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  • 1
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    Comprehensive analysis of human papillomavirus prevalence and the potential role of low-risk types in verrucous carcinoma
    Elsevier BV ; 2012
    In:  Modern Pathology Vol. 25, No. 10 ( 2012-10), p. 1354-1363
    Details
    In: Modern Pathology, Elsevier BV, Vol. 25, No. 10 ( 2012-10), p. 1354-1363
    Type of Medium: Online Resource
    ISSN: 0893-3952
    URL: Article
    DOI: 10.1038/modpathol.2012.91
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
    detail.hit.zdb_id: 2041318-X
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  • 2
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    Somatic mutation in PIK3CA is a late event in cervical carcinogenesis
    Wiley ; 2015
    In:  The Journal of Pathology: Clinical Research Vol. 1, No. 4 ( 2015-10), p. 207-211
    Details
    In: The Journal of Pathology: Clinical Research, Wiley, Vol. 1, No. 4 ( 2015-10), p. 207-211
    Abstract: Somatic mutations in cervical intraepithelial neoplasia (CIN) are largely unknown. Here, we profiled 35 cervical carcinomas and 23 CIN grade 2/3 (CIN2/3) for mutations in 48 cancer‐related genes using a Next Generation Sequencing‐based cancer panel. PIK3CA exon 9 was the most frequently mutated locus in cervical carcinoma and the only mutated locus detected in CIN2/3. These PIK3CA exon 9 mutation findings were verified in a large, independent series ( n  = 647) covering all stages of cervical carcinogenesis using high resolution melting‐guided Sanger sequencing. PIK3CA exon 9 mutation frequency was 37.1% (13/35; 95%CI 21.2–54.0%) in cervical carcinoma, and 2.4% (5/209; 95%CI 0.5–4.7%) in CIN3. No PIK3CA exon 9 mutations were detected in CIN2 (0/144), CIN1 (0/154) and normal cervix (0/105). In a third series of 46 CIN2/3 lesions from women with a known 5‐year history of preceding high‐risk human papillomavirus (hrHPV) infection, detection of PIK3CA exon 9 mutation was confined to 2 (5.4%; 95%CI 0.0–13.2%) CIN3 lesions with preceding hrHPV infection ≥5 years, and was absent in those with a short duration ( 〈 5 years) of preceding hrHPV infection. In conclusion, somatic mutation in PIK3CA represents a late event during cervical carcinogenesis, detected in a substantial subset of cervical carcinoma, but only in a minority of CIN3.
    Type of Medium: Online Resource
    ISSN: 2056-4538 , 2056-4538
    URL: Issue
    URL: Article
    DOI: 10.1002/cjp2.v1.4
    DOI: 10.1002/cjp2.27
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2814357-7
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  • 3
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    Detection of hypermethylated genes as markers for cervical screening in women living with HIV
    Wiley ; 2018
    In:  Journal of the International AIDS Society Vol. 21, No. 8 ( 2018-08)
    Details
    In: Journal of the International AIDS Society, Wiley, Vol. 21, No. 8 ( 2018-08)
    Abstract: To evaluate the performance of hypermethylation analysis of ASCL 1 , LHX 8 and ST 6 GALNAC 5 in physician‐taken cervical scrapes for detection of cervical cancer and cervical intraepithelial neoplasia ( CIN ) grade 3 in women living with HIV ( WLHIV ) in South Africa. Methods Samples from a prospective observational cohort study were used for these analyses. Two cohorts were included: a cohort of WLHIV who were invited for cervical screening ( n  =   321) and a gynaecologic outpatient cohort of women referred for evaluation of abnormal cytology or biopsy proven cervical cancer ( n  =   108, 60% HIV seropositive). Cervical scrapes collected from all subjects were analysed for hypermethylation of ASCL 1 , LHX 8 and ST 6 GALNAC 5 by multiplex quantitative methylation specific PCR ( qMSP ). Histology endpoints were available for all study subjects. Results Hypermethylation levels of ASCL 1 , LHX 8 and ST 6 GALNAC 5 increased with severity of cervical disease. The performance for detection of CIN 3 or worse ( CIN 3 + ) as assessed by the area under the receiver operating characteristic ( ROC ) curves ( AUC ) was good for ASCL 1 and LHX 8 ( AUC 0.79 and 0.81 respectively), and moderate for ST 6 GALNAC 5 ( AUC 0.71). At a threshold corresponding to 75% specificity, CIN 3 + sensitivity was 72.1% for ASCL 1 and 73.8% for LHX 8 and all samples from women with cervical cancer scored positive for these two markers. Conclusions Hypermethylation analysis of ASCL 1 or LHX 8 in cervical scrape material of WLHIV detects all cervical carcinomas with an acceptable sensitivity and good specificity for CIN 3 + , warranting further exploration of these methylation markers as a stand‐alone test for cervical screening in low‐resource settings.
