CagA status of Helicobacter pylori infection and p53 gene mutations in gastric adenocarcinoma

Paula P. Magalhães1, Dulciene M.M. Queiroz1,3, Anamaria A. Camargo2 and Andrew J.G. Simpson2

1 Universidade Federal de Minas Gerais, Laboratory of Research in Bacteriology, Belo Horizonte, Minas Gerais, Brazil and
2 Ludwig Institute for Cancer Research, São Paulo, São Paulo, Brazil

Dear Sir,

We read with great interest the research findings of Dr Shibata et al. (1) regarding the association between p53 mutation and CagA+ Helicobacter pylori infection. The authors searched for p53 gene mutations by SSCP and, when necessary, by direct sequencing of DNA samples obtained from tumor specimens of patients with gastric adenocarcinoma. Helicobacter pylori infection and CagA status were investigated by ELISA for serum IgG antibodies.

Undoubtedly, the use of sera obtained prior to cancer diagnosis greatly improves the sensitivity of H.pylori detection and CagA status investigation. However, it should be pointed out that the interval between serum collection and cancer diagnosis was extremely variable, from 2 years to more than three decades, which makes possible that some patients have already had premalignant lesions, such as atrophy, an adverse condition for H.pylori survival, when serum was obtained. The fact that some samples were drawn many years before carcinoma diagnosis increases the chance of acquiring infection with other H.pylori strains, including CagA+ ones. Also, it must be mentioned the possibility of changing the bacterium CagA status, what may be achieved by selective loss of parts of the cag pathogenicity island (2). It may be added that the combination of H.pylori- and CagA-/H. pylori+ groups for statistical analysis could lead to a biased result.

We have been investigating p53 somatic mutations in exons 5–8 by direct sequencing of DNA isolated from distal gastric carcinoma patients. In contrast to the results reported by Shibata et al., we observed that only six of 43 (13.9%) H.pylori+ patients harbored mutations, one of them in exons 5 and 6. Also, all mutations we detected were substitutions. We cultured H.pylori strains from all patients and investigated their cagA status by PCR. The frequency of cagA+ strains we found (42/43, 97.7%) was higher than that observed by Shibata et al. (61/74, 82.4%, for distal gastric cancer). It should be highlighted that the high prevalence we detected is meaningful as cagA+ strains were found in ~65% of Brazilian patients with gastritis only (3).

The differences observed between our findings and those reported by Shibata et al. can be due to particular characteristics of each population studied.

Although cagA+H.pylori infection has been related to distal gastric carcinoma, we think that there is no clear biological evidence for associating CagA+ strains with higher prevalence of p53 gene mutations in gastric adenocarcinoma yet, at least in some geographical areas.

Notes

3 To whom correspondence should be addressed Email: dqueiroz{at}medicina.ufmg.br Back

References

  1. Shibata,A., Parsonnet,J., Longacre,T.A., Garcia,M.I., Pulingandla,B., Davis,R.E., Vogelman,J.H., Orentreich,N. and Habel,L.A. (2002) CagA status of Helicobacter pylori infection and p53 gene mutations in gastric adenocarcinoma. Carcinogenesis, 23, 419–424.[Abstract/Free Full Text]
  2. Sozzi,M., Crosatti,M., Kim,S.K., Romero,J. and Blaser,M.J. (2001) Heterogeneity of Helicobacter pylori cag genotypes in experimentally infected mice. FEMS Microbiol. Lett., 203, 109–114.[CrossRef][ISI][Medline]
  3. Queiroz,D.M.M., Mendes,E.N., Rocha,G.A., Oliveira,A.M.R., Oliveira,C.A., Magalhães,P.P., Moura,S.B., Cabral,M.M.D.A. and Nogueira,A.M.M.F. (1998) cagA-positive Helicobacter pylori and risk for developing gastric carcinoma in Brazil. Int. J. Cancer, 78, 135–139.[CrossRef][ISI][Medline]




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