Human papillomavirus not detected in esophageal adenocarcinoma tumor specimens

Antonsson, Annika; Knight, Lani; Whiteman, David C.

doi:10.1016/j.canep.2016.01.014

Cited by 25 publications

(17 citation statements)

References 14 publications

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“…While the association between HPV and EC remains under discussion despite all evidences (Antonsson et al , 2016), the etiological role of BPV in EC is well established (Borzacchiello et al , 2003). EC in cattle is a self-limiting disease, being directly associated to BPV-4 infection (Borzacchiello et al , 2003; Masuda et al , 2011).…”

Section: Bpv-associated Malignant Neoplasmsmentioning

confidence: 99%

“…Scarce epidemiological data about EC in cattle are available. In humans, EC has a variable incidence according to geographic area (Bjørge et al , 1997; Syrjänen, 2002; Guo et al , 2012; Nasrollahzadeh et al , 2015; Antonsson et al , 2016). Among countries with high EC incidence are China, Singapore, Iran, South Africa and Brazil (Bey et al , 1976; Han et al , 1996; Syrjänen, 2002; Guo et al , 2012).…”

Section: Bpv-associated Malignant Neoplasmsmentioning

confidence: 99%

“…Studies based on PCR also show a low correlation between HPV and EC, mainly in clinical samples from Australia (Antonsson et al , 2010; Antonsson et al , 2016). These results can be attributed to the origin of clinical samples, since Australia is not considered a high-risk area for HPV-associated EC.…”

Section: Bpv-associated Malignant Neoplasmsmentioning

confidence: 99%

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Papillomaviruses: a systematic review

et al. 2017

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In the last decades, a group of viruses has received great attention due to its relationship with cancer development and its wide distribution throughout the vertebrates: the papillomaviruses. In this article, we aim to review some of the most relevant reports concerning the use of bovines as an experimental model for studies related to papillomaviruses. Moreover, the obtained data contributes to the development of strategies against the clinical consequences of bovine papillomaviruses (BPV) that have led to drastic hazards to the herds. To overcome the problem, the vaccines that we have been developing involve recombinant DNA technology, aiming at prophylactic and therapeutic procedures. It is important to point out that these strategies can be used as models for innovative procedures against HPV, as this virus is the main causal agent of cervical cancer, the second most fatal cancer in women.

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Section: Bpv-associated Malignant Neoplasmsmentioning

confidence: 99%

Section: Bpv-associated Malignant Neoplasmsmentioning

confidence: 99%

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Papillomaviruses: a systematic review

et al. 2017

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“…Recent findings from Antonsson et al[88] showed the results of DNA quality testing (b-globin) through PCR and evaluation of the presence of HPV DNA in 241 histologically confirmed archived EAC and GEJAC (gastro-esophageal junction adenocarcinomas) tissue specimens from a population-based study in Australia. With a 97% DNA yield and acceptable quality in 233/241 specimens (201 EAC, 32 GEJAC), each sample was tested three times for HPV DNA.…”

Section: Hpv and Esophageal Cancermentioning

confidence: 99%

Human papillomavirus and gastrointestinal cancer: A review

Bucchi¹,

Stracci²,

Buonora³

et al. 2016

WJG

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Human papillomavirus (HPV) is one of the most common sexually transmitted infections worldwide. Exposure to HPV is very common, and an estimated 65%-100% of sexually active adults are exposed to HPV in their lifetime. The majority of HPV infections are asymptomatic, but there is a 10% chance that individuals will develop a persistent infection and have an increased risk of developing a carcinoma. The International Agency for Research on Cancer has found that the following cancer sites have a strong causal relationship with HPV: cervix uteri, penis, vulva, vagina, anus and oropharynx, including the base of the tongue and the tonsils. However, studies of the aetiological role of HPV in colorectal and esophageal malignancies have conflicting results. The aim of this review was to organize recent evidence and issues about the association between HPV infection and gastrointestinal tumours with a focus on esophageal, colorectal and anal cancers. The ultimate goal was to highlight possible implications for prognosis and prevention.

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“…69,70 Previously published studies using PCR techniques that showed negative results were due to poor tissue classification, suboptimal testing methodology exacerbated by low viral load, old specimen samples susceptible to DNA/RNA degradation, as well as ethnic and regional variations. [71][72][73][74][75] Instead of fresh frozen material, almost all of these retrospective investigations used paraffin-embedded tissue, which yields a significant false negative HPV PCR DNA result. 68 Some studies misclassified as negative used only nondysplastic BE.…”

Section: Hpv and Adenocarcinoma Of The Esophagusmentioning

confidence: 99%

Risk factors for esophageal cancer: emphasis on infectious agents

El‐Zimaity

Pilato

Ringressi

et al. 2018

Annals of the New York Academy of Sciences

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Risk factors for esophageal cancer include genetic factors (such as tylosis) and infectious agents. A variety of organisms have been implicated in esophageal carcinogenesis, either directly or indirectly. In this review, we explore the normal esophageal flora and how it may be controlled, and also the variety of organisms that may affect esophageal carcinogenesis, either directly or indirectly. The organisms with potential direct effects in squamous cell carcinoma include human papillomavirus (HPV), Epstein-Barr virus, and polyoma viruses. Interestingly, HPV is now implicated in esophageal adenocarcinoma (EAC), not in its initiation but in the development of dysplasia, in which HPV33 in particular has been associated. Indirectly, Helicobacter pylori has been associated with EAC by, initially, causing increased acid secretion that increases acid reflux, and by reducing lower esophageal sphincter pressure, which increases gastroesophageal reflux; the latter increases the risk of Barrett's esophagus, and hence EAC. Conversely, subsequent atrophic gastritis may normalize that risk.

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Human papillomavirus not detected in esophageal adenocarcinoma tumor specimens

Abstract: We found no evidence of HPV DNA in esophageal adenocarcinoma tumor cells. HPV is unlikely to cause EAC or GEJAC.

Cited by 25 publications

References 14 publications

Papillomaviruses: a systematic review

Papillomaviruses: a systematic review

Human papillomavirus and gastrointestinal cancer: A review

Risk factors for esophageal cancer: emphasis on infectious agents

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