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:: Volume 29, Issue 1 (3-2021) ::
Journal of Ilam University of Medical Sciences 2021, 29(1): 87-95 Back to browse issues page
Evaluation of Gene Expression Alterations of ATM, TP53, and POLM in Gastric Biopsy Specimens of Patients with Gastritis and its Association with Helicobacter Pylori Infection
Armin Ghameshloo1 , Ali Rashidi-nezhad * 2, Masoud Alebouyeh3 , Abas Shakouri4
1- Dept of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
2- Maternal, Fetal and Neonatal Research Center, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran , arashidinezhad@tums.ac.ir
3- Pediatric Infections Research Center, Research Institute for Children's Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran
4- Genetic Ward, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
Abstract:   (1896 Views)
Introduction: Gastritis is one of the most common diseases affecting the stomach. Helicobacter pylori infection could lead to DNA damage in gastric epithelial cells, followed by error-prone DNA repair pathways that increase the accumulation of damage at the site of DNA double-stranded breaks, exacerbate genome instability, and facilitate the emergence of gastric cancer. This study aimed to examine the expression level of ATM, POLM, and TP53 genes involving in the DNA Damage Response and the cell cycle arrest in the gastric precancerous stage.
Materials & Methods: Among 180 gastric biopsy specimens, 30 samples taken from patients with moderate chronic gastritis infected by H. Pylori were regarded as the case group, and 30 other samples taken from non-infected patients with mild chronic gastritis were regarded as control. Following that, RNA extraction and cDNA synthesis was performed. Afterward, the expression levels of ATM, POLM, and TP53 genes were evaluated by the Real-Time PCR method.
Ethics code: 98-02-27-43392
Findings: The ATM, POLM, and TP53 genes in the cases showed a 4.07, 3.35, and 5.13 increase in the gene expression at the transcriptional level, compared to the controls.
Discussion & Conclusions: In general, ATM, POLM, and TP53 genes showed a higher increased expression level in the case group, compared to the controls, which might indicate the activation of noted genes after H. pylori infection. This may subsequently activate the error-prone DNA repair and non-homologous recombination pathways.
Keywords: ATM, POLM, TP53 genes, DNA double stranded breaks, Gastritis, H. pylori
Full-Text [PDF 746 kb]   (668 Downloads)    
Type of Study: Research | Subject: genetic mlvkly
Received: 2020/08/6 | Accepted: 2021/01/20 | Published: 2021/03/30
1. Sipponen P, Maaroos HI. Chronic gastritis. Scand J Gastroenterol 2015;50:657-67. doi.10.3109/00365521.2015.1019918
2. Wotherspoon AC, Hidalgo C, Falzon MR, Isaacson PG. Helicobacter pylori associated gastritis and primary Bcell gastric lymphoma. Lancet 1991 9;338:1175-6. doi.10.1016/0140-6736(91)92035-z
3. Asaka M, Takeda H, Sugiyama T, Kato M. What role does H.pylori play in gastric cancer? 1 th ed. WB Saunders Publication. 1997;P.133-8.
4. Martel C, Ferlay J, Franceschi S, Vignat J, Bray F, Forman D, et al. Global burden of cancers attributable to infections in 2008 a review and synthetic analysis. Lancet Oncol 2012;13:607-15. doi.10.1016/S1470-2045(12)70137-7
5. Ishaq S, Nunn L. H. pylori and gastric cancer a state of the art review. Gastroenterol Hepatol Bed Bench2015;8:6-14.
6. Gebert B, Fischer W, Haas R. The H.pylori vacuolating cytotoxin from cellular vacuolation to immunosuppressive activities. Rev Physiol Biochem Pharmacol2004;152:205-20. doi.10.1007/s10254-004-0027-3
7. Saadat I, Higashi H, Obuse C, Umeda M, Kamiya N, Saito Y, et al. H.pylori cagA targets par1/mark kinase to disrupt epithelial cell polarity. Nature2007;447:330-3. doi. 10.1038/nature05765
8. Peek RM, Vaezi MF, Falk GW, Goldblum JR, Perez GI, Richter JE, et al. Role of H. pylori cagA strains and specific host immune responses on the development of premalignant and malignant lesions in the gastric cardia. Int J Cancer1999;82:520-4. doi.10.1002/(SICI)1097-0215(19990812)82
9. Rawla P, Barsouk A. Epidemiology of gastric cancer global trends risk factors and prevention. Gastroenterol Rev 2019;14:26-38. doi.10.5114/pg.2018.80001
10. Khoshdel AR, Ziaei M, Ghaffari HR, Azadi S, Alimohamadi Y. [The prediction number of new cases and death of gastric cancer among Iranian military community during 2007-19]. Mult Cancer Inv2018;02:14-9. (Persian). doi.10.30699/acadpub.mci.2.2.14
11. Stanley W, Ashley JM. Daly stomatch in seymourI schwartz principle of surg. 7th ed. Sunders Publication.1999;P.1201-6.
