P53 Arg72Pro Polymorphism in Gastric Cancer Patients

Souza, Lessileia Gomes de; Lima, Jacqueline Miranda de; Silva, Ismael Dale Cotrim Guerreiro da; Forones, Nora Manoukian

doi:10.1007/s12029-009-9078-7

Cited by 12 publications

(5 citation statements)

References 20 publications

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“…Six studies examined the association of TP 53 codon 72 polymorphism and gastric cancer [27, 31, 41, 44, 55, 68]. Allele frequency of Pro among controls ranged from 27 to 38% across studies.…”

Section: Resultsmentioning

confidence: 99%

Risk factors for gastric cancer in Latin America: a meta-analysis

Bonequi

Meneses-González

Correa

et al. 2012

Cancer Causes Control

123

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Background Latin America has among the highest gastric cancer incidence rates in the world, for reasons that are still unknown. In order to identify region-specific risk factors for gastric cancer, we conducted a meta-analysis summarizing published literature. Methods Searches of PubMed and regional databases for relevant studies published up to December 2011 yielded a total of 29 independent case-control studies. We calculated summary odds ratios (OR) for risk factors reported in at least five studies, including socioeconomic status (education), lifestyle habits (smoking and alcohol use), dietary factors (consumption of fruits, total vegetables, green vegetables, chili pepper, total meat, processed meat, red meat, fish and salt) and host genetic variants (IL1B-511T, IL1B-31C, IL1RN*2, TNFA-308A, TP53 codon 72 Arg and GSTM1 null). Study-specific ORs were extracted and summarized using random-effects models. Results Chili pepper was the only region-specific factor reported in at least five studies. Consistent with multifactorial pathogenesis, smoking, alcohol use, high consumption of red meat or processed meat, excessive salt intake and carriage of IL1RN*2 were each associated with a moderate increase in gastric cancer risk. Conversely, higher levels of education, fruit consumption, and total vegetable consumption were each associated with a moderately decreased risk. The other exposures were not significantly associated. No prospective study data were identified. Conclusion Risk factor associations for gastric cancer in Latin America are based on case-control comparisons that have uncertain reliability, particularly with regard to diet; the specific factors identified and their magnitudes of association are largely similar to those globally recognized. Future studies should emphasize prospective data collection and focus on region-specific exposures that may explain high gastric cancer risk.

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Section: Resultsmentioning

confidence: 99%

Risk factors for gastric cancer in Latin America: a meta-analysis

Bonequi

Meneses-González

Correa

et al. 2012

Cancer Causes Control

123

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“…In addition, the RR variants suppress transformation of primary cells to a higher degree than the P type [20]. There is a lower risk of gastric cancer among Asians with the Pro/Pro genotype than those with Arg/Arg genotypes [21]. Also, gastritis harboring patients with the PP variant are prone to diffuse-type gastric cancer [22].…”

Section: Discussionmentioning

confidence: 99%

Profile and Frequency of p53 Gene Alterations in Gastritis Lesions from Iran

Sadeghi¹,

Azimzadeh²,

Vahedi³

et al. 2010

Digestion

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Background: It has been frequently shown that p53 alterations have an important role in the development of gastric cancers but there is no data on p53 alteration in gastric cancer and its precancerous lesions from Iran although this country experiences one of the highest gastric cancer incidence and mortality rates in the world. The purpose of this study was to do a comprehensive assessment of p53 alterations in the Iranian population of gastritis patients and to evaluate the association between p53 alterations, microsatellite status and clinicopathological aspects. Methods: After DNA extraction, PCR sequencing was done for exons 2–7. Also microsatellite status was evaluated using five microsatellite markers: NR-27, NR-21, NR-24, BAT-25 and BAT-26. Results: The highest rate of alteration was seen in codons 72 (85.6%, SNP) and 248 (30.9%, mutation). Also, we found 2 new mutations in codons 9 and 146. In contrast with previous work, transition at the CpG codons was relatively rare. Nucleotide alterations were more prevalent in the Helicobacter pylori-positive group but not significantly. Neither nuclear staining for p53 protein nor microsatellite instability was seen in gastritis lesions. Conclusion: p53 alterations might contribute to the pathogenesis of gastritis and perhaps gastric cancer in Iran. However, the different spectrum seen here implies other mechanism(s) in gastritis and gastric cancer development in the Iranian population.

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“…Three additional papers identified from the reference list of reviews and retrieved articles were included, leaving 26 studies for full publication review. Of these, 5 were excluded (1 was duplicate 24; 2 were not case‐control studies 25, 26, 2 did not report usable data 27, 28), thus, 21 papers 1, 22, 23, 29–46 which included 5,867 gastric cancer cases and 7,001 controls, were found to conform our inclusion criteria. Twenty‐one studies, including 7 population‐based case‐control studies and 14 hospital‐based case‐control studies were included in this meta‐analysis.…”

Section: Resultsmentioning

confidence: 99%

“…It was believed that variation in the function of genes responsible for DNA repair mechanisms, cell cycle control, and weakened tumor suppression in the presence of carcinogen‐mediated cell damage was an attractive mechanism for understanding interindividual variation in gastric cancer susceptibility 43, 48, 49. The p53 gene acts basically as a transcription factor, involved in the preservation of genomic integrity by activating regulatory molecules of many cellular pathways, including the cell cycle progression, DNA repair, apoptosis, cell differentiation, and angiogenesis 50, 51.…”

Section: Discussionmentioning

confidence: 99%