Absence of human papillomavirus sequences in ovarian pathologies

Trottier, Anne-Marie; Provencher, Diane; Mes‐Masson, Anne‐Marie; Vauclair, R; Coutlée, François

doi:10.1128/jcm.33.4.1011-1013.1995

Cited by 30 publications

(25 citation statements)

References 20 publications

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“…Interestingly, three tumors were localized in the ovary. The presence of HPV DNA in ovarian cancers was reported by some researchers [Mai et al, 1996;Pins et al, 1997], while others found no HPV in several ovarian pathologies [Sworn et al, 1995;Trottier et al, 1995].…”

Section: Discussionmentioning

confidence: 85%

HPV16 and HPV18 in genital tumors: Significantly different levels of viral integration and correlation to tumor invasiveness

Badaracco¹,

Venuti²,

Sedati³

et al. 2002

Journal of Medical Virology

121

103

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The integration of the high-risk HPV16 and HPV18 types into the cell genome is considered an important step in malignant transformation. The relationship between the physical status of the virus and clinical/pathological parameters was studied by type-specific and multiplex PCR for E6, E2, and E1 sequences in 86 genital tumors from different sites, consisting of 69 invasive carcinomas (including 5 microinvasive carcinomas), 9 carcinomas in situ, 6 severe dysplasias, and 2 moderate dysplasias. Forty tumors contained HPV16 (46.6%), 7 HPV18 (8.1%), and 39 both viruses (45.3%). HPV16 DNA was found either as pure integrant (35.4%), or pure episome (36.7%), or a mixture of both (27.8%). Conversely, all 46 lesions containing HPV18 showed pure integrated forms. The physical status of both types was not related to the tumor site, the tumor/node/metastasis stage, or the histological differentiation grade of the invasive carcinomas. HPV16 integration was significantly associated with invasiveness. Interestingly, in double infections when HPV16 coexisted with HPV18, its genome was found more frequently in episomal form than in single infections where, conversely, it was mostly integrated (P < 0.0001), suggesting a sort of competition for cell integration sites. The complete HPV18 integration, even in pre-neoplastic lesions, indicates a different behavior in genital transformation compared with HPV16 and may reflect a major aggressiveness of this viral type. In conclusion, virus typing in conjunction with the evaluation of the integration status may provide a better prognostic evaluation together with an improved diagnosis.

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Section: Discussionmentioning

confidence: 85%

HPV16 and HPV18 in genital tumors: Significantly different levels of viral integration and correlation to tumor invasiveness

Badaracco¹,

Venuti²,

Sedati³

et al. 2002

Journal of Medical Virology

121

103

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“…In reviewing the reference list in these articles, we identified one more article. Of the 35 identified studies, 22 were considered relevant after thorough examination. The remaining 13 studies were excluded for the following reasons: they were case reports ( n = 4) ; the data from these were included in another study ( n = 3) ; the paper reported HPV prevalence in serum and not HPV DNA in ovarian cancer tissue ( n = 1) ; endometrial and ovarian cancer were not differentiated ( n = 1) ; the information about how data were acquired was inadequate ( n = 1) ; the study included fewer than five ovarian cancer cases ( n = 1) ; the study only included borderline tumors ( n = 1) or the study was retracted after publication because of an error ( n = 1) .…”

Section: Resultsmentioning

confidence: 99%

“…The characteristics of the studies included are presented in Table . In most studies, the subjects were women with ovarian cancer of epithelial origin , and ovarian cancer was classified into histological subtypes , serous ovarian cancer being the most common. Two publications failed to report the type of ovarian malignancy .…”

Section: Resultsmentioning

confidence: 99%

Prevalence of human papillomavirus in epithelial ovarian cancer tissue. A meta‐analysis of observational studies

Svahn

Faber

Christensen

et al. 2013

Acta Obstet Gynecol Scand

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“…66,67 Previous studies have uniformly failed to demonstrate the presence of HPV in primary ovarian carcinomas. [68][69][70] Nevertheless, the view that these are metastatic has been challenged and discussed in the literature, the alternative being that the neoplastic change in the ovary occurs as a part of a field change to a common oncogenic insult. It is postulated that this may be facilitated by transtubal transfer of HPVinfected or transformed cells and disruption of the ovarian surface due to ovulatory injury in women in their reproductive years.…”

Section: Synchronous Cervical and Ovarian Neoplasmsmentioning

confidence: 93%

Synchronous tumours of the female genital tract

Singh

2010

Histopathology

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About 1-2% of women with gynaecological cancers are found to have two or more simultaneous independent primary malignancies. Low stage multiple primaries must be distinguished from metastasis from one to other site for correct management. Synchronous tumours in the ovary and endometrium are the commonest combination. Most of these can be accurately categorised by standard histological criteria. Molecular testing has been advocated for valuable adjunctive information in ambiguous cases but must be interpreted with clinicopathological correlation: loss of heterozygosity, pTEN or beta-catenin gene mutational analysis, microsatellite instability and most recently gene expression profiling have all been used. The pattern of beta-catenin immunohistochemical expression has been reported to be of value. A very low percentage of women with synchronous primaries in the uterus and ovary are HNPCC patients and testing for mismatch repair gene mutations is unnecessary in all cases, even if young; the diagnosis of HNPCC should be based on standard criteria. Women with endometrial cancer under 50 are more likely than older patients to have a synchronous ovarian cancer. Rarer combinations of synchronous tumours are less well studied but may also represent a mixture of unusual patterns of metastasis and multifocal origin; these are discussed briefly.

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Absence of human papillomavirus sequences in ovarian pathologies

Cited by 30 publications

References 20 publications

HPV16 and HPV18 in genital tumors: Significantly different levels of viral integration and correlation to tumor invasiveness

HPV16 and HPV18 in genital tumors: Significantly different levels of viral integration and correlation to tumor invasiveness

Prevalence of human papillomavirus in epithelial ovarian cancer tissue. A meta‐analysis of observational studies

Synchronous tumours of the female genital tract

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