Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study

Sanjosé, Sílvia de; Quint, Wim; Alemany, Laia; Geraets, D.T.; Klaustermeier, Joellen; Lloveras, Belén; Tous, Sara; Félix, Ana; Bravo, Luis Eduardo; Shin, Hai Rim; Vallejos, Carlos S.; Ruı́z, Patricia Alonso de; Lima, Marcus Aurelho de; Guimerà, Núria; Clavero, Omar; Alejo, María; Llombart‐Bosch, Antonio; Chou, Cheng-Yang; Tatti, Sílvio; Kasamatsu, Elena; Iljazović, Ermina; Odida, Michael; Prado, Renato Luiz; Seoud, Muhieddine; Grce, Magdalena; Usubütün, Alp; Jain, Asha; Suarez, Gustavo Adolfo Hernandez; Lombardi, Luis Estuardo; Banjo, Aekunbiola; Menéndez, Clara; Domingo, Efren J.; Velasco, Julio; Nessa, Ashrafun; Chichareon, Saibua; Qiao, You‐Lin; Lerma, Enrique; Garland, Suzanne M.; Sasagawa, Toshiyuki; Ferrera, Annabelle; Hammouda, Doudja; Mariani, Luciano; Pelayo, Adela; Steiner, I; Oliva, Esther; Meijer, Chris J.L.M.; Al-Jassar, Waleed; Cruz, Eugénia; Wright, Thomas; Puras, A; Llave, Cecilia; Tzardi, Maria; Αγοραστός, Θεόδωρος; García-Barriola, Victoria; Clavel, Christine; Ordi, Jaume; Andújar, Miguel; Castellsagué, Xavier; Sánchez, Gloria Inés; Nowakowski, Andrzej; Bornstein, Jacob; Muñóz, Núbia; Bosch, F. Xavier

doi:10.1016/s1470-2045(10)70230-8

Cited by 2,150 publications

(2,252 citation statements)

References 23 publications

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“…In agreement with results reported in a nearby country having comparable socioeconomic status,16 our results indicated that the prevalence of HPV infection of any genotypes in Saudi CxCa patients (77%) is below the estimated worldwide range (85%‐99%) 3, 4, 17. Statistical analysis revealed that this rate is significantly lower than the lowest (85%) global estimation (1 sample z‐test; 95% CI, 71% ‐ 82%; P = .001).…”

Section: Discussionsupporting

confidence: 91%

“…However, its incidence is not uniform in various populations having different socioeconomic and national human development levels; a large majority of the global burden occurs in less‐developed regions, and the lowest rates are in western Asia 1. Infection with human papillomavirus (HPV) stands out as being the main cause among all known risk factors, and high‐risk HPVs drive the major carcinogenic events in the pathogenesis of CxCa, with an estimated worldwide prevalence ranging between 85% and 99% 2, 3, 4. In contrast, CxCa incidence is low in a few countries, even though they lack national screening programs 5.…”

Section: Introductionmentioning

confidence: 99%

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Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence

Al-Harbi

Judia

Khoja

et al. 2017

Cancer

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BACKGROUNDCervical cancer is a predominantly human papillomavirus (HPV)‐driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C single nucleotide polymorphism (SNP) presumed to affect cancer incidence.METHODSPatients treated between 1990 and 2012 were reviewed, and a series of 232 invasive cervical cancer cases were studied and compared with 313 matched controls without cancer. SNP was genotyped by way of direct sequencing. HPV linear array analysis was used to detect and genotype HPV in tumor samples.RESULTSThe incidence of cervical cancer revealed bimodal peaks at 42.5 years, with a slighter rebound at 60.8 years. Among all cases, 77% were HPV‐positive and 16 HPV genotypes were detected—mostly genotypes 16 (75%) and 18 (9%)—with no difference by age, histology, or geographical region. Although the TP53 G72C genotype was not associated with overall cervical cancer risk, it was significantly associated with HPV positivity (odds ratio, 0.57; 95% confidence interval, 0.36‐0.90; P = .016). Furthermore, the variant C allele was significantly overtransmitted in the population (P < .0003).CONCLUSIONCervical cancer incidence displays bimodal curve peaking at a young age with secondary rebound at older age. The combination of relative low HPV infection and variant TP53 72C allele overtransmission provide a plausible explanation for the low incidence of cervical cancer in our population. Therefore, HPV screening and host SNP genotyping may provide more relevant biomarkers to gauge the risk of developing cervical cancer. Cancer 2017;123:2459–66. © 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence

Al-Harbi

Judia

Khoja

et al. 2017

Cancer

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“…On the other hand, HPV18 and 45 showed a low PPV for CIN2/3+ despite being responsible for a considerable proportion of invasive cancers 31, 32. This discrepancy, already observed in many studies having high‐grade CIN as the endpoint,6, 10, 33, 34 could result from a different natural history of cell transformation induced by HPV18 and 45.…”

Section: Discussionmentioning

confidence: 93%

Human papilloma virus genotyping for the cross‐sectional and longitudinal probability of developing cervical intraepithelial neoplasia grade 2 or more

