2015
DOI: 10.1016/j.cgh.2014.12.018
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Does Human Papillomavirus Cause Esophageal Adenocarcinoma?

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Cited by 3 publications
(2 citation statements)
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“…The estimated prevalence of HPV in EAC (12%) is slightly lower than the estimate from a previous systematic review containing only 5 studies (35%) and the estimated prevalence within esophageal squamous cell carcinoma (22.2%). The prevalence is also considerably lower than previous estimates of the prevalence of HPV infection in squamous cell carcinoma of the uterine cervix and adenocarcinoma of the uterine cervix (~83.5%) [59], indicating that should any causal role in EAC exist, it is likely to be less dominant than the role of HPV in cervical cancer [60]. A less dominant role is perhaps to be expected as the orogenital transmission route may be particularly limited for lower parts of the esophagus, where EAC is common.…”
Section: Discussioncontrasting
confidence: 58%
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“…The estimated prevalence of HPV in EAC (12%) is slightly lower than the estimate from a previous systematic review containing only 5 studies (35%) and the estimated prevalence within esophageal squamous cell carcinoma (22.2%). The prevalence is also considerably lower than previous estimates of the prevalence of HPV infection in squamous cell carcinoma of the uterine cervix and adenocarcinoma of the uterine cervix (~83.5%) [59], indicating that should any causal role in EAC exist, it is likely to be less dominant than the role of HPV in cervical cancer [60]. A less dominant role is perhaps to be expected as the orogenital transmission route may be particularly limited for lower parts of the esophagus, where EAC is common.…”
Section: Discussioncontrasting
confidence: 58%
“…A comparison within studies assessing HPV prevalence in samples from individuals with EAC and individuals free from cancer using the same methodology suggested the prevalence of HPV was significantly higher in EAC samples. This adds to research not included in the review which found that HPV viral load was increased along the dysplasia-metaplasia-adenocarcinoma pathway [61], and found that persistence of HPV after ablation for BE was associated with dysplasia [60,62]. In addition, evidence from HPV transgenic mouse models indicates these mice are more susceptible to esophageal cancer [63].…”
Section: Discussionmentioning
confidence: 98%