    Type of Medium: Online Resource
    ISSN: 1758-2652 , 1758-2652
    URL: Issue
    URL: Article
    DOI: 10.1002/jia2.2018.21.issue-8
    DOI: 10.1002/jia2.25165
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2467110-1
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  • 4
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    Genomic profiling identifies common HPV-associated chromosomal alterations in squamous cell carcinomas of cervix and head and neck
    Springer Science and Business Media LLC ; 2009
    In:  BMC Medical Genomics Vol. 2, No. 1 ( 2009-12)
    Details
    In: BMC Medical Genomics, Springer Science and Business Media LLC, Vol. 2, No. 1 ( 2009-12)
    Abstract: It is well known that a persistent infection with high-risk human papillomavirus (hrHPV) is causally involved in the development of squamous cell carcinomas of the uterine cervix (CxSCCs) and a subset of SCCs of the head and neck (HNSCCs). The latter differ from hrHPV-negative HNSCCs at the clinical and molecular level. Methods To determine whether hrHPV-associated SCCs arising from different organs have specific chromosomal alterations in common, we compared genome-wide chromosomal profiles of 10 CxSCCs (all hrHPV-positive) with 12 hrHPV-positive HNSCCs and 30 hrHPV-negative HNSCCs. Potential organ-specific alterations and alterations shared by SCCs in general were investigated as well. Results Unsupervised hierarchical clustering resulted in one mainly hrHPV-positive and one mainly hrHPV-negative cluster. Interestingly, loss at 13q and gain at 20q were frequent in HPV-positive carcinomas of both origins, but uncommon in hrHPV-negative HNSCCs, indicating that these alterations are associated with hrHPV-mediated carcinogenesis. Within the group of hrHPV-positive carcinomas, HNSCCs more frequently showed gains of multiple regions at 8q whereas CxSCCs more often showed loss at 17p. Finally, gains at 3q24-29 and losses at 11q22.3-25 were frequent ( 〉 50%) in all sample groups. Conclusion In this study hrHPV-specific, organ-specific, and pan-SCC chromosomal alterations were identified. The existence of hrHPV-specific alterations in SCCs of different anatomical origin, suggests that these alterations are crucial for hrHPV-mediated carcinogenesis.
    Type of Medium: Online Resource
    ISSN: 1755-8794
    URL: Article
    DOI: 10.1186/1755-8794-2-32
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2009
    detail.hit.zdb_id: 2411865-5
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  • 5
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    HPV‐mediated cervical carcinogenesis: concepts and clinical implications
    Wiley ; 2006
    In:  The Journal of Pathology Vol. 208, No. 2 ( 2006-01), p. 152-164
    Details
    In: The Journal of Pathology, Wiley, Vol. 208, No. 2 ( 2006-01), p. 152-164
    Abstract: Persistent infection with a high‐risk human papillomavirus (hrHPV) is generally accepted as a necessary cause of cervical cancer. However, cervical cancer is a rare complication of an hrHPV infection since most such infections are transient, not even giving rise to cervical lesions. On average, it takes 12–15 years before a persistent hrHPV infection may ultimately, via consecutive premalignant stages (ie CIN lesions), lead to an overt cervical carcinoma. This argues that HPV‐induced cervical carcinogenesis is multi‐step in nature. In this review, the data from hrHPV‐mediated in vitro transformation studies and those obtained from analysis of clinical specimens have been merged into a cervical cancer progression model. According to this model, a crucial decision maker in the early stages following infection involves individual susceptibility for certain HPV types depending on the genetic make‐up of immune surveillance determinants. Once a CIN lesion has developed, altered transcriptional regulation of the viral E6/E7 oncogenes, resulting in genomic instability and distinguishing the process of cell transformation from a productive viral infection, probably provides the subsequent important step towards malignancy. The additional (epi)genetic alterations that subsequently accumulate in high‐grade CIN lesions may result in overt malignancy via immortality and growth conditions that gradually become less sensitive to growth‐modulating influences mediated by cytokines and cell–cell and cell–matrix adhesions. The potential implications of hrHPV testing and some other biomarkers deduced from this model for cervical screening and the clinical management of CIN disease are also discussed. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.v208:2
    DOI: 10.1002/path.1866
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 1475280-3
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  • 6
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    Repression of MAL tumour suppressor activity by promoter methylation during cervical carcinogenesis : Promoter methylation represses MAL in cervical cancer
    Wiley ; 2009
    In:  The Journal of Pathology Vol. 219, No. 3 ( 2009-11), p. 327-336
    Details
