Asian Pacific Journal of Cancer Prevention

Asian Pacific Journal of Cancer Prevention (아시아태평양암예방학회)
권호 표지
DOI QR코드

DOI QR Code

Detection of p53 Common Intron Polymorphisms in Patients with Gastritis Lesions from Iran

  • Sadeghi, Rouhallah Najjar (Research Center for Gastroenterology and Liver Diseases, Taleghani Hospital) ;
  • Damavand, Behzad (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Vahedi, Mohsen (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Mohebbi, Seyed Reza (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Zojazi, Homayon (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Molaei, Mahsa (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Zali, Mohamad Reza (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences)
  • Published : 2013.01.31
Download PDF
⟨ Previous Next ⟩

Abstract

Background: p53 alterations have been implicated in the development of many cancers, such as gastric cancer, but there is no evidence of p53 intron alterations in gastritis lesions. The aim of this study was to investigate the p53 intron alterations in gastritis along with p53 and mismatch repair protein expression and microsatellite status. Materials and Methods: PCR-sequencing was conducted for introns 2-7 on DNA extracted from 97 paired samples of gastritis lesions and normal adjacent tissue. Abnormal accumulation of p53 and mismatch repair proteins was investigated using immunohistochemistry. In addition, microsatellite status was evaluated with reference to five mononucleotide markers. Results: Gastritis cases included 41 males and 56 females in the age range of 15-83 years, 87.6% being H.pylori positive. IVS2+38, IVS3ins16 and IVS7+72 were the most polymorphic sites. Their minor allele frequency values were as follows: 0.38, 0.21 and 0.06, respectively. Samples with GG genotype at IVS2+38 and CT at IVS7+72 had no insertion. Moreover, most of the stable samples (91.9 %) had a G allele at IVS2+38. All of the samples were IHC negative for p53 protein, microsatellite stable and expressed mismatch repair proteins. p53 alterations were prominent in the H. Pylori+ group, but without statistical significance. Conclusions: According to our results, some p53 polymorphisms such as IVS2+38, IVS3ins16 and IVS7+72, because of their correlations together or with microsatellite status may contribute to gastritis development. However, so far effects on p53 expression and function remain unclear. Therefore, a comprehensive survey is needed to delineate their biological significance.

