Papillomavirus, p53 alteration and primary carcinoma of the vulva

Pilotti, Silvana; Donghi, R.; D'Amato, Lucia; Giarola, Monica; Longoni, Alberto; Torre, Gabriella Della; Palo, Giuseppe De; Rilke, F

doi:10.1016/s0959-8049(05)80442-3

Cited by 21 publications

(10 citation statements)

References 5 publications

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“…In agreement with other reports, we show that HPV infection associated with VIN III lesions occurred predominantly in younger patients, and was not related to p53 expression (6,15,16,21). In spite of having detected only nine patients with superficially invasive vulvar carcinomas between 1983 and 1995, our intention was to identify any similarity with the VIN III or with the invasive carcinoma group.…”

Section: Discussionsupporting

confidence: 93%

“…It seems that HPV is related to a minority of cases, especially in younger women, with the basaloid variant of squamous carcinoma and associated vulvar intraepithelial neoplasia (VIN) (1,2,9,10). HPV DNA is detected in about 10-20% of all vulvar squamous cell carcinomas (6,11,12), and in 50-80% of the basaloid subtype of invasive carcinoma (2,5,8,11). However, most vulvar carcinomas occur in older patients, are predominantly of the usual keratinizing type and are associated with lichen sclerosus and squamous hyperplasia, suggesting that vulvar carcinomas may have different etiologies, with HPV and other factors possibly playing a significant role and are still a matter of debate (1,2,9,(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

“…Inactivation of its tumor suppressing activity seems to be an almost universal step in the development of human malignancies and may also be related to tumor progression (2,4,6,7). p53 inactivation in vulvar carcinomas can occur either by interaction with HPV E6 oncoprotein, or by p53 gene mutation in the absence of the virus.…”

Section: Introductionmentioning

confidence: 99%

“…p53 inactivation in vulvar carcinomas can occur either by interaction with HPV E6 oncoprotein, or by p53 gene mutation in the absence of the virus. In addition, several cellular proteins and events can also interfere with or inhibit p53-mediated transactivation functions (2)(3)(4)(5)(6)(7)13). p53 expression has been described in 50 to 88% of cases of vulvar squamous cell carcinoma (2,5,6,(15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

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Human papillomavirus infection and p53 protein expression in vulvar intraepithelial neoplasia and invasive squamous cell carcinoma

Engelman

Andrade

Vassallo

2003

Braz J Med Biol Res

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The etiopathogenesis of vulvar intraepithelial neoplasia (VIN III) and invasive squamous cell carcinoma are largely unknown. Since there are few studies on Brazilian patients, our purpose was to determine the frequency of human papillomavirus (HPV) infection and the expression of p53 in these lesions, and associate them with other factors such as age, morphological subtypes, multicentric and multifocal disease. Thirty-eight cases of VIN III, nine of superficially invasive carcinoma, and 55 of invasive vulvar carcinoma were retrospectively evaluated from 1983 to 1995 for the presence of HPV by immunohistochemistry and in situ hybridization, and for p53 protein expression by immunohistochemistry on paraffin sections. All cases for whom material (slides and paraffin blocks) and clinical data were available were included. HPV and p53 were detected in 57.9 and 21.1% of the VIN III lesions, 33.3 and 66.7% of superficially invasive carcinomas, and 7.3 and 58.2% of invasive squamous cell carcinomas, respectively. HPV infection was associated with younger age in the VIN III and invasive carcinoma groups. In the latter, HPV infection was associated with the basaloid variant. p53 expression rate was higher in superficially invasive and invasive lesions and was not related to HPV infection. Our findings are similar to others and support the hypothesis that there are two separate entities of the disease, one associated with HPV and the other unrelated, with p53 inactivation possibly being implicated in some of the cases. Correspondence

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Human papillomavirus infection and p53 protein expression in vulvar intraepithelial neoplasia and invasive squamous cell carcinoma

Engelman

Andrade

Vassallo

2003

Braz J Med Biol Res

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“…Many reports show that alterations in p53 may affect the carcinogenesis of the vulva more than that of the cervix, in which HPV infection predominates as a causative agent (3)(4)(5)(6). More recent data suggest that the overexpression of p53 protein is a late event and that the gene is a useful marker to predict lymph node metastasis in squamous cell carcinoma (7)(8)(9)(10).…”

mentioning

confidence: 99%

Loss in 3p and 4p and Gain of 3q Are Concomitant Aberrations in Squamous Cell Carcinoma of the Vulva

Jee

Kim

et al. 2001

Modern Pathology

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Neoplasm of the vulva is a rare malignancy accounting for <5% of all female genital-tract cancer. However, in recent years the incidence of vulva intraepithelial neoplasia, known to serve as a precursor to carcinoma, has increased in young women generating considerable interest in its pathogenesis. Genetic changes at the molecular level in precursor or invasive vulvar tumors are not well investigated, and DNA copy number changes have not been reported until now. We used comparative genomic hybridization (CGH) to analyze genetic alterations in 10 primary invasive squamous cell carcinomas of the vulva. Chromosomal aberrations were identified in 8/10 cases. The most frequent chromosomal losses were 4p13-pter (five cases), 3p (four cases), and 5q (two cases), and less frequent losses were detected at 6q, 11q, and 13q (one case each). The most frequent chromosomal gains were 3q (four cases) and 8p (three cases), and less frequent gains were found in 9p, 14, 17, and 20q (one case each). The pattern of chromosomal imbalance in vulvar cancer detected by CGH was revealed to be very similar to that in cervical cancers, despite regional differences in their prevalence. These results suggest that the pathogenic pathways in vulvar and cervical carcinomas may be similar and that the genetic background may be common to these two squamous cell carcinomas.

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p53 protein overexpression is common and independent of human papillomavirus infection in squamous cell carcinoma of the vulva

Kagie¹,

Kenter²,

Tollenaar³

et al. 1997

Cancer

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METHODS.Immunohistochemical methods for the detection of p53 protein and consensus primer polymerase chain reaction (PCR) were used, followed by direct 1 Department of Gynecology, Leiden University sequencing of the PCR product for the evaluation of HPV subtype infection. SixtyMedical Centre, The Hague, The Netherlands.six patients with squamous cell carcinoma of the vulva were available for this study. pending on the method of detection and the carcinoma subtype.5-8

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Papillomavirus, p53 alteration and primary carcinoma of the vulva

Cited by 21 publications

References 5 publications

Human papillomavirus infection and p53 protein expression in vulvar intraepithelial neoplasia and invasive squamous cell carcinoma

Human papillomavirus infection and p53 protein expression in vulvar intraepithelial neoplasia and invasive squamous cell carcinoma

Loss in 3p and 4p and Gain of 3q Are Concomitant Aberrations in Squamous Cell Carcinoma of the Vulva

p53 protein overexpression is common and independent of human papillomavirus infection in squamous cell carcinoma of the vulva

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