Transmission of High-Risk Human Papillomavirus (HPV) between Parents and Infant: a Prospective Study of HPV in Families in Finland

Rintala, Marjut; Grénman, Seija; Puranen, Mirja; Isolauri, Erika; Ekblad, Ulla; Kero, Pentti; Syrjänen, Stina

doi:10.1128/jcm.43.1.376-381.2005

Cited by 173 publications

(219 citation statements)

References 28 publications

Supporting

Mentioning

204

Contrasting

Unclassified

Order By: Relevance

“…Studies have demonstrated that oral infection by HPV is not uncommon [3,9]. However, evidence suggests that virtually all immune competent patients clear the viral infections [10][11][12][13], supporting the hypothesis that most individuals experience only transient infection.…”

Section: Introductionmentioning

confidence: 92%

B7-H1 Expression Model for Immune Evasion in Human Papillomavirus-Related Oropharyngeal Squamous Cell Carcinoma

Ukpo

Thorstad

Lewis

2012

Head and Neck Pathol

122

104

View full text Add to dashboard Cite

Human papillomavirus (HPV) is associated with oropharyngeal squamous cell carcinomas. Persistent viral infection is postulated to lead to carcinogenesis, although infection of benign adjacent epithelium is not typically observed. It is known that immune evasive tumor cells can provide an ideal niche for a virus. The B7-H1/ PD-1 cosignaling pathway plays an important role in viral immune evasion by rendering CD8? cytotoxic T cells anergic. We hypothesized that HPV-related oropharyngeal squamous cell carcinomas express B7-H1 as a mechanism for immune evasion. A tissue microarray was utilized, for which HPV E6/E7 mRNA by in situ hybridization was previously performed. Immunohistochemistry was performed to detect B7-H1 and staining was characterized by pattern, distribution, and intensity. B7-H1 was expressed by 84 of the 181 (46.4 %) cases. Both tumor cell membranous and cytoplasmic expression were present and cytoplasmic expression was identified in some peritumoral lymphocytes. Expression was analyzed in several different ways and then considered binarily as positive versus negative. Tumors expressing B7-H1 were more likely to be HPV positive (49.2 vs. 34.1 %, p = 0.08). B7-H1 expression showed no correlation with disease recurrence in the entire cohort (OR = 1.09, p = 0.66), HPV positive cohort (OR = 0.80, p = 0.69) or HPV negative cohort (OR = 2.02, p = 0.22). However, B7-H1 expression intensity did correlate with the development of distant metastasis (p = 0.03), and B7-H1 intensity of 3? (versus all other staining) showed a strong trend towards distant metastasis in the HPV positive (OR = 6.67, p = 0.13) and HPV negative (OR = 9.0, p = 0.13) cohorts. There was no correlation between B7-H1 expression and patient survival for any of the different ways in which staining was characterized, whether binarily, by distribution, intensity, or combined scores. B7-H1 is expressed in the majority of oropharyngeal squamous cell carcinomas with transcriptionally-active HPV. This suggests that B7-H1 expression by tumor cells may play a role in harboring persistent HPV infection.

show abstract

Section: Introductionmentioning

confidence: 92%

B7-H1 Expression Model for Immune Evasion in Human Papillomavirus-Related Oropharyngeal Squamous Cell Carcinoma

Ukpo

Thorstad

Lewis

2012

Head and Neck Pathol

122

104

View full text Add to dashboard Cite

show abstract

“…In addition, in two independent studies, HPV 16 has been found to be present in breast tumours that occur in European women with HPV 16-associated cervical cancer (Hennig et al, 1999;Widschwendter et al, 2004). Virions (virus particles) are shed from desquamating keratinocytes (the target cells for HPV infections) and high-risk HPVs can be transmitted by close human nonsexual contact (Bryan and Brown, 2001;Rintala et al, 2005). Accordingly, we speculate that HPVs may be transmitted by hand from the female perineum to the breast which could occur, for example, during showering or bathing.…”

Section: ----------------------------C------------------------------4mentioning

confidence: 99%

Identification of human papillomavirus DNA gene sequences in human breast cancer

et al. 2005

View full text Add to dashboard Cite

Human papilloma viruses (HPVs) are accepted as being carcinogenic in human cervical and anogenital cancers. The suspicion that HPVs may also have a role in human breast cancer is based on the identification of HPVs in human breast tumours and the immortalisation of normal human breast cells by HPV types 16 and 18. For this investigation, DNA that had been previously extracted and fresh frozen at À701C from 50 unselected invasive ductal breast cancer specimens were screened by polymerase chain reaction (PCR) for HPV type 16, 18 and 33 gene sequences. We show that HPV 18 gene sequences are present in DNA extracted from breast tumours in Australian women. Overall, 24 (48%) of the 50 samples were HPV positive. Overall no correlations with tumour grade, patient survival, steroid receptor status, ERB-2, p53 expression and mutation were observed. Human papilloma viruses may have a role in human breast cancer. We speculate that HPVs may be transmitted by hand from the female perineum to the breast. It is accepted that human papillomavirus (HPV) types 16 and 18 are carcinogenic, and that probably HPV types 31 and 33 are also carcinogenic in human cervical and anogenital cancers (IARC, 1995). The suspicion that HPVs may also have a role in human breast cancer is based on the identification of HPVs in human breast tumours and the immortalisation of normal human breast cells by HPV 16 and 18 (Band et al, 1990;De Villiers et al, 2005).Human papilloma virus 16 has been identified in breast tumours in Italian women and breast tumours in Norwegian women who had previous cervical neoplasia (Hennig et al, 1999). Human papilloma virus 33 has been identified in breast cancer in Chinese and Japanese women (Yu et al, 1999) MATERIALS AND METHODSFor this investigation, DNA that had been previously extracted and fresh frozen at À70 O C from 50 unselected invasive ductal breast cancer specimens were screened by polymerase chain reaction (PCR) for HPV type 16, 18 and 33 gene sequences. The DNA samples were amplified twice per sample using GenomiPhit DNA Amplification Kit (Amersham Biosciences). The DNA quality was confirmed by PCR, amplifying 268 bp of the b-globin gene. These samples were then screened for the presence of HPV by PCR using primers that could detect 140 bp in the E6 region of HPV 16, 18 and 33 (Yu et al, 1999). DNA extracted from cervical cancer cell lines HeLa and SiHa cells were used as positive controls for HPV 18 and 16, respectively. Plasmid plink 322 HPV 33 was used as a positive control for HPV 33. DNA from leukaemia Raji cells was used a negative control. The PCR products were separated on 7.6% PAGE and visualised by SYBR Green I (Molecular Probes). The screening was repeated five times using different batches of DNA samples amplified by the GenomiPhit DNA Amplification Kit (Amersham Biosciences). Human papilloma virus-positive samples were sequenced (there was sufficient material to sequence 18 of 24 HPV-positive samples).Grade of tumour and survival of patients were known for each sample. Screening for exons 5...

