Kahn JA.. HPV vaccination for the prevention of cervical intraepithelial neoplasia. N Engl J Med 361: 271-278

Division of Adolescent Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
New England Journal of Medicine (Impact Factor: 55.87). 08/2009; 361(3):271-8. DOI: 10.1056/NEJMct0806938
Source: PubMed


A sexually active 18-year-old woman presents to her internist for an annual examina- tion. During the review of her family history, she notes that her mother recently re- ceived a diagnosis of "pre-cervical cancer" and underwent a loop electrosurgical exci- sion procedure. The patient's mother has advised her to get the "cervical-cancer shot." Should this patient receive a human papillomavirus (HPV) vaccine, and how effective would vaccination be in preventing cervical cancer? The Clinical Problem Genital HPV infection is usually acquired through sexual contact and is extremely common. In a nationally representative study of women in the United States, 25% of persons between the ages of 14 and 19 years and 45% of persons between the ages of 20 and 24 years were HPV-positive.1 It is estimated that more than 80% of both men and women in the United States will be infected with HPV at some point in their lives.2 HPV is often acquired within months after the first sexual intercourse: in a study of university women who had recently had sexual intercourse for the first time and reported having only one partner, almost 30% became HPV-positive within 1 year.3 Although HPV infection is usually asymptomatic, anogenital warts or can- cers or other HPV-associated cancers develop in a subgroup of infected women and men. The clinical outcome of greatest significance for public health is cervical cancer. Globally, cervical cancer is the second most frequent cancer among women; each year, approximately 490,000 women receive this diagnosis and 270,000 die from cervical cancer.4 In the United States, the implementation of cytologic screening programs with the Papanicolaou (Pap) test has led to a decrease in rates of cervical cancer, since screening identifies precancerous cervical lesions that can be treated before they prog- ress to cancer. Despite such screening, in 2008, approximately 11,000 women in the United States received a diagnosis of cervical cancer and 3900 died from the disease.5 The direct medical costs associated with the prevention and treatment of HPV- related anogenital warts and cervical disease in the United States are estimated to be $4.0 billion annually,6 and productivity losses due to deaths from cervical can- cer are estimated to be $1.3 billion annually.7

