Immunohistochemical study of p53, p21 and PCNA in pterygium

Ueda, Yasuo; Kanazawa, Suketaka; Kitaoka, Takashi; Dake, Yoshinori; Ohira, Akihiro; Ouertani, A.; Amemiya, Tsugio

doi:10.1078/0065-1281-00584

Cited by 32 publications

(32 citation statements)

References 18 publications

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“…We and other researchers (Dushku and Reid, 1997;Dushku et al, 1999;Tan et al, 1997Tan et al, , 2000Chowers et al, 2001;Ueda et al, 2001;Weinstein et al, 2002;Perra et al, 2006;Schneider et al, 2006) found pterygium cells to be p53 positive by IHC. The antip53 antibody and cutoff level (10% cell staining) that we used was the same as that used by Weinstein et al (2002) and by Tsai et al (2005b); however, the previously reported frequencies of 53.8 and 22.8%, respectively, differed from our finding of 24/36.…”

Section: Discussionmentioning

confidence: 99%

“…The frequency of p53 mutations in cancer patients can vary among different races (Beroud and Soussi, 2003), and our country is quite miscegenated. Ueda et al (2001) demonstrated that the incidence of immunoreactivity for p53 is affected by race differences in the development of pterygium as well as by environmental factors. This accumulated p53 protein is apparently mostly inactive, at least in terms of how it affects apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Abnormal levels of p53 protein have been found in the epithelium; many researchers feel that pterygium is a UV-related, uncontrolled, cell proliferation consistent with that of a tumor (Ueda et al, 2001;Weinstein et al, 2002). The p53 tumor suppressor gene is one of the most commonly mutated genes observed in human tumors and has been noted in more than 50% of all human cancers (Tsai et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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TP53 gene expression, codon 72 polymorphism and human papillomavirus DNA associated with pterygium

Rodrigues

Arruda²,

Silva³

et al. 2008

Genet. Mol. Res.

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ABSTRACT. Pterygium is a disease of unknown origin and pathogenesis that can be vision threatening. Several researchers believe that pterygium is UV-related and that abnormal expression of p53 protein and infection with human papillomavirus (HPV) are risk factors for pterygium, but their experiments have been inconclusive. We investigated its relation with p53 protein expression, p53 gene codon 72 polymorphism and infection with HPV DNA. Pterygial samples were obtained from 36 patients; 21 normal conjunctival samples were used as controls. Expression of p53 protein was studied by immunohistochemistry, using the antibody DO-7. Analysis for the p53 genotype was made by polymerase chain reaction, using specific primers for the arginine and proline alleles, and an analysis for HPV was made of the pterygium patients and control group. Fourteen of the 36 pterygial specimens were positive for abnormal p53 expression. Thirty-one of the patients were heterozygotic and three were homozygotic for the proline allele; two were homozygotic for the arginine allele; in the control group 12 of 21 were heterozy- gotic and seven of these 21 were homozygotic for the proline allele; two were homozygotic for the arginine allele. Twenty-one of the pterygium patients were positive for HPV; HPV type 1 was found in nine of these, type 2 in seven and both types in five. Only two of the 21 controls had HPV; both had type 16. We suggest that abnormal expression of p53, p53 codon 72 polymorphisms and HPV DNA are required co-factors for the development of pterygium.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TP53 gene expression, codon 72 polymorphism and human papillomavirus DNA associated with pterygium

Rodrigues

Arruda²,

Silva³

et al. 2008

Genet. Mol. Res.

