p53 polymorphism and risk of cervical cancer

Hildesheim, Allan; Schiffman, Mark; Brinton, Louise A.; Fraumeni, Joseph F.; Herrero, Rolando; Bratti, M. Concepción; Schwartz, Peter E.; Mortel, Rodrigue; Barnes, Willard A.; Greenberg, Mitchell; McGowan, Larry; Scott, David; Martin, Maureen P.; Herrera, Jesús; Carrington, Mary

doi:10.1038/25040

Cited by 95 publications

(62 citation statements)

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“…A number of studies have been done in various populations to find the distribution of p53 genotype and to correlate it with predisposition and prognosis of cancers such as the cervix, 12,[17][18][19] lung, 20 -25 esophagus 26 and head and neck SCC. 27 The allele frequencies in the present study is found to be 0.55 (Arg) and 0.45 (Pro) as per the Hardy-Weinberg equilibrium.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Nagpal

Patnaik

Das

2001

Intl Journal of Cancer

136

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Key words: p53 polymorphism; HPV; oral cancerOral squamous cell carcinoma (OSCC) is the sixth most common malignancy and is a major cause of cancer morbidity and mortality worldwide. The overall survival percentage has not changed in recent years, despite extensive research on the biological and molecular aspects of oral SCC. Among the more pressing problems in clinical management are the lack of early detection and the high incidence of local-regional recurrence, even with aggressive surgical therapy. OSCC incidence accounts for up to 40% of all malignancies in India and South East Asia. 1 Moreover differences have been observed in the clinico-pathological and molecular pathological profile in the tobacco smoking and alcoholassociated oral cancers in the USA, UK, France, Japan, etc. and the chewing tobacco-associated oral cancers, particularly in the Indian sub-continent. 2 In India, oral leukoplakias have been reported to show a significant tendency to malignant transformation from 0.13 to 6% and rising to 14% or higher in cases of dysplasia. 3,4 Epidemiological studies reveal the betel quid and tobacco chewing habit as an important risk factor in the etiology of oral cancer in India. Since carcinogenesis is a multi-step process, therefore, in addition to insult by tobacco-associated intra oral carcinogens, several additional factors, such as genetic susceptibility of individuals and external agents, such as dietary factors and viruses (human papillomavirus, HPV, and Epstein-Baar virus, EBV), may play a synergetic role in oral tumorigenesis. [5][6][7][8] HPVs are a very heterogenous group of DNA viruses. Almost 90 HPV types have been described; 30 of these types are associated with anogenital cancers, forming either the high-risk types (HPV16 and HPV18) that are associated with anogenital invasive tumour and their precursor lesions or the low-risk types (HPV6 and HPV11) that rarely progress to malignancy. Analysis of viral genome has revealed that 2 early genes, E6 and E7, of high risk HPVs (16/18) are transforming genes that are responsible for maintenance of tumorigenic phenotype. 6,9,10 Genetic polymorphism at the genes involved in tumorigenesis may determine individual susceptibility of cancer. The genotype distribution of p53 codon 72 polymorphism is significantly different among ethnic groups. 11 Storey et al. 12 recently reported the probable correlation between p53 polymorphism and HPV associated cervical tumorigenesis. They showed that population homozygous for Arg-72 (arginine) is about 7 times more susceptible to development of cervical cancer than heterozygotes. However, this has been subject of much debate. Makni et al. 13 recently showed the substantial inter-laboratory variation in the proportion of Arg/Arg, Arg/Pro (proline) and Pro/Pro.In spite of its great relevance, so far only 2 contradictory reports have been proposed on the status of HPV in oral cancer on Indian population. The work on South Indian population has indicated 42% HPV-16 infection and 47% of HPV-18 infection, 7 whereas the r...

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Section: Discussionmentioning

confidence: 99%

Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Nagpal

Patnaik

Das

2001

Intl Journal of Cancer

136

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“…Interlaboratory variation in ascertaining p53 genotypes may lead to an underestimation or inability to detect an association. A number of independent studies since Storey's original findings have found no increased risk associated with arginine homozygosity (23)(24)(25)(26)(27)(28)(29)(30) (Table 1). Studies involving European population samples (Norway, United Kingdom, Netherlands, Sweden, Germany, and France) of cervical carcinomas and/or squamous intraepithelial lesions (SILs) in Hardy-Weinberg equilibrium do not confirm Storey's findings, regardless of HPV status.…”

