HPV oligonucleotide microarray-based detection of HPV genotypes in cervical neoplastic lesions☆

Kim, Chan Joo; Jeong, Jeongmi Kim; Park, Misun; Park, Tae Shin; Park, Tae Chul; Namkoong, Sung Eun; Park, Jong Sup

doi:10.1016/s0090-8258(02)00069-0

Cited by 76 publications

(84 citation statements)

References 32 publications

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“…This method is based on the polymerase chain reaction with an advantage to detect single and multiple infection of 22 HPV genotypes at once and has reported to be a very sensitive method comparable with Hybrid Capture II assay. 17,22 In the present study, we found that the overall HPV prevalence in the cervical adenocarcinoma among Korean women was 90%, and HPV 16 (42%) appeared to be more prevalent than HPV 18 (29%), which was followed by HPV 16 þ 18 (7%) and HPV 33 (5%). It is of interest that the particular subtypes such as endometrioid and villoglandular type were predominantly associated with HPV 16.…”

Section: Discussionmentioning

confidence: 46%

Prevalence of human papillomavirus DNA in various histological subtypes of cervical adenocarcinoma: a population-based study

Kim

et al. 2005

Modern Pathology

115

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The role of human papilloma virus (HPV) infection in the development of cervical carcinoma is well established, however, the prevalence of HPV DNA in cervical adenocarcinoma varies from study to study. It appears to be caused by a number of factors, one of which is that cervical adenocarcinomas comprise a heterogeneous group of multiple subtypes. To clarify the impact of HPV infection on the development of cervical adenocarcinoma with diverse histological subtypes, we performed a population-based study in Korean women from 15 different institutes for the status of HPV infection in adenocarcinoma of uterine cervix. A total of 432 cervical adenocarcinomas from 1997 to 2001 were reviewed and classified according to the modified WHO classification. For 135 cases, HPV typing was performed with HPV DNA chip (82 cases) and PCR HPV typing (53 cases), using formalin-fixed, paraffin-embedded archival tissue. The overall prevalence of HPV infection in cervical adenocarcinoma was 90%. The infection of HPV 16 and/or HPV 18 accounted for 78% of HPV-positive adenocarcinomas. Multiple HPV types were found in 13% of the cases. The HPV DNA was rarely detected in minimal deviation adenocarcinoma. Interestingly, HPV 16 was a predominant type in endometrioid and villoglandular types, whereas HPV 16 and HPV 18 were detected with equal prevalence in other subtypes. In conclusion, HPV infection, mostly HPV 16 and HPV 18, is highly associated with most of the cervical adenocarcinomas, whereas endometrioid and villoglandular type have a different pattern of HPV infection status. Minimal deviation adenocarcinoma does not seem to be related with HPV infection. Modern Pathology (2005) 18, 528-534, advance online publication, 22 October 2004; doi:10.1038/modpathol.3800316Keywords: cervical adenocarcinoma; HPV infection; HPV DNA Chip; PCR-based HPV typingThe incidence and proportion of adenocarcinoma relative to squamous cell carcinoma in the uterine cervix has been increasing over the past several decades. Recent reports indicated that the adenocarcinoma accounted for 20-25% in uterine cervical cancer compared with only 5-15% in the past. [1][2][3] The epidemiologic risk for cervical adenocarcinoma is similar to those for invasive squamous cell carcinoma, such as multiple sexual partners and the early onset of sexual intercourse, which are related to the risk factors of human papilloma virus (HPV) infection. 4 Whereas the role of HPV infection in the development of cervical squamous cell carcinoma is well established, the pathogenetic role of the HPV in the cervical adenocarcinoma is still

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Section: Discussionmentioning

confidence: 46%

Prevalence of human papillomavirus DNA in various histological subtypes of cervical adenocarcinoma: a population-based study

Kim

et al. 2005

Modern Pathology

115

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“…Cervical cancer cell lines were stained with FITC-labeled anti-HLA class I (Beckman Coulter, Fullerton, CA) and analyzed as above. [49][50][51][52][53][54][55][56][57] peptide-specific CTLs can be generated and lyse E6-transduced 293T cells…”

Section: Tetramer Construction and Flow Cytometric Analysismentioning

confidence: 99%

“…A CTL line that could lyse peptide-pulsed autologous B-LCL was successfully generated from the CIN patient but not from healthy volunteer donors. Intracellular cytokine staining demonstrated that E6 [49][50][51][52][53][54][55][56][57] peptidepulsed autologous B-LCL induced IFN-g production in 52.7% of CD3 1 cells from the CTL line, whereas induction with the other 2 peptides was negligible (Fig. 1a).…”