show abstract

“…Peripartum vertical transmission of HPV infection to infants has been reported. 33 However, although the incidence of cervical cancer is higher in South than in North America because of differences in screening practices, HPV infection prevalence is quite similar. We consider it less likely that the behavior of these viruses would differ by geography; however, we cannot entirely exclude the possibility of a critical cofactor (e.g.…”

mentioning

confidence: 99%

Human retinoblastoma is not caused by known pRb‐inactivating human DNA tumor viruses

Gillison¹,

Chen²,

Goshu³

et al. 2007

Intl Journal of Cancer

View full text Add to dashboard Cite

Retinoblastomas occur as the consequence of inactivation of the tumor suppressor retinoblastoma protein (pRb), classically upon biallelic inactivation of the RB1 gene locus. Recently, human papillomavirus (HPV) genomic DNA has been detected in retinoblastomas. To investigate the possibility that oncoproteins encoded by pRb-inactivating DNA tumor viruses play a role in the pathogenesis of human retinoblastoma, 40 fresh-frozen tumors were analyzed for the presence of HPV, adenovirus (HAdV) and polyomavirus (BKV, JCV and SV40) genomic DNA sequences by real-time polymerase chain reaction (PCR). Tumors were screened for genetic and epigenetic alterations in all 27 exons of the RB1 gene locus and promoter by exonic copy number detection, sequencing and methylation-specific PCR of the promoter region. Retinoblastoma tumors from children with bilateral familial (n 5 1), bilateral nonfamilial (n 5 1) and unilateral nonfamilial (n 5 38) disease were analyzed. Inactivating modifications to the RB1 gene locus were identified on both the alleles in 27 tumors, one allele in 8, and neither allele in 5 cases. A median of over 107,000 tumor cells were analyzed for viral genomic DNA in each PCR reaction. All tumor samples were negative for 37 HPV types, 51 HAdV types, BKV and JCV genomic sequences. Very low copy number (0.2-260 copies per 100,000 tumor cells) SV40 genomic DNA detected in 8 of 39 samples was demonstrated to be consistent with an artifact of plasmid-derived SV40. In contrast to recent reports, we obtained substantial quantitative evidence indicating that neither HPV nor any other pRb-inactivating human DNA tumor viruses play a role in the development of retinoblastoma, regardless of RB1 genotype. ' 2006 Wiley-Liss, Inc.Key words: human papillomavirus; retinoblastoma; virus; causation Retinoblastoma is a rare childhood cancer of the retina, classically initiated by loss or mutation of both alleles of the retinoblastoma gene (RB1) during retinal development. Children with an inherited or de novo germline mutation in the RB1 gene develop bilateral or unilateral retinoblastoma with high penetrance, accounting for 40% of cases. In the majority of remaining cases, unilateral tumors occur as a consequence of somatic mutations that inactivate both RB1 alleles. Upon detailed analysis, mutations of the RB1 promoter or coding region can be identified in 92% of suspected RB1 alleles either as heterozygous germline mutations in heritable cases or as biallelic mutations in retinoblastoma tumors. 1 However, no RB1 inactivating event has been identified in 8% of RB1 alleles, leaving open the possibility that some retinoblastomas may be caused by alternative genetic or epigenetic events that modify retinoblastoma protein (pRB) function.The RB1 gene on chromosome 13q14 encodes a nuclear phosphoprotein (the tumor suppressor pRb) that plays a key regulatory role in the cell cycle check point between G1 and entry into Sphase. 2 In addition to mutations in the RB1 gene, pRb function can be abrogated by oncoproteins from several DNA tum...

show abstract

Transmission of High-Risk Human Papillomavirus (HPV) between Parents and Infant: a Prospective Study of HPV in Families in Finland

Cited by 173 publications

References 28 publications

B7-H1 Expression Model for Immune Evasion in Human Papillomavirus-Related Oropharyngeal Squamous Cell Carcinoma

B7-H1 Expression Model for Immune Evasion in Human Papillomavirus-Related Oropharyngeal Squamous Cell Carcinoma

Identification of human papillomavirus DNA gene sequences in human breast cancer

Human retinoblastoma is not caused by known pRb‐inactivating human DNA tumor viruses

Contact Info

Product

Resources

About