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Helicobacter pylori Infection and a P53 Codon 72 Single Nucleotide Polymorphism: a Reason for an Unexplained Asian Enigma

  • Pandey, Renu ;
  • Misra, Vatsala ;
  • Misra, Sri Prakash ;
  • Dwivedi, Manisha ;
  • Misra, Alok
  • Published : 2014.11.28

Abstract

Aim: P53, the most commonly mutated tumor suppressor gene in all types of human cancer, is involved in cell cycle arrest and control of apoptosis. Although p53 contains several polymorphic sites, the codon 72 polymorphism is by far more common. There are divergent reports but many studies suggest p53 pro/pro SNP may be associated with susceptibility to developing various cancers in different regions of the world. The present study aimed to find any correlation between H. pylori infection and progression of carcinogenesis, by studying apoptosis and the p53 gene in gastric biopsies from north Indian population. Materials and Methods: A total of 921 biopsies were collected and tested for prevalence of H. pylori by rapid urease test (RUT), imprint cytology and histology. Apoptosis was studied by the TUNEL method. Analysis of p53 gene polymorphism at codon 72 was accomplished by PCR using restriction enzyme BstU1. Observation: Out of 921 samples tested 56.7% (543) were H. pylori positive by the three techniques. The mean apoptotic index (AI) in the normal group was 2.12, while gastritis had the maximum 4.24 followed by gastric ulcer 2.28, gastropathy 2.22 and duodenal ulcer 2.08. Mean AI in cases with gastric cancer (1.72) was less than the normal group. The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% & 33.66%) as compared to p53 pro/pro variant (25.74%) inthe healthy population. Conclusions: The North Indian population harbors Arg or Pro/Arg SNP that is capable of withstanding stress conditions; this may be the reason of low incidence of gastric disease in spite of high infection with H. pylori. There was no significant association with H. pylori infection and AI. However, there is increased apoptosis in gastritis which may occur independent of H. pylori or p53 polymorphism.

