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本文引用的文献

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Evidence of ultraviolet type mutations in xeroderma pigmentosum melanomas.着色性干皮病黑色素瘤中紫外线类型突变的证据。
Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6279-84. doi: 10.1073/pnas.0812401106. Epub 2009 Mar 27.
2
The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis.原发性和转移性黑色素瘤的基因表达谱产生了肿瘤进展和转移的一个转变点。
BMC Med Genomics. 2008 Apr 28;1:13. doi: 10.1186/1755-8794-1-13.
3
Epidemiology of melanoma in Puerto Rico, 1987-2002.1987 - 2002年波多黎各黑色素瘤的流行病学
P R Health Sci J. 2007 Dec;26(4):343-8.
4
Polymorphisms in the DNA repair genes XPC, XPD, and XPG and risk of cutaneous melanoma: a case-control analysis.DNA修复基因XPC、XPD和XPG的多态性与皮肤黑色素瘤风险:一项病例对照分析。
Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2526-32. doi: 10.1158/1055-9965.EPI-06-0672.
5
Melanoma.黑色素瘤
N Engl J Med. 2006 Jul 6;355(1):51-65. doi: 10.1056/NEJMra052166.
6
Reconstructing the population history of Puerto Rico by means of mtDNA phylogeographic analysis.通过线粒体DNA系统地理学分析重建波多黎各的人口历史。
Am J Phys Anthropol. 2005 Sep;128(1):131-55. doi: 10.1002/ajpa.20108.
7
UV dose determines key characteristics of nonmelanoma skin cancer.紫外线剂量决定了非黑素瘤皮肤癌的关键特征。
Cancer Epidemiol Biomarkers Prev. 2004 Dec;13(12):2006-11.
8
Some geographical aspects of the mortality from melanoma in Europeans.欧洲人黑色素瘤死亡率的一些地理特征。
Med J Aust. 1956 Jun 30;43(26):1082-7.
9
DNA repair and nonmelanoma skin cancer in Puerto Rican populations.波多黎各人群中的DNA修复与非黑色素瘤皮肤癌
J Am Acad Dermatol. 2003 Sep;49(3):433-9. doi: 10.1067/s0190-9622(03)00918-6.
10
Repair of UV light-induced DNA damage and risk of cutaneous malignant melanoma.紫外线诱导的DNA损伤修复与皮肤恶性黑色素瘤风险
J Natl Cancer Inst. 2003 Feb 19;95(4):308-15. doi: 10.1093/jnci/95.4.308.

在长期暴露于高强度阳光的人群中,DNA修复能力在皮肤黑素瘤风险中的作用。

The role of DNA repair capacity in melanoma skin cancer risk in a population chronically exposed to high levels of sunlight.

作者信息

Matta Jaime L, Rodriguez Giovanna, Villa Jaime, Ruiz Abigail

出版信息

Ochsner J. 2010 Summer;10(2):75-82.

PMID:21603361
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3096198/
Abstract

Puerto Rican residents are exposed to some of the highest levels of environmental ultraviolet radiation in the world; paradoxically, the melanoma incidence in Puerto Rico is lower than that of the US mainland. The overall objective of this case-control pilot study was to test the hypotheses that (1) persons with melanoma have a significantly lower DNA repair capacity (DRC) in relation to controls matched by age, (2) decline in DRC is associated with vertical depth of melanoma invasion, and (3) DRC is associated with anatomical tumor location. Controls (n  =  124) were examined by dermatologists; cases (n  =  62) were histopathologically confirmed. The mean DRC ± 1 SE of controls was 6.46% ± 0.3. Melanoma patients (n  =  62) had a mean decrease in DRC of 3% (6.25% ± 0.5), which was not statistically different from controls (P  =  0.697). No significant differences in DRC were evident in participants with either in situ or malignant melanoma tumors; neither were such differences evident when evaluating anatomical location of tumors (ie, non-sun-exposed versus sun-exposed). DRC generally declined in participants with increased depth of melanoma tumor penetration when compared with controls and those with small in situ tumors. These findings should be examined in a larger-scale population study that includes participants with more advanced metastatic melanoma.

摘要

波多黎各居民暴露于世界上一些最高水平的环境紫外线辐射中;矛盾的是,波多黎各的黑色素瘤发病率低于美国本土。本病例对照试点研究的总体目标是检验以下假设:(1)与年龄匹配的对照组相比,黑色素瘤患者的DNA修复能力(DRC)显著更低;(2)DRC的下降与黑色素瘤侵袭的垂直深度相关;(3)DRC与肿瘤的解剖位置相关。对照组(n = 124)由皮肤科医生进行检查;病例组(n = 62)经组织病理学确诊。对照组的平均DRC±1个标准误为6.46%±0.3。黑色素瘤患者(n = 62)的DRC平均下降3%(6.25%±0.5),与对照组相比无统计学差异(P = 0.697)。原位或恶性黑色素瘤肿瘤患者的DRC均无明显差异;在评估肿瘤的解剖位置(即非阳光暴露部位与阳光暴露部位)时也无此类差异。与对照组和原位小肿瘤患者相比,黑色素瘤肿瘤浸润深度增加的参与者的DRC通常会下降。这些发现应在一项更大规模的人群研究中进行检验,该研究纳入更多晚期转移性黑色素瘤患者。