Keywords

References

  1. Angelopoulou K, Levesque MA, Katsaros D, et al (1998). Exon 5 of the p53 gene is a target for deletions in ovarian cancer. Clin Chem, 44, 72-7.
  2. Bai L, Zhu WG (2006). p53: structure, function and therapeutic applications. J Cancer Mol, 2, 141-53.
  3. Boussioutas A, H Li, J Liu, et al (2003). Distinctive patterns of gene expression in premalignant gastric mucosa and gastric cancer. Cancer Res, 63, 2569-77.
  4. Brueckl WM, Heinze E, Milsmann C, et al (2004). Prognostic significance of microsatellite instability in curatively resected adenocarcinoma of the small intestine. Cancer Lett, 203, 181-90. https://doi.org/10.1016/j.canlet.2003.08.013
  5. Brusa G, Benvenuti M, Mazzacurati L, et al (2003). p53 loss of function enhances genomic instability and accelerates clonal evolution of murine myeloid progenitors expressing the p (210) BCR-ABL tyrosine kinase. Haematologica, 88, 622-30.
  6. Buhard O, Suraweera N, Lectard A, et al (2004). Quasimonomorphic mononucleotide repeats for high-level microsatellite instability analysis. Dis Markers, 20, 251-7. https://doi.org/10.1155/2004/159347
  7. Carstens M, Krempler A, Triplett A, et al (2004). Cell cycle arrest and cell death are controlled by p53-dependent and p53-independent mechanisms in tsg101-deficient cells. J Biol Chem, 279, 35984-994. https://doi.org/10.1074/jbc.M400408200
  8. Davis RL, Homer VM, George PM, Brennan SO (2009). A deep intronic mutation in FGB creates a consensus exonic splicing enhancer motif that results in afibrinogenemia caused by aberrant mRNA splicing, which can be corrected in vitro with antisense oligonucleotide treatment. Hum Mutat, 30, 221-7. https://doi.org/10.1002/humu.20839
  9. Fenoglio Preiser C, Wang J, Stemmermann G, Noffsinger A (2003). TP53 and gastric carcinoma: a review. Hum Mutat, 21, 258-70. https://doi.org/10.1002/humu.10180
  10. Furihata M, Takeuchi T, Matsumoto M, et al (2002). p53 mutation arising in Arg72 allele in the tumorigenesis and development of carcinoma of the urinary tract. Clin Cancer Res, 8, 1192-5.
  11. Gemignani F, Moreno V, Landi S, et al (2003). A TP53 polymorphism is associated with increased risk of colorectal cancer and with reduced levels of TP53 mRNA. Oncogene, 23, 1954-56.
  12. Hamamoto T, Yokozaki H, Semba S, et al (1997). Altered microsatellites in incomplete-type intestinal metaplasia adjacent to primary gastric cancers. Br Med J, 50, 841-6.
  13. Higashimoto Y, Saito S, Tong XH, et al (2000). Human p53 is phosphorylated on serines 6 and 9 in response to DNA damage-inducing agents. J Biol Chem, 275, 23199-203. https://doi.org/10.1074/jbc.M002674200
  14. Kashiwagi K, Watanabe M, Ezaki T, et al (2000). Clinical usefulness of microsatellite instability for the prediction of gastric adenoma or adenocarcinoma in patients with chronic gastritis. Br J Cancer, 82, 1814-8. https://doi.org/10.1054/bjoc.1999.1154
  15. Kim S, Bhang C, Min K, et al (2002). p53 mutations and microsatellite instabilities in the subtype of intestinal metaplasia of the stomach. J Korean Med Sci, 17, 490-6. https://doi.org/10.3346/jkms.2002.17.4.490
  16. Koshiol J, Hildesheim A, Gonzalez P, et al (2009). Common genetic variation in TP53 and risk of human papillomavirus persistence and progression to CIN3/cancer revisited. Cancer Epidemiol Biomarkers Prev, 18, 1631-7. https://doi.org/10.1158/1055-9965.EPI-08-0830
  17. Leung W, Kim J, Kim J, et al (2000). Microsatellite instability in gastric intestinal metaplasia in patients with and without gastric cancer. Am J Pathol, 156, 537-43. https://doi.org/10.1016/S0002-9440(10)64758-X
  18. Li J, Shi X, Lv S, et al (2005). Effect of Helicobacter pylori infection on p53 expression of gastric mucosa and adenocarcinoma with microsatellite instability. World J Gastroenterol, 11, 4363-6.
  19. Li YQ, Li YL, Gu QR, et al (2005). p53 gene intron 7 polymorphism and its association with oral neoplasms. Zhonghua Kou Qiang Yi Xue Za Zhi, 40, 386-9.
  20. Malekzadeh R, Derakhshan MH, Malekzadeh Z (2009). Gastric cancer in Iran: epidemiology and risk factors. Arch Iran Med, 12, 576-83.
  21. Maunakea AK, Nagarajan RP, Bilenky M, et al (2010). Conserved role of intragenic DNA methylation in regulating alternative promoters. Nature, 466, 253-57. https://doi.org/10.1038/nature09165
  22. Mehrabian A, Esna-Ashari F, Zham H, et al (2010). Gastric cancer prevalence, according to survival data in Iran. Iranian J Public Hlth, 39, 27-31.
  23. Molaei M, Mansoori BK, Ghiasi S, et al (2010). Colorectal cancer in Iran: Immunohistochemical profiles of four mismatch repair proteins. Int J Colorectal Dis, 25, 63-9. https://doi.org/10.1007/s00384-009-0784-1
  24. Murakami K, Fujioka T, Okimoto T, et al (1999). Analysis of p53 gene mutations in Helicobacter pylori-associated gastritis mucosa in endoscopic biopsy specimens. Scand J Gastroenterol, 34, 474-7.
  25. Najjar SR, Azimzadeh P, Vahedi M, et al (2011). Profile and frequency of p53 gene alterations in gastritis lesions from Iran. Digestion, 83, 65-75. https://doi.org/10.1159/000320690
  26. Romiti A, Moretti A, Vecchione A, et al (1998). Analysis of p53 expression in precancerous and malignant gastric mucosa. Oncol Rep, 5, 109-13.
  27. Shamsher MK, Chuzhanova NA, Friedman B, et al (2000). Identification of an intronic regulatory element in the human protein C (PROC) gene. Hum Genet, 107, 458-65. https://doi.org/10.1007/s004390000391
  28. Shiao Y, Rugge M, Correa P, et al (1994). p53 alteration in gastric precancerous lesions. Am J Pathol, 144, 511.
  29. Smith M, Fornace AJJ (1996). The two faces of tumor suppressor p53. Am J Pathology, 148, 1019-22.
  30. Sogame N, Kim M, Abrams JM (2003). Drosophila p53 preserves genomic stability by regulating cell death. Proc Natl Acad Sci USA, 100, 4696-701. https://doi.org/10.1073/pnas.0736384100
  31. Thongsuksai P, Boonyaphiphat P, Puttawibul P, Sudhikaran W (2010). Specific intronic p53 mutation in esophageal squamous cell carcinoma in Southern Thailand. World J Gastroenterology: WJG, 16, 5359. https://doi.org/10.3748/wjg.v16.i42.5359
  32. Wang-Gohrke S, Becher H, Kreienberg R, et al (2002). Intron 3 16 bp duplication polymorphism of p53 is associated with an increased risk for breast cancer by the age of 50 years. Pharmacogen. Genomics, 12, 269-72.
  33. Wang-Gohrke S, Weikel W, Risch H, et al (1999). Intron variants of the p53 gene are associated with increased risk for ovarian cancer but not in carriers of BRCA1 or BRCA2 germline mutations. Br J Cancer, 81, 179-83. https://doi.org/10.1038/sj.bjc.6690669
  34. Whibley C, Pharoah P, Hollstein M (2009). p53 polymorphisms: cancer implications. Nat Rev Cancer, 9, 95-107. https://doi.org/10.1038/nrc2584
  35. Wu X, Zhao H, Amos CI, et al (2002). p53 genotypes and haplotypes associated with lung cancer susceptibility and ethnicity. J Natl Cancer Inst, 94, 681-90. https://doi.org/10.1093/jnci/94.9.681
  36. Xinarianos G, Liloglou T, Prime W, et al (2002). p53 status correlates with the differential expression of the DNA mismatch repair protein MSH2 in non small cell lung carcinoma. Int J Cancer, 101, 248-52. https://doi.org/10.1002/ijc.10598
  37. Yamada H, Shinmura K, Okudela K, et al (2007). Identification and characterization of a novel germ line p53 mutation in familial gastric cancer in the Japanese population. Carcinogenesis, 28, 2013-8. https://doi.org/10.1093/carcin/bgm175
  38. Yamamoto H, Perez-Piteira J, Yoshida T, et al (1999). Gastric cancers of the microsatellite mutator phenotype display characteristic genetic and clinical features. Gastroenterology, 116, 1348-57. https://doi.org/10.1016/S0016-5085(99)70499-3
  39. Zeraati H, Mahmoudi M, Kazemnejad A, Mohammed K (2005). Postoperative life expectancy in gastric cancer patients and its associated factors. Saudi Med J, 26, 1203-7.

