Bankstown Hospital - Grand Rounds - Further Reading

Welcome to the Grand Rounds Further Reading List, Gastroenterology edition, brought to you by the Clinical Library, on Level 4, next to the Auditorium.

This library guide is to help support you in your professional development. Please give us feedback so we can improve this list in the future.

Some sections are under construction and will be ready later in the year. If you are presenting at a later Grand Rounds, please contact lynne.roberts3@health.nsw.gov.au and tell us about the content of your paper so we can add appropriate resources to the list for when you present. your paper.

If you have any questions, please contact the Clinical Library on 9722 8250 or email SWSLHD-BankstownLibrary@health.nsw.gov.au or visit us Monday to Fridays, 8.30am - 5.00pm.

All journal articles are available via CIAP, or by request from the Clinical Library, via our online request form.

Baj, J., et al. (2022). "The Involvement of Human Papilloma Virus in Gastrointestinal Cancers." Cancers 14(11): 2607 FULL TEXT @ SWSLHD Libraries https://www.mdpi.com/2072-6694/14/11/2607

Mounting evidence suggests a relationship between Human Papilloma Virus (HPV) infection and the occurrence of neoplastic transformations within oral, pharyngeal, and anal cancers. Other segments of the intestinal tract can also be involved. Knowledge about the association between HPV infection and gastrointestinal carcinogenesis is crucial for both cancer prevention and patient care. Unfortunately, definite conclusions cannot be drawn yet, due to the high number of contradictions in the published papers.

Rajendra, K. and P. Sharma (2022). "Viral Pathogens in Oesophageal and Gastric Cancer." Pathogens 11(4): 476 FULL TEXT @ SWSLHD Libraries https://www.mdpi.com/2076-0817/11/4/476

Tumour virology was born with the discovery by Peyton Rous in 1911 of a filterable agent in chicken cellular extracts that caused neoplasia in healthy chickens. Universally, 20% of all human cancers have a viral aetiology. Viruses are involved at various stages of the carcinogenesis pathway, depending on the viral pathogen, and likely require co-factors. Multiple risk factors have been associated with oesophageal and gastric malignancy, including carcinogenic pathogens. These viruses and bacteria include human papillomavirus (HPV) [oesophageal cancer], Epstein–Barr virus (EBV) [proximal stomach cancer], and Helicobacter pylori (HP) [non-cardia stomach cancer]. Viruses such as EBV have been firmly established as causal for up to 10% of gastric cancers. HPV is associated with 13 to 35% of oesophageal adenocarcinoma but its role is unclear in oesophageal squamous cell carcinomas. The causal relationship between hepatitis B (HBV), cytomegalovirus (CMV), HPV, and John Cunningham (JCV) and gastric neoplasia remains indeterminate and warrants further study. The expression of viral antigens by human tumours offers preventive and therapeutic potential (including vaccination) and has already been harnessed with vaccines for HPV and HBV. Future goals include viral protein-based immunotherapy and monoclonal antibodies for the treatment of some of the subset of EBV and HPV-induced gastro-esophageal cancers.
    

Rajendra, S. and P. Sharma (2023). "Causal Link of Human Papillomavirus in Barrett Esophagus and Adenocarcinoma: Are We There Yet?" Cancers 15(3): 873 FULL TEXT @ SWSLHD LIBRARIES https://www.mdpi.com/2072-6694/15/3/873

Esophageal cancer is a relatively common malignancy worldwide with a high mortality (5-year survival of <15%). Despite screening, surveillance, improved imaging and treatment, the exponential rise in OAC continues. The strongest risk factors for OAC are chronic heartburn and metaplastic transformation of the lower third of the esophagus (Barrett’s esophagus). The risk profile includes Caucasian race, male gender older age, obesity and smoking. Although the tumor risk in BO has been progressively revised downwards, the exponential rise in OAC remains unchecked. This paradox points to an unidentified missing link. Relatively recently, we provided the world’s initial data for a strong association of biologically relevant hr-HPV with BD and OAC. Since then, systematic reviews and meta-analysis have documented HPV DNA prevalence rates in OAC of between 13 to 35%. In this review, we provide some evidence for a probable causal relationship between hr-HPV and OAC. This is challenging given the multifactorial etiology and long latency. Increasingly, high-risk HPV (hr-HPV) is regarded as a risk factor for OAC. This discovery will aid identification of a sub-group of high-risk progressors to esophageal cancer by surveillance and the development of effective preventive strategies including vaccination.

Sharma, P., et al. (2020). "Importance of investigating high-risk human papillomavirus in lymph node metastasis of esophageal adenocarcinoma." World J Gastroenterol 26(21): 2729-2739 FULL TEXT @ SWSLHD Libraries https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284187/
    High-risk human papillomavirus has been suggested as a risk factor for esophageal adenocarcinoma. Tumor human papillomavirus status has been reported to confer a favorable prognosis in esophageal adenocarcinoma. The size of the primary tumor and degree of lymphatic spread determines the prognosis of esophageal carcinomas. Lymph node status has been found to be a predictor of recurrent disease as well as 5-year survival in esophageal malignancies. In human papillomavirus driven cancers, e.g. cervical, anogenital, head and neck cancers, associated lymph nodes with a high viral load suggest metastatic lymph node involvement. Thus, human papillomavirus could potentially be useful as a marker of micro-metastases. To date, there have been no reported studies regarding human papillomavirus involvement in lymph nodes of metastatic esophageal adenocarcinoma. This review highlights the importance of investigating human papillomavirus in lymph node metastasis of esophageal adenocarcinoma based on data derived from other human papillomavirus driven cancers.

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