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confidence: 99%

“…Both leukocyte DNA and/or DNA extracted from tissues were used with similar results. In fact, in one study that used samples from Costa Rica, the Eastern United States, and Oregon, a decreased risk for cervical cancer was associated with p53 arginine homozygosity (25). In this study, we further investigate the linkage of p53 arginine homozygosity in the spectrum of cervical neoplasia using a variation of Storey's method, as well as a restriction fragment length polymorphism (RFLP)-based method applied to DNA extracted from paraffin sections under microscopic control.…”

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confidence: 99%

Polymorphism at Codon 72 of p53 Is Not Associated with Cervical Cancer Risk

et al. 2000

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P53 allelic polymorphism at codon 72 has been studied as a possible predisposing factor for cervical carcinogenesis with inconsistent results. Storey and colleagues recently published the interesting finding of a 7-fold increased risk for cervical cancer in women homozygous for the arginine allele at codon 72. This stimulated a number of independent investigations, the majority of which found no association of cervical cancer and arginine homozygosity.With the use of a modified Storey method for determining codon 72 allelotypes, DNA was examined from 431 microdissected, formalin-fixed, archival cervical conization specimens ranging from low-grade squamous lesions to invasive cancer. An alternative independent method using restriction fragment length polymorphism analysis was performed on all arginine homozygotes and all indeterminate cases for confirmation and final allelotype assignment.With the use of Storey's method alone, logistic regression suggested an association (odds ratio, 1.42) between arginine homozygosity and invasive disease. However, with the use of the combined method for accurate allelotyping, this trend disappeared (odds ratio, 1.00), the discordance was clearly resolvable as being due to methodologic variables.With the use of two separate methods for codon 72 allelotyping and accounting for a number of the issues raised in previously published reports, there is no increased risk for invasive cervical cancer associated with arginine homozygosity at codon 72 of p53.KEY WORDS: Cervix, Neoplasia, p53, Papillomavirus, Polymorphism.Mod Pathol 2000;13(4):373-378Human papillomaviruses (HPVs) are epitheliotropic double-stranded DNA viruses that have been implicated in cervical carcinogenesis. More than 100 HPV genotypes have been identified. Traditionally, HPV genotypes, which are frequently identified in cervical neoplasms, have been segregated into those with a low risk and those with a high risk for malignant transformation. HPV types 6 and 11 are the prototypes of low-risk viruses that are most frequently found in low-grade squamous intraepithelial lesions (LSIL) and condylomata. HPV 16, 18, 31, and 45 account for approximately 80% of invasive cervical carcinomas, and the HPV 16 -related group is overrepresented in high-grade squamous intraepithelial lesions (HSIL) and squamous cancers compared with the HPV 18 -related viruses. The expression of HPV mRNA and proteins provides a coherent model for cervical carcinogenesis (1-3). Within the HPV genomes, the E6 and E7 genes are the driving forces behind epithelial proliferation and transformation. These transcribed genes are conserved and expressed within all HPV-infected pathologies. In many high-risk cervical dysplasias and invasive carcinomas, the E6 and E7 proteins are restrictively transcribed from the HPV genome integrated into the host DNA (4 -6). The link between oncogenesis and the transforming properties of HPV infection was identified by the interaction between these proteins and host cellular tumor suppressor gene products. Specifically, E7...

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“…However reported data on the prevalence of p53 polymorphism in cervical cancer patients are controversial and the ethnic group characteristics seem to be an important reason for discrepancies in the frequency of this polymorphism (Brenna, 2004;Wang, 1999;Wu, 2004;Pegoraro, 2002;Klug, 2001;Szarka, 2000;Agorastos, 2000;Hildesheim, 1998;Bhattacharya, 2002). Moreover, other potential confounding factors should be also considered including the sample size, the source of DNA and the detection techniques used.…”

Section: Topics On Cervical Cancer With An Advocacy For Prevention 200mentioning

confidence: 99%

Evaluation of p53, p16INK4a and E-Cadherin Status as Biomarkers for Cervical Cancer Diagnosis

Mzibri¹,

Attaleb²,

Hassani³

et al. 2012

Topics on Cervical Cancer With an Advocacy for Prevention

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p53 polymorphism and risk of cervical cancer

Cited by 95 publications

References 1 publication

Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Polymorphism at Codon 72 of p53 Is Not Associated with Cervical Cancer Risk

Evaluation of p53, p16INK4a and E-Cadherin Status as Biomarkers for Cervical Cancer Diagnosis

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