Absence of Human Papillomavirus E6–E7 Transforming Genes from HPV 16 and 18 in Malignant Ovarian Carcinoma

Chen, Timothy R.; Chan, Philip J.; Seraj, Ibrahim M.; King, Alan

doi:10.1006/gyno.1998.5255

Cited by 16 publications

(27 citation statements)

References 15 publications

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“…Therefore, the involvement of HPV infection in epithelial ovarian cancer has been an interesting issue. However, previous studies in different laboratories provided highly controversial results (Kaufman et al, 1987;Leake et al, 1989;Beckmann et al, 1991;Lai et al, 1992Lai et al, , 1994Duggan et al, 1995;Runnebaum et al, 1995;Sworn et al, 1995;Trottier et al, 1995;Anwar et al, 1996;Kedzia et al, 1996;Mai et al, 1996;Zimna et al, 1997;Manolitsas et al, 1998;Anttila et al, 1999;Chen et al, 1999;Ip et al, 2002). We report here that HPV-16 was found in a series of histologically characterised epithelial ovarian carcinomas from Chinese women.…”

mentioning

confidence: 56%

“…To date about 16 additional reports on HPV infection in ovarian tumours were found in the MEDLINE. Among these, 10 analysed more than 10 tumour specimens in each report (Leake et al, 1989;Beckmann et al, 1991;Lai et al, 1992Lai et al, , 1994Runnebaum et al, 1995;Trottier et al, 1995;Zimna et al, 1997;Anttila et al, 1999;Chen et al, 1999;Ip et al, 2002). Only in four of the 10 studies, HPV infection was found in ovarian cancers (Lai et al, 1992(Lai et al, , 1994Zimna et al, 1997;Ip et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

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Detection of human papillomavirus-16 in ovarian malignancy

Guo

et al. 2003

Br J Cancer

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Human papillomavirus is the causal factor for cervical cancer. However, the role of HPV infection in ovarian cancer is unclear. This study aimed to determine the presence of human papillomavirus-16 (HPV-16) in ovarian cancer tissues. Archived human ovarian cancer tissues (N ¼ 54 cases, 50 are epithelial cancer, four are nonepithelial cancer) embedded in paraffin blocks were used. Controls are 30 nonmalignant ovarian tissue blocks. In situ hybridisation (ISH) and immunohistochemistry (IHC) were used to detect the presence of HPV-16 and p53 expression. In all, 52 or 36% of the epithelial ovarian tumours detected by ISH or IHC, respectively, were HPV-16 E6 positive. In contrast, only 6.7% of normal ovarian tissues were HPV-16 positive proved by ISH. Human papillomavirus-16 infection was significantly higher in cancer tissues compared to controls with an odds ratio of 16.7 (95% confidence interval [CI] ¼ 3.2 -71.4, Po0.01). No significant correlation between HPV-16 infection and histological types of cancer was found (P40.05). p53 gene expression was detected in 42% epithelial ovarian cancers. No correlation between p53 expression and HPV-16 infection was found. The results showed the presence of HPV-16 E6 in ovarian carcinoma, suggesting that HPV infection might play a role in ovarian carcinogenesis.

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confidence: 56%

Section: Discussionmentioning

confidence: 99%

Detection of human papillomavirus-16 in ovarian malignancy

Guo

et al. 2003

Br J Cancer

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“…HPV is not considered an etiologic agent in the pathogenesis of primary ovarian tumors 3,7,11,18,34,40,45,52,53,61,64 ; hence, any observed diffuse expression of p16 in ovarian carcinomas (particularly the common serous type which constitutes most of the tumors analyzed in the studies referenced) would not be expected to be the result of HPV-induced molecular alterations. The lack of diffuse p16 expression in virtually all primary ovarian tumors analyzed in the current study is consistent with this concept and provides immunohistochemical evidence that HPV is not involved in the pathogenesis of primary ovarian mucinous and endometrioid tumors.…”

Section: Discussionmentioning

confidence: 90%

“…Biotin-labeled HPV probe solutions (Dako Corporation, Carpinteria, CA) were applied to individual sections. These included a wide spectrum probe (cocktail of HPV 6,11,16,18,31,33,45,51) and separate type specific probes for HPV 16 and HPV 18. Detection of hybridized probe was performed by tyramide catalyzed signal amplification using the Dako Genpoint Kit (Dako).…”

Section: Hpv Dna Detectionmentioning

confidence: 99%

p16 Expression in Primary Ovarian Mucinous and Endometrioid Tumors and Metastatic Adenocarcinomas in the Ovary

