High prevalence of mutations at codon 249 of the p53 gene in hepatocellular carcinomas from Senegal

Coursaget, Pierre; Depril, N.; Chabaud, Martine; Nandi, Rajesh; Mayelo, V.; LeCann, P.; Yvonnet, B

doi:10.1038/bjc.1993.258

Cited by 97 publications

(51 citation statements)

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“…A similar frequency of 17p loss has been reported previously (Yumoto et al, 1995). A mis-sense mutation with replacement of arginine by serine at codon 249 has been reported previously in HCCs from Qidong, Shanghai and other geographical areas where aflatoxin and HBV are present Hsu et al, 1991;Ozturk et al, 1991;Coursaget et al, 1993). LOH of 17 p without identified p53 gene mutation or positive p53 immunohistochemistry was present in 29% of HCCs in our study.…”

Section: Microsatellite Instability and Loh Of Chromosomes 1p 4q 13supporting

confidence: 90%

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

et al. 1999

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The major risk factors for hepatocellular carcinomas (HCC) in high incidence areas include infection with hepatitis B and C viruses (HBV, HCV) and exposure to aflatoxin. Genetic alterations in 24 liver resection specimens from Shanghai and Qidong were studied. Hepatitis B virus was integrated in all patient samples, and a null phenotype for the GSTM1 enzyme was present in 63% of patients. Alteration of p53 was present in 95% (23/24) of cases: mutations of the p53 gene in 12 HCC, p53 overexpression in 13 and loss of heterozygosity (LOH) of chromosome 17p in 17. All seven HCCs with a p53 mutation from Qidong and three of five from Shanghai had the aflatoxin-associated point mutation with a G to T transversion at codon 249, position 3. No HCC had microsatellite instability. LOH of chromosome 4q, 1p, 16q and 13q was present in 50%, 46%, 42% and 38%, respectively, and 4q was preferentially lost in HCCs containing a p53 mutation: LOH of 4q was present in 75% (9/12) of HCC with, but only 25% (3/12) of HCC without, a p53 gene mutation ( P = 0.01). These data indicate a possible interaction between p53 gene mutation and 4q loss in the pathogenesis of HCC. © 1999 Cancer Research Campaign

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Section: Microsatellite Instability and Loh Of Chromosomes 1p 4q 13supporting

confidence: 90%

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

et al. 1999

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“…Array of literature described that incidence of 249Ser mutation was high in patients having HCC compare to other neoplasms (Liu et al, 2002). There is a relation between aflotoxin B1 exposure and the G-T transversion in codon 249 in 50% of Southeast Asian patients (Hsu et al, 1991) and 67% from Senegal (Coursaget et al, 1993). The substitution of arginine by serine in the p53 protein causing folding abnormality of the DNA binding domain on the protein (Igetei et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

p53 Exon 4 (codon 72) Polymorphism and Exon 7 (codon 249) Mutation in Breast Cancer Patients in Southern Region(Madurai) of Tamil Nadu

Vijayaraman¹,

Veluchamy²,

Murugesan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: We investigated the association between polymorphisms in the p53 tumor suppressor gene and breast cancer risk in women especially in the Southern part of India. Methods: Genotyping was performed for 50 breast cancer women and 50 controls to determine the status of p53 exon 4 codon 72 polymorphism and exon 7 codon 249 mutation and their possible role in breast cancer risk. Results: Frequency of Arg/Arg at codon 72 was 18% in controls and 28% in patients, Arg/Pro frequency was 56% and 66% , Pro/Pro genotype was 8% in controls and 8% in patients. No significance was observed for breast cancer risk with either Arg/Arg or Pro/ Pro genotype in codon 72 polymorphism. Similarly, mutation analysis of exon 7 codon 249 revealed that 72% of breast cancer patients have mutation, which is not statistically significant. However, there is a strong association between increase in exon 7 codon 249 mutation and exposure to pollution. Conclusion: The results suggested that there is no risk for exon 4 with Arg/Arg or Pro/Pro polymorphisms in the p53 gene and there is no strong correlation between breast cancer patients and mutation in exon 7 codon 249 in South Indian women.Keywords: Breast cancer -p53 -exon 4 codon 72 -exon 7 codon 249 -South India

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“…The p53 tumour-suppressor gene has been shown to be mutated in HCCs at variable frequencies (0-67%) (Buetow et al, 1989;Kress et al, 1992;Coursaget et al, 1993;Nishida et al, 1993;Teramoto et al, 1994;Vesey et al, 1994;Kazachkov et al, 1996;Honda et al, 1998). The relationship between p53 and HBV or HCV has also been found to play a central role in the regulation of carcinogenesis and proliferation of HCC (Henkler et al, 1995;Wang et al, 1995;Lunn et al, 1997;Ray et al, 1997).…”

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confidence: 99%

Absence of mutation of the p73 gene localized at chromosome 1p36.3 in hepatocellular carcinoma

et al. 1998

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Summary Accumulating evidence has demonstrated that aberration of the p53 tumour-suppressor gene is one of the pivotal genetic events in hepatocellular carcinogenesis. Recent reports suggest that the product of hepatitis B virus (HBV) interacts with p53 and that the hepatitis C virus (HCV) core protein reduces p53 expression. A novel p73 gene, which is related to p53, has recently been identified and mapped to chromosome 1p36.3, which is a locus of multiple tumour-suppressor genes for many cancers, including hepatocellular carcinoma (HCC) and neuroblastoma. Here, we investigated mRNA expression, allelotype and mutation of p73 in 48 HCCs obtained from untreated patients. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that p73 mRNA was expressed ubiquitously at low levels in all the tumour tissues, as well as in the adjacent normal liver tissues. The frequency of p73 loss of heterozygosity was observed in 20% of HCCs, but PCR-single strand conformation polymorphism (SSCP) analysis showed no mutations in the 48 tumours except for three types of polymorphisms. These results suggest that p73 may play a role in hepatocellular carcinogenesis in a different manner from a Knudson twohit model. The regulatory mechanism of interaction between p73 and hepatitis viruses remains to be determined.Keywords: p73; hepatocellular carcinoma; p53; mutation; mRNA expression; 1p36.3 164British Journal of Cancer (1999) 79(1), 164-167 © 1999 Cancer Research Campaign Received 18 February 1998 Revised 11 May 1998 Accepted 13 May 1998Correspondence to: A Nakagawara, Division of Biochemistry, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuoh-ku, Chiba 260-8717, Japan Analysis of p73 in hepatocellular carcinoma 165

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High prevalence of mutations at codon 249 of the p53 gene in hepatocellular carcinomas from Senegal

Cited by 97 publications

References 9 publications

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

p53 Exon 4 (codon 72) Polymorphism and Exon 7 (codon 249) Mutation in Breast Cancer Patients in Southern Region(Madurai) of Tamil Nadu

Absence of mutation of the p73 gene localized at chromosome 1p36.3 in hepatocellular carcinoma

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