色性干皮病似乎是DNA修复在普通人群BCC中作用的一个有效范例。

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