Section: Hpv-16 E6mentioning

confidence: 99%

“…14 Bortezomib is a selective but reversible inhibitor of both standard proteasomes and immunoproteasomes. [15][16][17][18] In the present study, using a reverse immunological approach, we identified an HLA-A*2402-restricted HPV-16 E6-derived nonameric epitope, E6 [49][50][51][52][53][54][55][56][57] . A CD8 1 T cell clone, specific for this epitope, initially failed to recognize untreated HPV-16 1 cervical cancer cell lines; however, recognition was evident on bortezomib treatment, particularly with simultaneous IFN-g treatment in combination.…”

mentioning

confidence: 99%

“…A CD8 1 T cell clone, specific for this epitope, initially failed to recognize untreated HPV-16 1 cervical cancer cell lines; however, recognition was evident on bortezomib treatment, particularly with simultaneous IFN-g treatment in combination. Furthermore, induction of E6 [49][50][51][52][53][54][55][56][57] -specific T cells detectable by HLA-A24/E6 [49][50][51][52][53][54][55][56][57] tetramers was possible in 5 of 7 patients with HPV-16 1 high grade cervical intraepithelial neoplasia (CIN) or cervical cancer by in vitro stimulation with the E6 [49][50][51][52][53][54][55][56][57] peptide. These results indicate E6 [49][50][51][52][53][54][55][56][57] to be an endogenously processed HLA-A*2402-restricted CTL epitope, and the limited supply of HPV-16 E6 peptides observed in cervical cancer cells may be, at least in part, overcome by coadministration of IFN-g and bortezomib.…”

mentioning

confidence: 99%

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Identification of an HLA‐A24‐restricted cytotoxic T lymphocyte epitope from human papillomavirus type‐16 E6: The combined effects of bortezomib and interferon‐γ on the presentation of a cryptic epitope

Akatsuka

Nawa

Kondo

et al. 2006

Intl Journal of Cancer

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About 50% of cervical cancers are associated with human papillomavirus type 16 (HPV-16), and since the HPV-16 E6 and E7 oncoproteins are constitutively expressed in the tumor cells, they are attractive targets for cytotoxic T lymphocyte (CTL)-mediated immunotherapy. Nevertheless, only a limited number of HPV-16 E6 epitopes have been identified to date. Using reverse immunological methods, we have generated a CTL clone against the HPV-16 E6 49-57 epitope restricted by HLA-A*2402, which is the most common allele in Japan and relatively frequent worldwide, capable of lysing 293T cells transduced with HLA-A*2402 and HPV-16 E6. Although it was unable to recognize the SiHa cervical cancer cell line positive for HPV-16 and HLA-A*2402, the cells became susceptible to lysis when transduced with E6-E7 genes, which was unexpectedly offset by pretreatment with interferon (IFN)-c alone. Interestingly, however, combined pretreatment with a proteasome inhibitor, bortezomib and IFN-c fully restored CTL-mediated lysis of the original SiHa cells. Furthermore, such intervention of 2 of 4 other cervical cancer cell lines expressing HPV-16 E6 and HLA-A*2402 was found to induce IFN-c production by specific CTLs. Tetramer analysis further revealed that induction of E6 49-57 -specific T cells was possible in 5 of 7 patients with HPV-16-positive high grade cervical intraepithelial neoplasia or cervical cancer by in vitro stimulation with E6 49-57 peptide. Thus, these findings together indicate that E6 49-57 is a candidate epitope for immunotherapy and immunological monitoring of such patients. ' 2006 Wiley-Liss, Inc.Key words: cytotoxic T lymphocyte; tumor immunity; epitope, cervical neoplasm; bortezomib Cervical cancer, the second most common cancer in women worldwide, with 250,000 new cases diagnosed each year, 1 is causally linked with human papillomavirus (HPV), the first proposed necessary cause of a human cancer as assessed by the World Health Organization. 2 High-risk HPV-16 is the most common type in all countries, with an overall prevalence of more than 50% in cervical cancers, 3 and 42.4% in Japanese patients. 4 Approximately 95% of HPV infections of the anogenital tract resolve spontaneously because of immune responses, 5 and the risk of cervical cancer is markedly increased in patients with immunodeficiency. [6][7][8] These findings suggest that the immune system plays a pivotal role in preventing development and progression of cervical cancer.Two HPV oncoproteins, E6 and E7, which can inhibit the tumor suppressors, p53 and RB respectively, are constitutively expressed in cervical cancer cells and appear to be required to maintain their malignant growth. 9 These viral oncoproteins, which are not present in normal cells, have been considered to be attractive targets for specific immunotherapy against cervical cancer, and identification and characterization of cytotoxic T lymphocyte (CTL) epitopes for HPV have facilitated the development of peptide vaccines against cervical cancer. Most of the CTL epitopes identified to date ...

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Human papillomavirus testing and molecular markers of cervical dysplasia and carcinoma

Dehn¹,

Torkko²,

Shroyer

2007

Cancer

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HPV oligonucleotide microarray-based detection of HPV genotypes in cervical neoplastic lesions☆

Cited by 76 publications

References 32 publications

Prevalence of human papillomavirus DNA in various histological subtypes of cervical adenocarcinoma: a population-based study

Prevalence of human papillomavirus DNA in various histological subtypes of cervical adenocarcinoma: a population-based study

Identification of an HLA‐A24‐restricted cytotoxic T lymphocyte epitope from human papillomavirus type‐16 E6: The combined effects of bortezomib and interferon‐γ on the presentation of a cryptic epitope

Human papillomavirus testing and molecular markers of cervical dysplasia and carcinoma

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