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“…However, pterygia display some tumourlike properties in their clinical appearance of local invasion and epithelial cell metaplasia. 2 Furthermore, the presence of oncogenic viruses, such as the human papilloma virus and herpes simplex virus, 3,4 loss of heterozygosity, 5 and abnormal p53 expression in pterygium lesions, 6,7 all suggest the possible neoplastic nature of pterygium. A model of pterygium formation is then proposed, in which genetic predisposition, environmental factors, and viral infections may participate in the multistep process.…”

Section: Introductionmentioning

confidence: 99%

Genetic polymorphism of hOGG1 and risk of pterygium in Chinese

Hc¹,

Cc²,

Wm³

et al. 2004

Eye

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Purpose Ultraviolet irradiation is known to cause oxidative DNA damage and is thought to be a major factor implicated in the pathogenesis of pterygium. The highly mutagenic 8-hydroxy-2 0 -deoxyguanosine, a marker for the evaluation of photo-oxidative DNA damage, can be repaired by human 8-oxoguanine glycosylase I (hOGG1). A transition of C to G at nucleotide position 1245 in exon 7 of the hOGG1 gene is associated with the substitution of cysteine for serine at codon 326. In this study, we investigated the association of the hOGG1 Ser326Cys polymorphism with pterygium in a Chinese population. Methods In all, 70 patients and 86 controls were enrolled in this study. The Ser326Cys polymorphism was determined by the polymerase chain reaction-restriction fragment-length polymorphism analysis. The association between this genetic polymorphism and risk of pterygium was examined by w 2 -test and logistic regression. Results The allelic frequencies for the Ser and Cys variants of hOGG1 gene were not significantly different between the two groups. However, when compared with Ser/ Ser and Ser/Cys genotypes combined, we found that the homozygous Cys/Cys genotype was more prevalent in pterygium patients than controls (P ¼ 0.024) with the odds ratio being 2.2 (95% CI: 1.1-4.5). In the pterygium group, the mean age of patients with the Cys/Cys genotype was younger than those with the other two genotypes (P ¼ 0.025). Conclusions Our findings suggest that the 1245C-G transition in exon 7 of the hOGG1 gene, which results in Ser326Cys substitution of the enzyme, might play a role in the susceptibility of humans to pterygium.

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“…86,87 This process is further amplified through elevated anti-apoptotic proteins survivin 88 and BCL-2. 89 The tumor-suppressor protein p53 is a widely studied factor in pterygia; normally present in low or undetectable levels within a cell, this protein functions to induce cell-cycle arrest, DNA repair or apoptosis.…”

Section: Role Of Hpv In P53 Tumor-suppressor Inactivationmentioning

confidence: 99%

Association of human papilloma virus with pterygia and ocular-surface squamous neoplasia

Girolamo

2011

Eye

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There are more microorganisms that colonize the human body than resident cells; some are commensal whereas others are pathogenic. Pathogenic microorganisms are sensed by the innate or adaptive immune system, an immune response is initiated, and the infection is often cleared. Some microorganisms have developed strategies to evade immune defenses, ensuring their long-term survival with potentially devastating consequences for the host. Approximately 18% of all cancers can be attributed to infective agents; the most common being Helicobacter pylori, Human papilloma virus (HPV) and Hepatitis B and C virus in causing stomach, cervical and liver carcinoma, respectively. This review focuses on whether HPV infection is necessary for initiating pterygia, a common benign condition and ocular-surface squamous neoplasia (OSSN), a rare disease with metastatic potential. The search engine PubMed was used to identify articles from the literature related to HPV and pterygium or conjunctival neoplasia. From 34 investigations that studied HPV in pterygia and OSSN, a prevalence rate of 18.6% (136/731) and 33.8% (144/426), respectively, was recorded. The variation in HPV prevalence (0-100%) for both disease groups may have arisen from study-design faults and the techniques used to identify the virus. Overall, the data suggest that HPV is not necessary for initiating either condition but may be a co-factor in susceptible hosts. Currently, over 60 million people worldwide have been immunized with HPV vaccines, but any effect on pterygium and OSSN development may not be known for some time as these lesions can evolve over decades or occur in older individuals.

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Immunohistochemical study of p53, p21 and PCNA in pterygium

Cited by 32 publications

References 18 publications

TP53 gene expression, codon 72 polymorphism and human papillomavirus DNA associated with pterygium

TP53 gene expression, codon 72 polymorphism and human papillomavirus DNA associated with pterygium

Genetic polymorphism of hOGG1 and risk of pterygium in Chinese

Association of human papilloma virus with pterygia and ocular-surface squamous neoplasia

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