    In: The Journal of Pathology, Wiley, Vol. 219, No. 3 ( 2009-11), p. 327-336
    Type of Medium: Online Resource
    ISSN: 0022-3417
    URL: Article
    DOI: 10.1002/path.2598
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 1475280-3
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  • 7
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    Abstract 4959: Deregulation of microRNA expression patterns during cervical carcinogenesis
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4959-4959
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4959-4959
    Abstract: At present little is known about the involvement of alterations in microRNA (miRNA) expression patterns during the development of cervical cancer. In this study we investigated genome-wide miRNA expression profiles in normal cervical squamous epithelium, high-grade precancerous lesions (CIN2/3), squamous cell carcinomas (SCC) and adenocarcinomas (AdCAs), all of which were high-risk HPV positive. In addition, miRNA expression profiles were integrated with previously generated genome-wide chromosomal profiles of the same samples. Unsupervised hierarchical clustering showed that miRNA expression profiling enables the distinction of normal cervical squamous epithelium, CIN2/3 lesions, SCCs and AdCAs. Differential miRNA expression analysis comparing normals, CIN2/3 lesions and SCCs identified early (temporal), late, and continuously differentially expressed miRNAs in cervical carcinogenesis (n=106). Differential expression of selected miRNAs could be validated by qRT-PCR in the same samples as well as in cervical scrapes of women with abnormal cytology and underlying high-grade CIN disease compared to control scrapes. In general, miRNAs located in the same cluster showed similar expression profiles, suggesting common regulatory mechanisms. For 5 of the 106 differentially expressed miRNAs, altered expression could be directly linked to underlying chromosomal alterations. Finally, cell viability assays indicated that ectopic expression of 2 selected miRNAs influenced cell proliferation in vitro, indicating functional relevance of differential miRNA expression during cervical carcinogenesis. In conclusion, deregulation of miRNA expression patterns occurs during cervical carcinogenesis and has functional relevance for cervical cancer development. Since deregulated miRNA expression in cervical (pre)malignant disease is reflected and detectable in cervical scrapes, miRNAs represent a highly promising class of disease markers for further improvement of the triage of high-risk HPV positive women. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4959. doi:10.1158/1538-7445.AM2011-4959
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-4959
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    HPV type-related chromosomal profiles in high-grade cervical intraepithelial neoplasia
    Springer Science and Business Media LLC ; 2012
    In:  BMC Cancer Vol. 12, No. 1 ( 2012-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2012-12)
    Abstract: The development of cervical cancer and its high-grade precursor lesions (Cervical Intraepithelial Neoplasia grade 2/3 [CIN2/3]) result from a persistent infection with high-risk human papillomavirus (hrHPV) types and the accumulation of (epi)genetic host cell aberrations. Epidemiological studies have demonstrated variable CIN2/3 and cancer risks between different hrHPV types. Recent genomic profiling studies revealed substantial heterogeneity in the chromosomal aberrations detected in morphologically indistinguishable CIN2/3 suggestive of varying cancer risk. The current study aimed to investigate whether CIN2/3 with different hrHPV types vary with respect to their chromosomal profiles, both in terms of the number of aberrations and chromosomal loci affected. Methods Chromosomal profiles were determined of 43 p16 INK4a -immunopositive CIN2/3 of women with long-term hrHPV infection (≥ 5 years). Sixteen lesions harboured HPV16, 3 HPV18, 14 HPV31, 1 HPV33, 4 HPV45, 1 HPV51, 2 HPV52 and 2 HPV58. Results Unsupervised hierarchical clustering analysis of the chromosomal profiles revealed two major clusters, characterised by either few or multiple chromosomal aberrations, respectively. A majority of 87.5% of lesions with HPV16 were in the cluster with relatively few aberrations, whereas no such unbalanced distribution was seen for lesions harbouring other hrHPV types. Analysis of the two most prevalent types (HPV16 and HPV31) in this data set revealed a three-fold increase in the number of losses in lesions with HPV31 compared to HPV16-positive lesions. In particular, losses at chromosomes 2q, 4p, 4q, 6p, 6q, 8q & 17p and gain at 1p & 1q were significantly more frequent in HPV31-positive lesions (FDR 〈 0.2). Conclusions Chromosomal aberrations in CIN2/3 are at least in part related to the hrHPV type present. The relatively low number of chromosomal aberrations observed in HPV16-positive CIN2/3 suggests that the development of these lesions is less dependent on genetic insult than those caused by other types like HPV31.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/1471-2407-12-36