Keywords

p53 polymorphism;Helicobacter pylori;gastric cancer;apoptotic index;North India

References

  1. Chua HW, Ng D, Choo S, et al (2010). Effect of MDM2 SNP309 and p53 codon 72 polymorphisms on lung cancer risk and survival among non-smoking Chinese women in Singapore. BMC Cancer, 10, 10-88. https://doi.org/10.1186/1471-2407-10-10
  2. Etienne MC, Chazal M, Laurent-Puig P, et al (2002). Prognostic value of tumoral thymidylate synthase and p53 in metastatic colorectal cancer patients receiving fluorouracil-based chemotherapy: phenotypic and genotypic analyses. J Clin Oncol, 20, 2832-43. https://doi.org/10.1200/JCO.2002.09.091
  3. Ferreira AC, Isomoto H, Moriyama M, et al (2008). Helicobacter and gastric malignancies. Helicobacter, 13, 28-34. https://doi.org/10.1111/j.1523-5378.2008.00633.x
  4. Forman D, Newell DG, Fullerton F, et al (1991). Association between infection with H. pylori and risk of gastric cancer: evidence from a prospective investigation. BMJ, 302, 1302-5. https://doi.org/10.1136/bmj.302.6788.1302
  5. Ghoshal UC, Tiwari S, Dhingra S, et al (2008). Frequency of H. pylori and CagA antibody in patients with gastric neoplasms and controls: the Indian enigma. Dig Dis Sci, 53, 1215-22. https://doi.org/10.1007/s10620-008-0229-7
  6. Gill HH, Desai HG, Majmudar P, Mehta PR, Prabhu SR (1993). Epidemiology of H. pylori: the Indian scenario. Indian J Gastroenterol, 12, 9-11.
  7. Yoshimura T, Shimoyama T, Tanaka M, et al (2000). Gastric mucosal inflammation and epithelial cell turnover are associated with gastric cancer in patients with H. pylori infection. J Clin Pathol, 53, 532-6. https://doi.org/10.1136/jcp.53.7.532
  8. Zhang Z, Yuan Y, Gao H (2001). Apoptosis, proliferation and p53 gene expression of H. pylori associated gastric epithelial lesions. World J Gastroenterol, 7, 779-82.
  9. Zhong Zhang , Yuan Yuan, Hua Gao, et al (2001). Apoptosis, proliferation and p53 gene expression of H. pylori associated gastric epithelial lesions. World J Gastroenterol, 7, 779-82.
  10. Bergamaschi D, Gasco M, Hiller L, et al (2003). p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis. Cancer Cell, 3, 387-402. https://doi.org/10.1016/S1535-6108(03)00079-5
  11. Bergamaschi D, Samuels Y, Sullivan A, et al (2006). iASPP preferentially binds p53 proline-rich region and modulates apoptotic function of codon 72-polymorphic p53. Nat Genet, 38, 1133-41. https://doi.org/10.1038/ng1879
  12. Gill HH, Desai HG (1992). H. pylori in north Indian subjects. Indian J Gastroenterol, 11, 146-7.
  13. Graham DY, Adam E, Reddy GT, et al (1991). Seroepidemiology of H. pylori infection in India. Comparison of developing and developed countries. Dig Dis Sci, 36, 1084-8. https://doi.org/10.1007/BF01297451
  14. Hollstein M, Sidransky D, Vogelstein B, Harris CC (1991). p53 Mutations inhuman cancers. Science. 253, 49-53. https://doi.org/10.1126/science.1905840
  15. Jain A, Buddhiraja S, Khurana B, et al (1999). Risk factors for duodenal ulcer in north India. Trop Gastroenterol, 20, 36-9.
  16. Jing G, Lv K, Jiao X (2012). The p53 Codon 72 Polymorphism and the risk of oral cancer in a Chinese han population. Genet Test Mol Biomarkers, 2012, 2.
  17. Kaeffer Bertrand (2011). Survival of exfoliated epithelial cells: a delicate balance between anoikis and apoptosis. J Biomed Biotechnol, 2011, 534139.
  18. Katelaris PH, Tippett GH, Norbu P, et al (1992). Dyspepsia, H. pylori, and peptic ulcer in a randomly selected population in India. Gut, 33, 1462-6. https://doi.org/10.1136/gut.33.11.1462
  19. Katkoori VR, Jia X, Shanmugam C, et al (2009). Prognostic significance of p53 codon 72 polymorphism differs with race in colorectal adenocarcinoma. Clin Cancer Res, 15, 2406-16. https://doi.org/10.1158/1078-0432.CCR-08-1719
