Asian-American variants of human papillomavirus 16 and risk for cervical cancer:: a case-control study
Asian-American variants of human papillomavirus 16 and risk for cervical cancer:: a case-control study
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DOI：
10.1093/jnci/93.17.1325
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发表时间：
2001-09-05
影响因子：
10.3
通讯作者：
Madrigal-de la Campa, A
中科院分区：
文献类型：
--
作者：
Berumen, J;Ordoñez, RM;Madrigal-de la Campa, A
人乳头瘤病毒16型（HPV16）有多种变体，每种变体都有不同的地理分布，其中一些变体与浸润性肿瘤的相关性更强。我们研究了墨西哥宫颈癌的高发病率（每10万女性中有50例）是否可能与致癌性HPV16变体的高流行率有关。
方法：从181例宫颈癌患者和181例年龄匹配的对照受试者（均来自墨西哥城）采集宫颈样本。通过E6/E7基因特异性聚合酶链反应检测HPV16，并通过对E6和L1/MY基因区域进行测序来确定HPV变体的类别和亚类。还收集了临床数据和肿瘤特征数据。所有统计检验均为双侧检验。
结果：在50.8%（181例中的92例）的宫颈癌患者的宫颈刮片中检测到HPV16，在11%（181例中的20例）的对照受试者中检测到HPV16。除1例外，所有HPV16阳性样本都包含欧洲（E）或亚裔美国人（AA）变体。在病例患者中发现AA和E变体的频率明显高于对照受试者（AA = 23.2%[181例中的42例]；E = 27.1%[181例中的49例]），而在对照受试者中（AA = 1.1%[181例中的2例]；E = 10%[181例中的18例]）（对于E或AA变体，病例与对照受试者相比，P <.001，卡方检验）。然而，癌症患者中AA变体的频率比对照受试者高21倍，而E变体的该比率仅为2.7（P =.006，卡方检验）。与AA变体相关的宫颈癌优势比（OR）（OR = 27.0；95%置信区间[CI] = 6.4至113.7）高于与E变体相关的优势比（OR = 3.4；95%CI = 1.9至6.0）。AA阳性病例患者（46.2±12.5岁[均值±标准差]）比E阳性病例患者（53.9±12.2岁）年轻7.7岁（P =.004，学生t检验）。AA变体与鳞状细胞癌和腺癌相关，而E变体仅与鳞状细胞癌相关（P =.014，费舍尔精确检验）。
结论：HPV16 AA变体的高频率出现，且似乎比E变体更具致癌性，这可能是墨西哥宫颈癌高发病率的原因之一。
Human papillomavirus 16 (HPV16) has a number of variants, each with a different geographic distribution and some that are associated more often with invasive neoplasias. We investigated whether the high incidence of cervical cancer in Mexico (50 cases per 100 000 women) may be associated with a high prevalence of oncogenic HPV16 variants. Methods: Cervical samples were collected from 181 case patients with cervical cancer and from 181 age-matched control subjects, all from Mexico City. HPV16 was detected with an E6/E7 gene-specific polymerase chain reaction, and variant HPV classes and subclasses were identified by sequencing regions of the E6 and L1/MY genes. Clinical data and data on tumor characteristics were also collected. All statistical tests were two-sided. Results: HPV16 was detected in cervical scrapes from 50.8% (92 of 181) of case patients and from 11% (20 of 181) of control subjects. All HPV16-positive samples, except one, contained European (E) or Asian-American (AA) variants. AA and E variants were found statistically significantly more often in case patients (AA = 23.2% [42 of 181]; E = 27.1% [49 of 181]) than in control subjects (AA = 1.1% [two of 181]; E = 10% [18 of 181]) (P < .001 for case versus control subjects for either E or AA variants, chi (2) test). However, the frequency of AA variants was 21 times higher in cancer patients than in control subjects, whereas that ratio for E variants was only 2.7 (P = .006, chi (2) test). The odds ratio (OR) for cervical cancer associated with AA variants (OR = 27.0; 95% confidence interval [CI] = 6.4 to 113.7) was higher than that associated with E variants (OR = 3.4; 95% CI = 1.9 to 6.0). AA-positive case patients (46.2 +/- 12.5 years [mean +/- standard deviation]) were 7.7 years younger than E-positive case patients (53.9 +/- 12.2 years) (P = .004, Student's t test). AA variants were associated with squamous cell carcinomas and adenocarcinomas, but E variants were associated with only squamous cell carcinomas (P = .014, Fisher's exact test). Conclusions: The high frequency of HPV16 AA variants, which appear to be more oncogenic than E variants, might contribute to the high incidence of cervical cancer in Mexico.