12. Hemati S, Rahmatian A, Talee G, Bastani E, Rahmatian A, Shams M, et al. Prevalence of H.pylori and Its seasonality in Ilam Iran. JJBS2021;14:187- 9.
13. Jang BG, Kim WH. Molecular pathology of gastric carcinoma. Pathobiology 2011;78:302-10. doi.10.1159/000321703
14. Gilley D, Tanaka H, Hande MP, Kurimasa A, Li GC, Oshimura M, et al. DNA PKcs is critical for telomere capping. Proc Natl Acad Sci USA 2001; 98:15084-8. doi.10.1073/pnas.261574698
15. Difilippantonio MJ, Zhu J, Chen HT, Meffre E, Nussenzweig MC, Max EE, et al. Dna repair protein Ku80 suppresses chromosomal aberrations and malignant transformation. Nature 2000;404:510-4. doi.10.1038/35006670
16. Ferguson DO, Alt FW. DNA double strand break repair and chromosomal translocation lessons from animal models. Oncogene 2001;20: 5572-9. doi.10.1038/sj.onc.1204767
17. Gao Y, Ferguson DO, Xie W, Manis JP, Sekiguchi JA, Frank KM, et al. Interplay of p53 and DNA repair protein XRCC4 in tumorigenesis genomic stability and development. Nature 2000;404:897-900. doi.10.1038/35009138
18. Zhu C, Mills KD, Ferguson DO, Lee C, Manis J, Fleming J, et al. Unrepaired DNA breaks in p53-deficient cells lead to oncogenic gene amplification subsequent to translocations. Cell 2002;109:811-21. doi.10.1016/s0092-8674(02)00770-5
19. Pfeiffer P, Goedecke W, Kuhfittig S, Obe G. Pathways of DNA double strand break repair and their impact on the prevention and formation of chromosomal aberrations. Cyt Gen Res 2004;104:7-13. doi.10.1159/000077460
20. Mills KD, Ferguson DO, Alt FW. The role of DNA breaks in genomic instability and tumorigenesis. Immunol Rev2003;194:77-95. doi.10.1034/j.1600-065x.2003.00060.x
21. Manxhuka S, Telaku S, Devolli E, Ahmetaj H, Sahatciu V, Kerliu A, et al. H.pylori gastritis updated Sydney classification applied in our material. Prilozi2009;30:45-60.
22. Kim JJ, Tao H, Carloni E, Leung WK, Graham DY, Sepulveda AR. H.pylori impairs DNA mismatch repair in gastric epithelial cells. Gastroenterology2002;123:542-53. doi.10.1053/gast.2002.34751
23. Malfertheiner P, Megraud F, Omorain CA, Atherton J, Axon ATR, Bazzoli F, et al. Management of H.pylori infection the maastricht florence consensus report. Gut 2012;61:646-64. doi.10.1136/gutjnl-2012-302084
24. Wong BCY, Lam SK, Wong WM, Chen JS, Zheng TT, Feng RE, et al. H. pylori eradication to prevent gastric cancer in a high risk region of china a randomized controlled trial. J Am Med Assoc 2004;291:187-94. doi.10.3748/wjg.v12.i11.1671
25. Kidane D, Murphy DL, Sweasy JB. Accumulation of abasic sites induces genomic instability in normal human gastric epithelial cells during H.pylori infection. Oncogenesis 2014;3:24-9. doi.10.1038/oncsis.2014.42
26. Tan P, Yeoh KG. Genetics and molecular pathogenesis of gastric adenocarcinoma. Gastroenterology 2015;149:1153-62. doi.10.1053/j.gastro.2015.05.059
27. Li N, Xie C, Lu NH. P53 a potential predictor of H.pylori infection associated gastric carcinogenesis? Oncotarget 2016;7:66276-86. doi.10.18632/oncotarget.11414
28. Zaika AI, Wei J, Noto JM, Peek RM. Microbial regulation of p53 tumor suppressor. Plos Pathol 2015;11:1005099. doi.10.1371/journal.ppat.1005099
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Ghameshloo A, Rashidi-nezhad A, Alebouyeh M, Shakouri A. Evaluation of Gene Expression Alterations of ATM, TP53, and POLM in Gastric Biopsy Specimens of Patients with Gastritis and its Association with Helicobacter Pylori Infection. J. Ilam Uni. Med. Sci. 2021; 29 (1) :87-95
URL: http://sjimu.medilam.ac.ir/article-1-6713-en.html

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Volume 29, Issue 1 (3-2021) Back to browse issues page
مجله دانشگاه علوم پزشکی ایلام Journal of Ilam University of Medical Sciences
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