  20. Koushik A, Tranah GJ, Ma J, et al (2006). p53 Arg72Pro polymorphism and risk of colorectal adenoma and cancer. Int J Cancer, 119, 1863-8. https://doi.org/10.1002/ijc.22057
  21. lARC monographs on the evaluation of carcinogenic risks to humans (1994). ISBN 92 832 12614, 1-61.
  22. Lee JM, Lee YC, Yang SY, et al (2000). Genetic polymorphisms of p53 and GSTP1, but not NAT2, are associated with susceptibility to squamous-cell carcinoma of the esophagus. Int J Cancer, 89, 458-64. https://doi.org/10.1002/1097-0215(20000920)89:5<458::AID-IJC10>3.0.CO;2-R
  23. Leite KR, Darini E, Canavez FC, et al (2005). H. pylori and cagA gene detected by polymerase chain reaction in gastric biopsies: correlation with histological findings, proliferation and apoptosis. Sao Paulo Med J, 123, 113-8.
  24. Levine AJ (1997). p53, the cellular gatekeeper for growth and division. Cell, 88, 323-31. https://doi.org/10.1016/S0092-8674(00)81871-1
  25. Levine AJ (2012). The evolution of the p53 family of genes. Cell Cycle, 11, 214-5. https://doi.org/10.4161/cc.11.2.18899
  26. Li Y, Prives C (2007). Are interactions with p63 and p73 involved in mutant p53 gain of oncogenic function? Oncogene, 26, 2220-5. https://doi.org/10.1038/sj.onc.1210311
  27. Liu KJ, Qi HZ, Yao HL, et al (2012). An updated meta-analysis of the p53 codon 72 polymorphism and gastric cancer risk. Mol Biol Rep, 39, 8265-75. https://doi.org/10.1007/s11033-012-1674-0
  28. Liu Y, Qin H, Zhang Y, et al (2011). P53 codon 72 polymorphism and colorectal cancer: a meta-analysis of epidemiological studies. Hepatogastroenterology, 58, 1926-9.
  29. Mannick EE, LE Bravo, G Zarama, et al (1996). Inducible nitric oxide synthase, nitrotyrosine, and apoptosis in H. pylori gastritis: effect of antibiotics and antioxidants. Cancer Research, 56, 3238-43.
  30. Mantovani F, Tocco F, Girardini J, et al (2007). The prolyl isomerase Pin1 orchestrates p53 acetylation and dissociation from the apoptosis inhibitor iASPP. Nat Struct Mol Biol, 14, 912-20. https://doi.org/10.1038/nsmb1306
  31. Matakidou A, Eisen T, Houlston RS (2003). TP53 polymorphisms and lung cancer risk: a systematic review and meta-analysis. Mutagenesis, 18, 377-85. https://doi.org/10.1093/mutage/geg008
  32. Misra SP, Dwivedi M, Misra V, Gupta SC (1993). Imprint cytology-a cheap, rapid and effective method for diagnosing H. pylori. Postgrad Med J, 69, 291-5. https://doi.org/10.1136/pgmj.69.810.291
  33. Misra V, Misra SP, Dwivedi M, Gupta SC, Bhargava V (2000). A topographic study of H. pylori density, distribution and associated gastritis. J Gastroenterol Hepatol, 15, 737-43. https://doi.org/10.1046/j.1440-1746.2000.02240.x
  34. Misra V, Misra SP, Singh MK, Singh PA, Dwivedi M (2007). Prevalence of H.pylori in patients with gastric cancer. Indian J Pathol Microbiol, 50, 702-7.
  35. Misra V, Pandey R, Misra SP, Dwivedi M (2014). H. pylori and gastric cancer: Indian enigma. World J Gastroenterol, 20, 1503-9. https://doi.org/10.3748/wjg.v20.i6.1503
  36. Moss SF (1998). Cellular markers in the gastric precancerous process, Aliment. Pharmacol Ther, 12, 91-109.
  37. Moss SF, J Calam, B Agarwal, S Wang, PR Holt (1996). Induction of gastric epithelial apoptosis by H. pylori, Gut, 38, 498-501. https://doi.org/10.1136/gut.38.4.498
  38. Nakamura T, Yao T, Kakeji Y, et al (2012). Depressed type of intramucosal differentiated-type gastric cancer has high cell proliferation and reduced apoptosis compared with the elevated type. Gastric Cancer, 16, 94-9.
  39. Nath G, Khanna AK, Jain AK, Gulati VK (2000). H. pylori does not cause gastric carcinoma in India. Natl Med J India, 13, 328-9.
  40. Pandey R, Misra V, Misra SP, et al (2010). H. pylori and gastric cancer. Asian Pac J Cancer Prev, 11, 583-8.
