p53 Mutations and Microsatellite Instabilities in the Subtype of Intestinal Metaplasia of the Stomach

Kim, Sung Soo; Bhang, Choon Sang; Min, Ki Ouk; Chae, Hiun Suk; Choi, Sang Wook; Lee, Chang Don; Lim, Keun Woo; Chung, In Sik; Park, Doo Ho

doi:10.3346/jkms.2002.17.4.490

Cited by 16 publications

(10 citation statements)

References 26 publications

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“…Missense alterations are more frequent than silent alteration in gastric cancer and its precancerous lesions [32,33,35,45], as seen in our study. They certainly have important effects on the p53 functions.…”

Section: Discussionsupporting

confidence: 68%

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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Section: Discussionsupporting

confidence: 68%

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

Sadeghi¹,

Azimzadeh²,

Vahedi³

et al. 2010

Digestion

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“…In line with former findings about infrequency of MSI in gastritis lesion (Kashiwagi et al, 2000;Kim et al, 2002;, the status of microsatellite in gastritis lesion was stable and few samples had variant alleles. The probable explain, is that MSI arises from loss of mismatch repair system whiles our samples express MMR proteins.…”

Section: Discussionsupporting

confidence: 88%

“…Maybe MMR defects and subsequent MSI happen later during malignant transformation of gastric mucosa. For example, MSI was reported up to 9.3% for intestinal metaplasia and 26.7% for gastric carcinoma (Hamamoto et al, 1997;Leung et al, 2000;Kim et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

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

Sadeghi

Damavand²,

Vahedi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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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.

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“…In gastric precancerous legions adjacent to GC, the frequency of MSI was different according to the markers examined for MSI detection (Semba et al, 1996;Hamamoto et al, 1997;Kobayashi et al, 2000;Leung et al, 2000;Jin et al, 2001;Kim et al, 2002;Lee et al, 2002;Zaky et al, 2008). In data using the Bethesda markers or closely related criteria, MSI was found in about 10% of cases except the studies by (0%) and Zaky et al (2008) (48.2%).…”

Section: Msi In Gastric Precancerous Legionsmentioning

confidence: 80%

“…To evaluate its role in gastric carcinogenesis, some studies discriminated between metaplasias that are adjacent to GC and those not coexisting with GC in evaluating legions for MSI (Semba et al, 1996;Hamamoto et al, 1997;Leung et al, 2000;Lee et al, 2002;. Previous results of MSI in gastric precancerous legions according to the markers and samples were summarized in Table 1 (Semba et al, 1996;Hamamoto et al, 1997;Endoh et al, 2000;Kashiwagi et al, 2000;Kim et al, 2000;Kobayashi et al, 2000;Leung et al, 2000;Jin et al, 2001;Kim et al, 2002;Lee et al, 2002;Garay et al, 2004;Liu et al, 2005;Zaky et al, 2008;Park et al, 2013). In gastric precancerous legions without GC, the frequency of MSI was low under 10% of cases except the studies by Semba et al (1996) (33.3%, 4/12) and Zaky et al (2008) (20.5%, 8/39).…”

Section: Msi In Gastric Precancerous Legionsmentioning

confidence: 99%

Microsatellite Instability of Nuclear and Mitochondrial DNAs in Gastric Carcinogenesis

Lee

Kim²

2014

Asian Pacific Journal of Cancer Prevention

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Genetic instability contributes to the development and progression of gastric cancer, one of the leading causes of cancer death worldwide. Microsatellite instability (MSI) has been hypothesized to be involved in carcinogenesis, althgough its mechanisms and exact roles in gastric cancer remain largely unknown. Our aim was to identify associated clinicopathological characteristics and prognostic value of MSI in gastric cancer and precancerous lesions including gastritis, metaplasia, dysplasia, and adenoma. Because mitochondrial DNA has a different genetic system from nuclear DNA, the results of both nuclear MSI and mitochondrial MSI in gastric cancer were reviewed. This review provides evidence that genetic instability of nuclear and mitochondrial DNAs contributes to early stages of gastric carcinogenesis and suggests possible roles in predicting prognosis.

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p53 Mutations and Microsatellite Instabilities in the Subtype of Intestinal Metaplasia of the Stomach

Cited by 16 publications

References 26 publications

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

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

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

Microsatellite Instability of Nuclear and Mitochondrial DNAs in Gastric Carcinogenesis

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