Cited by

  1. Effects of p53 Codon 72 and MDM2 SNP309 Polymorphisms on Gastric Cancer Risk among the Iranian Population vol.15, pp.17, 2014, https://doi.org/10.7314/APJCP.2014.15.17.7413
  2. Association of Cytokine Gene Polymorphisms with Gastritis in a Kazakh Population vol.15, pp.18, 2014, https://doi.org/10.7314/APJCP.2014.15.18.7763
  3. Microsatellite Instability of Nuclear and Mitochondrial DNAs in Gastric Carcinogenesis vol.15, pp.19, 2014, https://doi.org/10.7314/APJCP.2014.15.19.8027
  4. Clinicopathological and p53 Gene Alteration Comparison between Young and Older Patients with Gastric Cancer vol.15, pp.3, 2014, https://doi.org/10.7314/APJCP.2014.15.3.1375
  5. Intronic Polymorphisms of the SMAD7 Gene in Association with Colorectal Cancer vol.16, pp.1, 2015, https://doi.org/10.7314/APJCP.2015.16.1.41
  6. Are SMAD7 rs4939827 and CHI3L1 rs4950928 polymorphisms associated with colorectal cancer in Egyptian patients? vol.37, pp.7, 2016, https://doi.org/10.1007/s13277-016-4813-8