Vang

Gown²,

Farinola³

et al. 2007

American Journal of Surgical Pathology

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Distinction of primary ovarian epithelial tumors from metastatic adenocarcinomas is challenging for tumors exhibiting mucinous, endometrioid, or mixed endometrioid/mucinous differentiation. Metastatic carcinomas with these types of differentiation can be derived from several sites, including the gastrointestinal tract and the uterus. Most endocervical adenocarcinomas exhibit mucinous and/or endometrioid differentiation; they infrequently metastasize to the ovaries but may simulate primary ovarian tumors [both atypical proliferative (borderline) and carcinoma]. Most are high-risk human papillomavirus (HPV)-related and demonstrate diffuse p16 over-expression due to complex molecular mechanisms by which high-risk HPV transforming proteins interact with cell cycle regulatory proteins. The performance of this expression pattern for identifying metastatic endocervical adenocarcinomas in the ovaries among primary ovarian tumors and other metastatic adenocarcinomas having mucinous and/or endometrioid/endometrioidlike differentiation has not been evaluated. Immunohistochemical expression of p16 was assessed in 195 tumors, including 98 primary ovarian tumors (51 mucinous, 47 endometrioid, and 4 mixed mucinous-endometrioid tumors), 93 metastatic adenocarcinomas of known primary sites (colorectum: 34, endocervix: 19, pancreaticobiliary tract: 17, appendix: 7, stomach: 5), 11 metastatic adenocarcinomas of unknown origin (7 established as noncervical), and 4 adenocarcinomas of uncertain (primary ovarian vs. metastatic) origin. The HPV status of the endocervical adenocarcinomas was determined by in situ hybridization and polymerase chain reaction (when in situ hybridization was negative). Expression was assessed based on the percentage of moderately to strongly positive cells, estimated to the nearest 10%. Mean and median expression values for HPV-positive endocervical adenocarcinomas (99%, 100%; range 90% to 100%) were substantially higher than those for primary ovarian mucinous (5%, 0%; range 0% to 70%) and endometrioid (20%, 10%; range 0% to 100%) tumors, HPV-unrelated endocervical adenocarcinomas (0%, 0%; range 0% to 60%), metastatic adenocarcinomas of unknown origin (11%, 0%; range 0% to 30%), and adenocarcinomas of uncertain (primary ovarian vs. metastatic) origin (40%, 35%; range 0% to 90%); only the 15 HPV-positive endocervical adenocarcinomas and 6 other tumors had values of 80% or greater. Diffuse (>75% positive tumor cells) moderate to strong p16 expression is a sensitive (100%) and specific (97%) marker for identifying HPV-related endocervical adenocarcinomas metastatic to the ovary among the primary ovarian tumors and metastatic adenocarcinomas from other sites that are in the differential diagnosis of ovarian tumors having mucinous and/or endometrioid/endometrioidlike differentiation. p16 is useful as part of a panel of immunohistochemical markers for distinguishing primary ovarian tumors from metastases and, when diffusely positive, can suggest the cervix as a potential primary site for metastatic adenocarcinomas...

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“…HPV DNA was generally detected in endometrial cancer although at a much lower frequency than in cervical cancer [4][5][6][7][8][9][10][11][12][13]. However, reports on HPV DNA in ovarian cancer have been conflicting [5,7,10,[13][14][15][16][17][18][19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Comparison of Human Papillomavirus DNA Levels in Gynecological Cancers: Implication for Cancer Development

Yang¹,

Liu²,

Tsang³

et al. 2003

Tumor Biol

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We have previously demonstrated the presence of human papillomavirus (HPV) DNA in several gynecological cancers using conventional PCR. In the present study, to further understand the role of HPV in malignant transformation of these cancers, the infection rates and viral loads of HPV 16 and 18 in gynecological cancers were analyzed using real-time quantitative PCR (qPCR). HPV 16 DNA was detected in 61.0% (58/95), 15.2% (7/46) and 32.1% (18/56) of cases of cervical, endometrial and ovarian cancers, respectively. On the other hand, HPV 18 DNA was detected in 23.2% (22/95) of cervical cancers, 1.8% (1/56) of ovarian cancers, and in no cases of endometrial cancer. Thus, HPV 16 is much more prevalent than HPV 18 in malignancies of the female genital tract. We also found that both HPV 16 and 18 were significantly (p < 0.05) less frequently present in endometrial and ovarian cancers than in cervical cancer. The median copy numbers of HPV 16 DNA in endometrial and ovarian cancers were 3,500 and 7,590 copies/µg DNA, respectively. These amounts were also significantly (p < 0.05) lower than HPV 16 DNA in cervical cancer (492,800 copies/µg DNA). Thus, HPV 16 could be detected in all three types of gynecological cancer, whilst HPV 18 is extremely rare in endometrial and ovarian cancers. The lower HPV 16 infection rates and lower copy numbers when compared with cervical cancer tend to suggest that HPV plays a less essential role in the development of endometrial cancer and ovarian cancer.

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Absence of Human Papillomavirus E6–E7 Transforming Genes from HPV 16 and 18 in Malignant Ovarian Carcinoma

Cited by 16 publications

References 15 publications

Detection of human papillomavirus-16 in ovarian malignancy

Detection of human papillomavirus-16 in ovarian malignancy

p16 Expression in Primary Ovarian Mucinous and Endometrioid Tumors and Metastatic Adenocarcinomas in the Ovary

Comparison of Human Papillomavirus DNA Levels in Gynecological Cancers: Implication for Cancer Development

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