The distribution and differential risks of human papillomavirus genotypes in cervical preinvasive lesions: a Taiwan Cooperative Oncologic Group Study

Chen, Chi-An; Liu, C. Y.; Chou, Hung-Hsueh; Chou, Cheng-Yang; Ho, Chih‐Ming; Twu, Nae‐Fang; Kan, Yuen-Yee; Chuang, Mei-Hsing; Chu, Tang–Yuan; Hsieh, Chang‐Yao

doi:10.1111/j.1525-1438.2006.00655.x

Cited by 43 publications

(30 citation statements)

References 30 publications

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“…HPV 58 was reported to have a relatively high frequency in women from east Asia (Chen et al, 2006;Huang et al, 1997) and some regions of Central and South America Gonzalez-Losa Mdel et al, 2004), and it may be considered for production of second-generation HPV prophylactic vaccines. Little information, however, is available regarding physical status and gene variation of the HPV 58 genome in cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

Profile of physical status and gene variation of human papillomavirus 58 genome in cervical cancer

Enqi

Xiao

et al. 2009

Journal of General Virology

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Epidemiological studies have shown that human papillomavirus 58 (HPV 58) is found at a relatively high frequency in east Asia and some regions of Central and South America. To investigate the physical status of HPV 58 and analyse sequence variations of HPV 58 in cervical cancer patients, the HPV 58 genome in 37 HPV 58-positive cervical cancer specimens collected from China were investigated by a mapping analysis based on nested PCR and nucleotide sequencing. A pure integrated genome was found in 78.4 % (29/37) of specimens, which is much higher than that found in previous studies. Multiple disruptions were first found among the integrated HPV 58 genomes in 51.7 % (15/29) of specimens. Among the 7824 bp of the HPV 58 genome, 119 (1.52 %) nucleotide positions were found to be variable, and 45 of them lead to amino acid changes. Phylogenetic analyses, based on partial L1 sequences of 14 variants isolated in previous studies and this study, show that two main groups were observed in HPV 58 variants, the prototype or prototype-like group and the non-prototype-like group.

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Section: Introductionmentioning

confidence: 99%

Profile of physical status and gene variation of human papillomavirus 58 genome in cervical cancer

Enqi

Xiao

et al. 2009

Journal of General Virology

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“…Although, specimens with HPV 16, 18, 52, and 58 represent about 43% of all LSILs (Chen et al, 2006), they represented 73% of HSILs in our cohort study. As a result of the relatively small proportion of HPV 16 in women with LSILs in Taiwan, it seems that distinguishing the risk of cervical precancer among HPV 16-positive women from the lower risk posed by other oncogenic HPV types might have limited clinical value.…”

Section: Discussionmentioning

confidence: 99%

“…The Taiwan Cooperative Oncology Group (TCOG), conducted a multicenter study -T1899, (Sun et al, 2005;Chen et al, 2006). Of the 1246 participants, 936 underwent cervical biopsies for histological examinations.…”

Section: Methodsmentioning

confidence: 99%

Human papillomaviral load changes in low-grade squamous intraepithelial lesions of the uterine cervix

Cheng

Chu

et al. 2006

Br J Cancer

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To better predict risk of progression of low-grade squamous intraepithelial lesions (LSILs) of the uterine cervix in women with human papillomavirus (HPV) infections, 294 baseline cervical specimens from women with LSILs were evaluated. Specimens were tested for HPV DNA using hybrid capture 2 (HC2) and PCR-reverse line blotting. 65 LSILs with HPV DNA types 16, 18, 52, or 58 were examined for physical status, E2/E6 ratio and viral load at two time points, along with patient age. Women with LSILs whose viral loads increased between baseline and 6 month follow-up had a 45% risk of developing HSIL (OR ¼ 7.6, 95% CI ¼ 1.9 -29.4, Po0.01), as evaluated by real-time PCR and a 44% risk (OR ¼ 6.1, 95% CI ¼ 1. Human papillomavirus (HPV) plays an important role in the carcinogenesis of cervical cancer (Bosch et al, 1995;Walboomers et al, 1999). The most common oncogenic HPV type in preinvasive and cervical cancer is HPV 16, detectable in 21% of women with low-grade squamous intraepithelial lesions (LSILs) (Castle et al, 2005), in more than 50% of women with cervical intraepithelial neoplasia grade 3 (CIN 3), and women with cervical cancer in America and Europe (Bosch et al, 1995;Herrero et al, 2000; Munoz et al, 2003). HPV 18 causes 10 -15% of CIN 3 and cervical cancers (Bosch et al, 1995). In addition, HPV 18 also causes more than 35% of cervical adenocarcinomas, which are difficult to detect by current screening methods (Bosch et al, 1995). Additionally, HPV 52 and 58 are as prevalent as HPV 16 and 18 in patients with preinvasive and cervical cancer in Taiwan and Asian countries (Liaw et al, 1995;Huang et al, 1997;Ho et al, 2005Ho et al, , 2006. Approximately 50% of atypical squamous cells of undetermined significance (ASCUS) and 80% of LSILs are infected by oncogenic types of HPV (ALTS group, 2000;Solomon et al, 2001). HPV DNA testing for patients with ASCUS provides useful information and allows referral of patients for immediate colposcopy to detect highgrade squamous intraepithelial lesions (HSILs) and cancer (Solomon et al, 2001). In contrast, oncogenic HPV DNA testing is not informative for triage of patients with LSILs because a high percentage of LSIL patients are HPV positive (ALTS group, 2000). A repeat Pap smear in 3 -6 months or direct biopsy under colposcopy is generally used in clinical practice. Development of alternative triage strategies for women with LSILs would be valuable in distinguishing women with LSILs that have high probabilities of progression to HSILs from women with LSILs that have spontaneously regressed.As a result of the lack of sufficiently large prospective longitudinal follow-up studies and the different geographic distributions of HPV types, it has not been established how the risk of HSILs differs during transition by physical status of HPV 16, 18, 52, and 58 DNA (integrated versus episomal DNA) during longitudinal follow-up, viral loads (high vs low) and viral load change (increased vs not increased) between baseline and followup among women with LSILs. To examine this issue, we evalu...

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“…For India HPV 16 and 18 account for 82.5% (14). Some countries (Taiwan, Hong Kong, and Singapore who are primarily constituted of Han Chinese, who share common ancestors from the south-eastern coast of China) report a pattern of relative preponderance of HPV 52 and 58, after HPV 16 and 18 (15)(16)(17)(18)(19).…”

Section: Relative Contribution To Cervical Cancer By Oncogenic Hpv Gementioning

confidence: 99%

Cervical Cancer Burden and Prevention Strategies: Asia Oceania Perspective

Garland

Bhatla

Ngan

2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The Asia Oceania region contributes to more than 50% of cervical cancer cases worldwide. Yet cervical cancer is one of few cancers that can be prevented through comprehensive screening for precancerous lesions, with their subsequent treatment. Screening with cervical cytology, a very old technology, has reduced cervical cancer mortality and incidence when applied in comprehensive programs with high coverage and high quality assurance.

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The distribution and differential risks of human papillomavirus genotypes in cervical preinvasive lesions: a Taiwan Cooperative Oncologic Group Study

Cited by 43 publications

References 30 publications

Profile of physical status and gene variation of human papillomavirus 58 genome in cervical cancer

Profile of physical status and gene variation of human papillomavirus 58 genome in cervical cancer

Human papillomaviral load changes in low-grade squamous intraepithelial lesions of the uterine cervix

Cervical Cancer Burden and Prevention Strategies: Asia Oceania Perspective

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