Background <p>A causal role of high-risk HPV in oesophageal adenocarcinoma development has been hypothesised, but longitudinal evidence is limited. This study aims to investigate a potential causal role of infectious agents in the malignant progression of Barrett’s oesophagus.</p> Methods <p>Using a retrospective nested case-control study design, index Barrett’s biopsies were retrieved for individuals within the Northern Ireland Barrett’s oesophagus register who subsequently progressed to oesophageal adenocarcinoma (<i>n</i> = 150) and matched non-progressors (<i>n</i> = 298). Index Barrett’s biopsies were assessed for the presence of 142 infectious agents by multiplex polymerase chain reaction using the Luminex platform. RNA in-situ hybridisation assessed persistent transcriptional activity in subsequent tissue samples, for infectious agents detected more frequently in progressors.</p> Results <p>High-risk HPV genotypes (HPV16 and HPV18) were only identified in the index biopsies of progressors but not non-progressors (4% [5/150] versus 0% [0/298], <i>P</i> = 0.004), though no signs of persistence or transcriptional activity were observed in subsequent tissue. Prevalence of infections did not differ between progressors and non-progressors for any other infectious agents, including Helicobacter Pylori and Herpes.</p> Conclusion <p>Despite a higher prevalence of high-risk HPV in progressors than non-progressors, no evidence of transcriptionally active high-risk HPV was observed in subsequent samples, indicating presence in Barrett’s is likely non-causal.</p>

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Infectious agents and progression from Barrett’s oesophagus to oesophageal adenocarcinoma: a nested case-control study

  • Talita H. A. de Oliveira,
  • Lesley A. Anderson,
  • Stephanie G. Craig,
  • Helen G. Coleman,
  • Tarik Gheit,
  • Sandrine McKay-Chopin,
  • Jacqueline Jamison,
  • Damian T. McManus,
  • Christopher R. Cardwell,
  • Victoria Bingham,
  • Brian T. Johnston,
  • Jacqueline A. James,
  • Andrew T. Kunzmann

摘要

Background

A causal role of high-risk HPV in oesophageal adenocarcinoma development has been hypothesised, but longitudinal evidence is limited. This study aims to investigate a potential causal role of infectious agents in the malignant progression of Barrett’s oesophagus.

Methods

Using a retrospective nested case-control study design, index Barrett’s biopsies were retrieved for individuals within the Northern Ireland Barrett’s oesophagus register who subsequently progressed to oesophageal adenocarcinoma (n = 150) and matched non-progressors (n = 298). Index Barrett’s biopsies were assessed for the presence of 142 infectious agents by multiplex polymerase chain reaction using the Luminex platform. RNA in-situ hybridisation assessed persistent transcriptional activity in subsequent tissue samples, for infectious agents detected more frequently in progressors.

Results

High-risk HPV genotypes (HPV16 and HPV18) were only identified in the index biopsies of progressors but not non-progressors (4% [5/150] versus 0% [0/298], P = 0.004), though no signs of persistence or transcriptional activity were observed in subsequent tissue. Prevalence of infections did not differ between progressors and non-progressors for any other infectious agents, including Helicobacter Pylori and Herpes.

Conclusion

Despite a higher prevalence of high-risk HPV in progressors than non-progressors, no evidence of transcriptionally active high-risk HPV was observed in subsequent samples, indicating presence in Barrett’s is likely non-causal.