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    • "Preinvasive lesions of cervical cancer have also been classified in terms of squamous intraepithelial lesions (SILs). Cervical cancer is considered to be a preventable disease because of its relatively long period of precancerous lesions, such as cervical intraepithelial neoplasia (CIN) [4]. Several cytokines that modulate the immunologic response have been implicated in the development of cervical cancer [5]–[7]. "
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    ABSTRACT: Tumor necrosis factor- alpha (TNF-α) is an inflammatory cytokine which may play important role on the immune response may control the progression of cervical lesions. There is a possible association between TNF-α rs1800629 G/A polymorphism and cervical lesions, but previous studies report conflicting results. We performed a meta-analysis to comprehensively assess the association between TNF-α rs1800629 polymorphism and cervical lesions risk. Literature searches of Pubmed, Embase, Web of Science, and Wanfang databases were performed for all publications on the association between TNF-α rs1800629 polymorphism and cervical lesions through December 15, 2012. The pooled odds ratios (ORs) with their 95% confidence interval (95%CIs) were calculated to assess the strength of the association. Twenty individual case-control studies from 19 publications with a total of 4,146 cases and 4,731 controls were finally included into the meta-analysis. Overall, TNF-α rs1800629 polymorphism was significantly associated with increased risk of cervical lesions under two main genetic comparison models (For A versus G: OR 1.22, 95%CI 1.04-1.44, P = 0.017; for AA versus GG: OR 1.32, 95%CI 1.02-1.71, P = 0.034). Subgroup analysis by ethnicity further showed that there was a significant association between TNF-α rs1800629 polymorphism and increased risk of cervical lesions in Caucasians but not in Asians. Subgroup analysis by the types of cervical lesions showed that there was a significant association between TNF-α rs1800629 polymorphism and increased risk of cervical cancer (For A versus G: OR 1.24, 95%CI 1.05-1.47, P = 0.011; for AA versus GG: OR 1.31, 95%CI 1.01-1.70, P = 0.043; for AA/GA versus GG: OR 1.25, 95%CI 1.01-1.54, P = 0.039). The meta-analysis suggests that TNF-α rs1800629 polymorphism is associated with increased risk of cervical lesions, especially in Caucasians.
    PLoS ONE 08/2013; 8(8):e69201. DOI:10.1371/journal.pone.0069201 · 3.23 Impact Factor
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    • "Therefore, HPV vaccines might also be a potential value in the prevention of OSCC. It is reported that, the HPV vaccines, which prevent infection with the HPV16/18 that cause 70% of cervical cancer, may lead to further decrease [35], [36]. Up to now, the definite effectiveness of the HPV vaccine in preventing OSCC has kept unknown. "
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    ABSTRACT: Previous studies indicated that oral squamous cell carcinomas (OSCC) might be related to human papilloma virus (HPV) infection. However, up to now, there still lacks a large sample study to analyze the relationship between OSCC in a Chinese population and oral HPV infection. In the present study, we used a meta-analysis to evaluate the relationship of OSCC with HPV infection in a Chinese population. The reports on HPV and OSCC in a Chinese population published between January, 1994, and September, 2011 were retrieved via CNKI/WANFANG/OVID/MEDLINE databases. According to the inclusion criteria, we selected 18 eligible case-control studies. After testing the heterogeneity of the studies by the Cochran Q test, the meta-analyses for HPV and HPV16 were performed using the fixed effects model. The overall positive rates of HPV and HPV16 in OSCC were 58.0% (354/610; 95% confidence interval [CI], 54.1-61.9) and 47.47% (169/356; 95% CI: 42.3-52.7), respectively; which were significantly higher than those in normal controls 10.44% (26/249; 95% CI: 7.2-14.7) and 7.1% (13/182; 95% CI: 4.2-11.8). Quantitative meta-analysis revealed that, compared with normal controls, the combined odds ratios of OSCC with HPV or HPV16 infection were 12.7 (95% CI: 8.0-20.0) and 9.0 (95% CI: 5.1-15.6), respectively. Both Begg's test and funnel plots revealed that no publication bias was found in this present study (P>0.05). High incidences of HPV infection (mainly involving HPV16) were found in the samples of Chinese OSCC. For the Chinese population, HPV infection elevates the risk of OSCC tumorigenesis. Prophylactic HPV-vaccination may reduce the burden of HPV-related OSCC in China.
    PLoS ONE 05/2012; 7(5):e36294. DOI:10.1371/journal.pone.0036294 · 3.23 Impact Factor
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    • "Indeed, the miR-17-92 cluster has complex pro-and antitumorigenic roles under different cellular conditions (Mendell, 2008). It is known that the percentage of spontaneous regression decreases as CIN stages develop (Kahn, 2009), yet the reasons are not clear. Our results suggest that the gradual increasing levels of miR-133b from CIN 2 to invasive cervical carcinoma and the strong tumorigenic functions of miR-133b are likely to be a cellular factor contributing to this decreasing regression rate. "
    W Qin · P Dong · C Ma · K Mitchelson · T Deng · L Zhang · Y Sun · X Feng · Y Ding · X Lu · J He · H Wen · J Cheng ·
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    ABSTRACT: We report that elevated microRNA-133b (miR-133b) acts as an oncogene in human cervical carcinoma to promote tumorigenesis and metastasis. In situ hybridization confirmed that miR-133b is localized in proliferating human cervical carcinoma cells with levels progressively elevating throughout advancing stages. Cellular studies showed that miR-133b enhances cell proliferation and colony formation by targeting mammalian sterile 20-like kinase 2 (MST2), cell division control protein 42 homolog (CDC42) and ras homolog gene family member A (RHOA), which subsequently results in activation of the tumorigenic protein kinase B alpha (AKT1) and mitogen-activated protein kinase (ERK1 and ERK2, here abbreviated as ERK) signaling pathways. Mouse experiments revealed that upregulation of miR-133b in cervical carcinoma cells strongly promotes both in vivo tumorigenesis and independent metastasis to the mouse lung. The data indicates that upregulation of miR-133b shortens the latency of cervical carcinoma. Together, these findings suggest that miR-133b could be a potent marker for the early onset of cervical carcinoma.
    Oncogene 12/2011; 31(36):4067-75. DOI:10.1038/onc.2011.561 · 8.46 Impact Factor
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