Infectious Agents and Oesophageal Cancer

Dear Colleagues,

Fifteen to twenty percent of all human cancers worldwide are caused by infectious agents. Helicobacter pylori, high-risk human papillomavirus (hr-HPV), hepatitis B virus and hepatitis C are responsible for more than ninety percent of pathogen-related cancers These pathogens are involved in various steps of the carcinogenic pathway and probably require co-factors.

Oesophageal cancer is the 7th most common cancer in the world and 6th most common cause of cancer-related mortality.

Multiple risk factors are associated with oesophageal cancer. In the case of oesophageal squamous cell carcinoma (OSCC), the risk factors include excess alcohol and smoking in the West, betel nut chewing in India and South-East Asia, and drinking hot mate in South America. Others include poverty and ionising radiation. In 1982, Kari Syrjanen first suggested a link between human papillomavirus (HPV) and OSCC. It has been difficult to ascertain the true prevalence of HPV in OSCC given the widely varying reported rates between 0 and 100%. Not surprisingly, the association remains contentious.

In the case of oesophageal adenocarcinoma, chronic heartburn and Barrett’s oesophagus as well as smoking, obesity, older age, Caucasian race and a family history oesophageal cancer have been considered the traditional risk factors for the development of this malignancy. There is accumulating evidence for a probable relationship for high-risk HPV genotypes 16 and 18 in the etiology of a sub-group of OAC (25%) based on the published data. In fact, hr-HPV continues to gain traction as a risk factor for esophageal adenocarcinoma on the basis of more recent investigations, meta-analyses and reviews. Reported prevalence rates of the virus in OAC vary between 13 and 35%. Critical factors in the understanding of HPV oncogenesis in esophageal adenocarcinoma remain unresolved. Both genomic and proteomic studies will provide mechanistic insights for OAC with and without viral etiology. Furthermore, the confirmation of a distinct molecular signature via sequencing and proteomic analysis characteristic of HPV-positive esophageal malignancy would greatly aid risk stratification and improved/modified treatment protocols for patients, with the potential of reduced toxicity. The identification of a sub-group of high-risk progressors to esophageal cancer by surveillance and the development of effective preventive strategies including vaccination would have a great impact on public health. The potential histopathological reversal (regression) of a subset of patients with Barrett’s dysplasia via HPV therapeutic vaccination is the holy grail. The role of other viruses, namely Epstein–Barr virus (EBV), herpes simplex virus (HSV) and John Cunningham virus (JCV), in oesophageal cancer remains inconclusive.

The authors welcome articles both reviews and original research on the aetiology and or mechanistic insights into the pathobiology of pathogen-associated oesophageal cancer. Prognostic data associated with these cancers would also be considered for publication.

Prof. Dr. Shan Rajendra
Dr. Mohammed Rabiei
Guest Editors

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• oesophageal cancer
• human papillomavirus
• infection
• Barrett’s oesophagus
• cancer
• oesophageal adenocarcinoma
• oesophageal squamous cell carcinoma