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SV40在人类癌症中起作用吗?

Is there a role for SV40 in human cancer?

作者信息

Poulin Danielle L, DeCaprio James A

机构信息

Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.

出版信息

J Clin Oncol. 2006 Sep 10;24(26):4356-65. doi: 10.1200/JCO.2005.03.7101.

DOI:10.1200/JCO.2005.03.7101
PMID:16963733
Abstract

The question of whether Simian Virus 40 (SV40) can cause human tumors has been one of the most highly controversial topics in cancer research during the last 50 years. The longstanding debate began with the discovery of SV40 as a contaminant in poliovirus vaccine stocks that were used to inoculate approximately 100 million children and adults in the United States between 1955 and 1963, and countless more throughout the world. Concerns regarding the potential health risk of SV40 exposure were reinforced by studies demonstrating SV40's potential to transform human cells and promote tumor growth in animal models. Many studies have attempted to assess the relationship between the potential exposure of humans to SV40 and cancer incidence. Reports of the detection of SV40 DNA in a variety of cancers have raised serious concerns as to whether the inadvertent inoculation with SV40 has led to the development of cancer in humans. However, inconsistent reports linking SV40 with various tumor types has led to conflicting views regarding the potential of SV40 as a human cancer virus. Several recent studies suggest that older detection methodologies were flawed, and the limitations of these methods could account for most, if not all, of the positive correlations of SV40 in human tumors to date. Although many people may have been exposed to SV40 by polio vaccination, there is inadequate evidence to support widespread SV40 infection in the population, increased tumor incidence in those individuals who received contaminated vaccine, or a direct role for SV40 in human cancer.

摘要

在过去50年里,猿猴病毒40(SV40)是否会引发人类肿瘤的问题一直是癌症研究中最具争议的话题之一。这场长期的争论始于1955年至1963年间在美国用于接种约1亿儿童和成人的脊髓灰质炎疫苗库存中发现SV40作为污染物,在全世界范围内接种的人数更是不计其数。关于接触SV40潜在健康风险的担忧因多项研究而加剧,这些研究表明SV40在动物模型中有转化人类细胞并促进肿瘤生长的潜力。许多研究试图评估人类潜在接触SV40与癌症发病率之间的关系。在多种癌症中检测到SV40 DNA的报告引发了严重担忧,即意外接种SV40是否导致了人类癌症的发生。然而,将SV40与各种肿瘤类型联系起来的报告不一致,导致了关于SV40作为人类癌症病毒潜力的相互矛盾的观点。最近的几项研究表明,早期的检测方法存在缺陷,这些方法的局限性可以解释迄今为止SV40在人类肿瘤中大多数(如果不是全部)的正相关关系。尽管许多人可能通过脊髓灰质炎疫苗接种接触过SV40,但没有足够的证据支持人群中广泛存在SV40感染、接种受污染疫苗的个体肿瘤发病率增加或SV40在人类癌症中起直接作用。

相似文献

1
Is there a role for SV40 in human cancer?SV40在人类癌症中起作用吗?
J Clin Oncol. 2006 Sep 10;24(26):4356-65. doi: 10.1200/JCO.2005.03.7101.
2
Polio vaccines, Simian Virus 40, and human cancer: the epidemiologic evidence for a causal association.脊髓灰质炎疫苗、猴病毒40与人类癌症:因果关联的流行病学证据
Oncogene. 2004 Aug 23;23(38):6535-40. doi: 10.1038/sj.onc.1207877.
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Poliovirus vaccination during pregnancy, maternal seroconversion to simian virus 40, and risk of childhood cancer.孕期脊髓灰质炎疫苗接种、孕妇血清转化为猴病毒40以及儿童患癌风险
Am J Epidemiol. 2004 Aug 15;160(4):306-16. doi: 10.1093/aje/kwh219.
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Simian virus 40, poliovirus vaccines, and human cancer: research progress versus media and public interests.猿猴病毒40、脊髓灰质炎病毒疫苗与人类癌症:研究进展与媒体及公众利益
Bull World Health Organ. 2000;78(2):195-8.
5
Some oral poliovirus vaccines were contaminated with infectious SV40 after 1961.1961年后,一些口服脊髓灰质炎疫苗被具有传染性的猿猴空泡病毒40污染。
Cancer Res. 2005 Nov 15;65(22):10273-9. doi: 10.1158/0008-5472.CAN-05-2028.
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Simian virus 40 (SV40)-like DNA sequences not detectable in finnish mesothelioma patients not exposed to SV40-contaminated polio vaccines.在未接触过受猴病毒40型(SV40)污染的脊髓灰质炎疫苗的芬兰间皮瘤患者中未检测到SV40样DNA序列。
Mol Carcinog. 1999 Oct;26(2):93-9.
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Potential exposure to SV40 in polio vaccines used in Sweden during 1957: no impact on cancer incidence rates 1960 to 1993.1957年瑞典使用的脊髓灰质炎疫苗中潜在的SV40暴露:对1960年至1993年癌症发病率无影响。
Dev Biol Stand. 1998;94:227-33.
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Association of SV40 with human tumours.猴空泡病毒40(SV40)与人类肿瘤的关联。
Semin Cancer Biol. 2001 Feb;11(1):49-61. doi: 10.1006/scbi.2000.0346.
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Does simian virus 40 cause non-Hodgkin lymphoma? A review of the laboratory and epidemiological evidence.猿猴病毒40会引发非霍奇金淋巴瘤吗?实验室及流行病学证据综述。
Cancer Invest. 2005;23(6):529-36. doi: 10.1080/07357900500202820.
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J Natl Cancer Inst. 2004 Sep 15;96(18):1368-74. doi: 10.1093/jnci/djh266.

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