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
    detail.hit.zdb_id: 2041352-X
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  • 9
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    Development of a multiplex methylation-specific PCR as candidate triage test for women with an HPV-positive cervical scrape
    Springer Science and Business Media LLC ; 2012
    In:  BMC Cancer Vol. 12, No. 1 ( 2012-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2012-12)
    Abstract: Quantitative methylation-specific PCR (qMSP) analysis for determining the methylation status of (candidate) tumor suppressor genes has potential as objective and valuable test to triage high-risk human papillomavirus (hrHPV) positive women in cervical screening. Particularly combined methylation analysis of a panel of genes shows most promising clinical performance, with sensitivity levels that equal or exceed that of cytology. However, the wide application of such methylation marker panels is hampered by the lack of effective multiplex assays allowing simultaneous methylation detection of various targets in a single reaction. Here, we designed and analyzed a multiplex qMSP assay for three genes whose methylation was previously found to be informative for cervical (pre)cancer (i.e. CADM1, MAL and hsa-miR-124-2) as well as a reference gene β-actin. Based on our experience, we discuss the optimization of the parameters that provide a practical approach towards multiplex qMSP design. Methods Primers and PCR reagents were optimized for multiplex qMSP purposes and the resulting assay was analytically validated on serial dilutions of methylated DNA in unmethylated DNA, and compared with singleplex counterparts on hrHPV-positive cervical scrapings. Results Upon optimization, including primer redesign and primer limiting assays, the multiplex qMSP showed the same analytical performance as the singleplex qMSPs. A strong correlation between the obtained normalized ratios of the singleplex and multiplex qMSPs on cervical scrapes was found for all three markers: CADM1 (R 2 =0.985), MAL (R 2 =0.986) and hsa-miR-124-2 (R 2 =0.944). Conclusion Multiplex qMSP offers a promising approach for high-throughput diagnostic analysis of the methylation status of multiple genes, which after proper design and validation can be equally specific, sensitive and reproducible as its singleplex versions.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/1471-2407-12-551
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
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  • 10
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    Methylation-mediated silencing and tumour suppressive function of hsa-miR-124 in cervical cancer
    Springer Science and Business Media LLC ; 2010
    In:  Molecular Cancer Vol. 9, No. 1 ( 2010-12)
    Details
    In: Molecular Cancer, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2010-12)
    Abstract: A substantial number of microRNAs (miRNAs) is subject to epigenetic silencing in cancer. Although epigenetic silencing of tumour suppressor genes is an important feature of cervical cancer, little is known about epigenetic silencing of miRNAs. Since DNA methylation-based silencing of hsa-miR-124 occurs in various human cancers, we studied the frequency and functional effects of hsa-miR-124 methylation in cervical carcinogenesis. Results Quantitative MSP analysis of all 3 loci encoding the mature hsa-miR-124 (hsa-miR-124-1/-2/-3) showed methylation in cervical cancer cell lines SiHa, CaSki and HeLa as well as in late passages of human papillomavirus (HPV) type 16 or 18 immortalised keratinocytes. Treatment of SiHa cells with a demethylating agent reduced hsa-miR-124 methylation levels and induced hsa-miR-124 expression. In HPV-immortalised keratinocytes increased methylation levels were related to reduced hsa-miR-124 expression and higher mRNA expression of IGFBP7 , a potential hsa-miR-124 target gene. Ectopic hsa-miR-124 expression in SiHa and CaSki cells decreased proliferation rates and migratory capacity. Combined hsa-miR-124-1 and/or hsa-miR-124-2 methylation analysis of 139 cervical tissue specimens showed an increasing methylation frequency from 0% in normal tissues up to 93% in cervical carcinomas. Increased methylation levels of hsa-miR-124-1 and hsa-miR-124-2 were significantly correlated with reduced hsa-miR-124 expression in cervical tissue specimens. Combined hsa-miR-124-1 and/or hsa-miR-124-2 methylation analysis of 43 cervical scrapes of high-risk HPV positive women was predictive of underlying high-grade lesions. Conclusions DNA methylation-based silencing of hsa-miR-124 is functionally involved in cervical carcinogenesis and may provide a valuable marker for improved detection of cervical cancer and its high-grade precursor lesions.
    Type of Medium: Online Resource
    ISSN: 1476-4598
    URL: Article
    DOI: 10.1186/1476-4598-9-167
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 2091373-4
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