Mistro

Adcock

Carozzi

et al. 2018

Intl Journal of Cancer

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Human papilloma virus (HPV) testing is more sensitive but less specific than cytology. We evaluated stand‐alone genotyping as a possible triage method. During a multicentre randomised controlled trial comparing HPV testing to conventional cytology, HPV‐positive women were referred to colposcopy and followed up if no high‐grade lesion was detected. HPV‐positive samples were genotyped by GP5+/GP6+ primed polymerase chain reaction followed by reverse line blot. Genotypes were hierarchically ordered by positive predictive value (PPV) for CIN grade 2 or more (CIN2+), and grouped by cluster analysis into three groups (A, B and C in decreasing order). Receiver operating characteristic curves were computed. Among 2,255 HPV‐positive women with genotyping, 239 CIN2+ (including 113 CIN3+) were detected at baseline or during a 3‐year follow‐up. HPV33 had the highest PPV with CIN2+ and CIN3+ as the endpoint and when considering lesions detected at baseline or also during follow‐up. HPV16 and HPV35 were the second and third, respectively. Cross‐sectional sensitivity for CIN2+ at baseline was 67.3% (95% CI 59.7–74.2), 91.8% (95% CI 86.6–95.5) and 94.7% (95% CI 90.2–97.6), respectively, when considering as “positive” any of the HPV types in group A (33, 16 and 35), A or B (31, 52, 18, 59 and 58) and A or B or C (39, 51, 56, 45 and 68). The corresponding cross‐sectional PPVs for CIN2+ were 15.8% 95% (CI 13.2–18.7), 12.0% (95% CI 10.3–13.9) and 9.6% (95% CI 8.2–11.1), respectively. HPV33, 16 and 35 confer a high probability of CIN2+ but this rapidly decreases when adding other genotypes.

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“…4 Overall, single and multiple infections assessed by BS-L1-MPG. 5 Overall, single and multiple infections assessed by TS-E7-MPG assay.…”

Section: Transcriptionally Active Hpv Types In Cxca Tissues With Multmentioning

confidence: 99%

“…1,2 Epidemiological studies have demonstrated that 20 mucosal HPV types from five phylogenetically related species of the genus alpha (a5, a6, a7, a9 and a11-termed as ''high-risk clade'') are consistently found as single HPV infections in CxCa worldwide. [3][4][5][6] Based on their frequency in CxCa and available biological data, 12 of these types, i.e., types 16,18,31,33,35,39,45, 51, 52, 56, 58 and 59 have been defined as carcinogens (IARC Group 1A)-hereafter referred to as high-risk (HR)-HPV. For eight other types, in the high-risk clade, i.e., types 26, 53, 66, 67, 68, 70, 73 and 82, the combination of their low frequency, lack of data on their active transcription and their transforming potential in model systems, has led them to be classified as only probable/possible carcinogens (IARC Groups 2A and 2B)-hereafter referred to as possible highrisk (pHR)-HPV types.…”

mentioning

confidence: 99%

Biological activity of probable/possible high‐risk human papillomavirus types in cervical cancer

Halec

Schmitt

Dondog

et al. 2012

Intl Journal of Cancer

109

155

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Judging the carcinogenicity of human papillomavirus (HPV) types rarely found in cervical cancer (CxCa) is hindered by lack of studies of their biological activity in cancer tissues. To asses transcriptional activity of HPV types, we have developed ultrashort amplimer, splice-site specific, E6*I mRNA RT-PCR assays for 12 high-risk (HR)-HPV (IARC Group 1) and eight probable/ possible high-risk (pHR)-HPV types (IARC Group 2A/B carcinogens). Previously unreported E6*I splice sites of the six pHR-HPV types 26, 53, 67, 70, 73 and 82 were identified by cloning and sequencing. We analyzed 97 formalin-fixed paraffin-embedded (FFPE) Mongolian CxCa biopsies for presence of HPV DNA by two sensitive genotyping assays, for E6*I transcripts of all HR-/ pHR-HPV types identified and for expression of HPV surrogate markers p16 INK4a , pRb and p53. E6*I of at least one HR-/pHR-HPV was expressed in 94 (98%) of cancer tissues including seven with pHR-HPV types 26, 66, 70 or 82 as single transcribed types. Fifty-eight of E6*I mRNA transcribing cases were analyzable by immunohistochemistry and displayed p16 INK4a overexpression in 57 (98%), pRb downregulation in 56 (97%) and p53 downregulation in 36 (62%) tissues. The newly developed E6*I mRNA RT-PCR assays appeared to be highly sensitive method to analyze HPV transcription in FFPE materials. Our finding of viral oncogene transcription of pHR-HPV types 26, 66, 70 and 82 in cervical tumors, in the absence of any other transcriptionally active HR-type and with p16 INK4a overexpression and pRb downregulation, may support a reassessment of the carcinogenicity classification of these pHR-HPV types.Human papillomaviruses (HPV) with currently more than 150 types defined are a complex group differing in tropism and carcinogenic potential. Detection of HPV DNA in 99.7% of cervical cancer (CxCa) cases has established HPV as an etiological factor for CxCa development. 1,2 Epidemiological studies have demonstrated that 20 mucosal HPV types from five phylogenetically related species of the genus alpha (a5, a6, a7, a9 and a11-termed as ''high-risk clade'') are consistently found as single HPV infections in CxCa worldwide. [3][4][5][6] Based on their frequency in CxCa and available biological data, 12 of these types, i.e., types 16,18,31,33,35,39, 45, 51, 52, 56, 58 and 59 have been defined as carcinogens (IARC Group 1A)-hereafter referred to as high-risk (HR)-HPV. For eight other types, in the high-risk clade, i.e., types 26, 53, 66, 67, 68, 70, 73 and 82, the combination of their low frequency, lack of data on their active transcription and their transforming potential in model systems, has led them to be classified as only probable/possible carcinogens (IARC Groups 2A and 2B)-hereafter referred to as possible highrisk (pHR)-HPV types. 7 In the era of HPV-based cervical cancer precursor screening and of type-specific HPV vaccination, understanding the oncogenic properties of individual

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Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study

Cited by 2,150 publications

References 23 publications

Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence

Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence

Human papilloma virus genotyping for the cross‐sectional and longitudinal probability of developing cervical intraepithelial neoplasia grade 2 or more

Biological activity of probable/possible high‐risk human papillomavirus types in cervical cancer

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