Strofilas et al [29], rising speculations regarding a possible correlation of increased seroprevalence of CagA+ strains in colorectal cancer patients, compared to CagA- strains. In our study, the prevalence of H. pylori antibodies did not statistically differ between the two groups, in accordance to numerous previous case-control studies [30-33]. However, there are sufficient published data, supportive of increased H. pylori seroprevalence in colorectal cancer patients, highlighting the impact of the pathophysiological mechanisms described above as favorable for the development of colorectal neopla- sia [34-36]. Although recent meta-analyses indicate that H. pylori infection slightly increases the risk for the develop- ment of colorectal cancer (OR increased from 1.36 to 1.58) [2, 28], more studies need to be performed in order to either confirm or reject the association between H. pylori infection and colorectal cancer. Our results did not show a statistically significant in- creased in the seroprevalence of CagA+ strains in the colorectal cancer group. This finding is contradictory with the results of the research groups of Shmuely et al (2001) and Hartwich et al, who reported that CagA+ seropositiv- ity is associated with increased risk for both gastric and co- lonic cancer [35, 37]. It would be challenging to speculate that the enhanced inflammation status, both systemic and gastric, caused by the CagA+ strains could trigger the sys- tematic cytokines cascade, predisposing to the formation of premalignant lesions. Focusing in the focal gastric inflam- mation, the CagA+ strains, compared to CagA-, are associ- ated with increased hazard of chronic atrophic gastritis and consequently hypergastrinemia, which appears to be related to colorectal carcinogenesis, directly or indirectly. At last, it can be concluded that CagA+ strains may exert the metabo- lism of ammonia products in the large intestine, which can act as endogenous carcinogens, although further studies are required to confirm our hypotheses. The significance of gastrin and H. pylori infection in colorectal cancer progress still appears like a never-ending conquest. Our study did not reveal statistically significant differences in gastrin levels among colorectal cancer patients and controls. Additionally, no correlation occurred between gastrin levels and the site of colorectal cancer or the stage of the disease. Nevertheless, it appeared that in colorectal cancer patients with infiltrated lymph nodes, the levels of gastrin were statistically significantly higher compared to the patients with no lymph node infiltrations. It would be interesting to investigate in future studies the potential role of gastrin in the mechanisms of metastasis of the tumor cells. Regarding the seroprevalence of H. pylori infection in colorectal cancer patients, no statistically significance occurred between the two groups of our study. Moreover, therewere no statistical significant difference in the preva- lence of the CagA serotype in the colorectal cancer group, when compared to the control group. The specific role of he- licobacter pylori CagA+ strains should be examined further J Clin Med Res • 2012;4(3):172-176 in the effort to elucidate the impact of h. pylori infection in the colorectal cancer progress and also to examine the po- tential of being a target towards the inhibition of colorectal cancerogenesis. References 1. WHO. IARC monographs on the evaluation of carci- nogenic risks to humans: schistosomes, liver flukes and Helicobacter pylori, Vol 6, Lyon, France: IARC, 1994, pp. 177-240. 2. Zumkeller N, Brenner H, Zwahlen M, Rothenbacher D. Helicobacter pylori infection and colorectal cancer risk: a meta-analysis. Helicobacter. 2006;11(2):75-80. 3. Hakanson R, Sundler F. Trophic effects of gastrin. Scand J Gastroenterol Suppl. 1991;180:130-136. 4. Ryberg B, Axelson J, Hakanson R, Sundler F, Mattsson H. Trophic effects of continuous infusion of [Leu15]- gastrin-17 in the rat. Gastroenterology. 1990;98(1):33- 38. 5. Renga M, Brandi G, Paganelli GM, Calabrese C, Papa S, Tosti A, Tomassetti P, et al. Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia. Gut. 1997;41(3):330-332. 6. D’Onghia V, Leoncini R, Carli R, Santoro A, Giglioni S, Sorbellini F, Marzocca G, et al. Circulating gastrin and ghrelin levels in patients with colorectal cancer: correla- tion with tumour stage, Helicobacter pylori infection and BMI. Biomed Pharmacother. 2007;61(2-3):137-141. 7. Creutzfeldt W, Lamberts R. Is hypergastrinaemia danger- ous to man? Scand J Gastroenterol Suppl. 1991;180:179- 191. 8. Sirinek KR, Levine BA, Moyer MP. Pentagastrin stimu- lates in vitro growth of normal and malignant human colon epithelial cells. Am J Surg. 1985;149(1):35-39. 9. Chu M, Rehfeld JF, Borch K. Effects of gastric fundec- tomy and antrectomy on the colonic mucosa in the ham- ster. Digestion. 1992;53(1-2):28-34. 10. Sobhani I, Lehy T, Laurent-Puig P, Cadiot G, Ruszniews- ki P, Mignon M. Chronic endogenous hypergastrinemia in humans: evidence for a mitogenic effect on the co- lonic mucosa. Gastroenterology. 1993;105(1):22-30. 11. Orbuch M, Venzon DJ, Lubensky IA, Weber HC, Gi- bril F, Jensen RT. Prolonged hypergastrinemia does not increase the frequency of colonic neoplasia in pa- tients with Zollinger-Ellison syndrome. Dig Dis Sci. 1996;41(3):604-613. 12. Bombski G, Gasiorowska A, Orszulak-Michalak D, Ne- neman B, Kotynia J, Strzelczyk J, Janiak A, et al. Ele- vated plasma gastrin, CEA, and CA 19-9 levels decrease after colorectal cancer resection. Int J Colorectal Dis. 2003;18(2):148-152. 13. Hollande F, Imdahl A, Mantamadiotis T, Ciccotosto GD, Articles © The authors | Journal compilation © J Clin Med Res and Elmer Press™ | www.jocmr.org 175