  41. Pandith AA, Shah ZA, Khan NP, et al (2010). Role of TP53 Arg72Pro polymorphism in urinary bladder cancer predisposition and predictive impact of proline related genotype in advanced tumors in an ethnic Kashmiri population. Cancer Genet Cytogenet, 203, 263-8. https://doi.org/10.1016/j.cancergencyto.2010.08.010
  42. Parkin DM (2006). The global health burden of infection-associated cancers in the year. Int J Cancer, 118, 3030-44. https://doi.org/10.1002/ijc.21731
  43. Parsonnet J, Friedman GD, Vandersteen DP, et al (1991). H. pylori infection and the risk of gastric carcinoma. N Engl J Med, 325, 1127-31. https://doi.org/10.1056/NEJM199110173251603
  44. Peek Jr RM, SF Moss, KT Tham, et al (1997). H. pylori cagA+ strains and dissociation of gastric epithelial cell proliferation from apoptosis. J Natl Cancer Inst, 89, 863-8. https://doi.org/10.1093/jnci/89.12.863
  45. Peek Jr R M, MJ Blaser, DJ Mays, et al (1999). H. pylori strainspecific genotypes and modulation of the gastric epithelial cell cycle. Cancer Res, 59, 6124-31.
  46. Phukan RK, Narain K, Zomawia E, Hazarika NC, Mahanta J (2006). Dietary habits and stomach cancer in Mizoram, India. J Gastroenterol, 41, 418-24. https://doi.org/10.1007/s00535-006-1761-x
  47. Shepherd T, Tolbert D, Benedetti J, et al (2000). Alterations in exon 4 of the p53 gene in gastric carcinoma. Gastroenterology, 118, 1039-44. https://doi.org/10.1016/S0016-5085(00)70356-8
  48. Shepherd T, Tolbert D, Benedetti J, et al (2002). Alterations in exon 4 of the p53 gene in gastric carcinoma. Gastroenterology, 118, 1039-44.
  49. Singh K, Ghoshal UC (2006). Causal role of H. pylori infection in gastric cancer: an Asian enigma. World J Gastroenterol, 7, 1346-51.
  50. Soulitzis N, Sourvinos G, Dokianakis DN, Spandidos DA (2002). p53 codon 72 polymorphism and its association with bladder cancer. Cancer Lett, 179, 175-83. https://doi.org/10.1016/S0304-3835(01)00867-9
  51. Sousa H, Santos AM, Pinto D, Medeiros R (2011). Is there a biological plausability for p53 codon 72 polymorphism influence on cervical cancer development? Acta Med Port, 24, 127-34.
  52. Talley NJ, Zinsmeister AR, Weaver A, et al (1991). Gastric adenocarcinoma and H. pylori infection. J Natl Cancer Inst, 83, 1734-9. https://doi.org/10.1093/jnci/83.23.1734
  53. Targa AC, Cesar AC, Cury PM, Silva AE (2007). Apoptosis in different gastric lesions and gastric cancer: relationship with H. pylori, overexpression of p53 and aneuploidy. Genet Mol Res, 6, 554-65
  54. Thillainayagam AV, Arvind AS, Cook RS, et al (1991). Diagnostic efficiency of an ultrarapid endoscopy room test for H. pylori. Gut, 32, 467. https://doi.org/10.1136/gut.32.5.467
  55. Thomas M, Kalita A, Labrecque S, et al (1999). Two polymorphic variants of wild-type p53 differ biochemically and biologically. Mol Cell Biol, 19, 1092-100.
  56. Tommiska J, Eerola H, Heinonen M, et al (2005). Breast cancer patients with p53 Pro72 homozygous genotype have a poorer survival. Clin Cancer Res, 11, 5098-103. https://doi.org/10.1158/1078-0432.CCR-05-0173
  57. Vogelstein B, Lane D, Levine AJ (2002). Surfing the p53 network. Nature, 408, 307-10.
  58. Vousden KH, Lane DP (2007). p 53 in health and disease. Nat Rev Mol Cell Biol, 8, 275-83. https://doi.org/10.1038/nrm2147
  59. Walker KK, Levine AJ (1996). Identification of a novel p53 functional domain that is necessary for efficient growth suppression. Proc Natl Acad Sci USA, 93, 15335-40. https://doi.org/10.1073/pnas.93.26.15335
  60. Xu T, Xu ZC, Zou Q, Yu B, Huang XE (2012). P53 Arg72Pro polymorphism and bladder cancer risk-meta-analysis evidence for a link in Asians but not Caucasians. Asian Pac J Cancer Prev, 13, 2349-54. https://doi.org/10.7314/APJCP.2012.13.5.2349
  61. Yamaoka Y (2010). Mechanisms of disease: H. pylori virulence factors. Nat Rev Gastroenterol Hepatol, 7, 629-41.