Andrichi et al.'s meta-analysis[1] showed that Barretts oesophagus (BO) was associated with an increased risk of both colorectal adenomas and colorectal cancer (CRC). They concluded that if the risk estimates for CRC in BO patients reflects a real relationship, an established association will warrant a search for common genetic or environmental risk factors.

Some genetic alterations are common in both conditions[2]; we initially found that specialised intestinal metaplasia indicating BO appeared in a significant percentage of patients with colon tumours (12/23) compared with controls (2/14) and was associated with increased oesophageal mucosal expression of oncogenes Ki-67 and p53/Bcl-2[3] that indicated mainly increased proliferation leading to oncogenesis.

In this regard, Helicobacter pylori infection may be considered a promoter of both diseases. Our and others’ data[4] indicate that H. pylori infection might contribute to oesophageal adenocarcinoma progress in subpopulations with gastro-oesophageal reflux disease and BO. In this respect, gastrin, induced by H. pylori infection, is an oncogenic growth factor contributing to oesophageal, gastric and colon carcinogenesis and, in particular, playing a potential causal effect on neoplastic progression in BO and left side CRC showing, for instance, anti-apoptotic activity through upregulation of the anti-apoptotic Bcl-2 and stimulation of mutagenic and tumourigenic cyclooxygenase-2 expression.[4-6]

Moreover, H. pylori infection is mostly frequent in colonic adenomas and tumour tissues (documented by immunohistochemical stain) and is accompanied by increased cell proliferation (mainly enhanced Ki-67 and Bcl-2 expression) and impaired apoptotic (decreased Bax) processes, thereby indicating its potential pathogenetic role.[6-8]

Apart from upper gastrointestinal tract (UGT), H. pylori infection might also cause chronic inflammatory colon mucosal damage and stimulate cancer stem cells and/or recruit bone-marrow–derived stem cells, which may ultimately facilitate UGT and colon tumour formation and progression.[8-10] However, further studies are needed to elucidate the proposed pathophysiological mechanisms involved in H. pylori-associated colon oncogenesis; its eradication might inhibit these oncogenic processes.


  1. Top of page
  2. Acknowledgement
  3. References

Declaration of personal and funding interests: None.


  1. Top of page
  2. Acknowledgement
  3. References
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    Andrici J, Tio M, Cox MR, Eslick GD. Meta-analysis: Barrett's oesophagus and the risk of colonic tumours. Aliment Pharmacol Ther 2013; 37: 40110.
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    Kyrgidis A, Kountouras J, Zavos C, Chatzopoulos D. New molecular concepts of Barrett's esophagus: clinical implications and biomarkers. J Surg Res 2005; 125: 189212.
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    Kountouras J, Kouklakis G, Chatzopoulos D, et al. Large intestine tumors (LI-TU) and ultra-short Barrett's esophagus (US-BE) [abstract]. Gut 2001; 49(Suppl. III): A1097.
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    Kountouras J, Chatzopoulos D, Zavos C, et al. Helicobacter pylori infection might contribute to esophageal adenocarcinoma progress in subpopulations with gastroesophageal reflux disease and Barrett's esophagus. Helicobacter 2012; 17: 4023.
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    Kountouras J, Touloumis L, Karatzoglou P, et al. In situ H. pylori infection and oncogenes’ expression in patients with colorectal cancer [abstract]. Gut 2004; 53(Suppl. VI): A270.
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