Characterization of human papillomavirus type 6b DNA isolated from an invasive squamous carcinoma of the vulva

Kasher, M S; Roman, Ann

doi:10.1016/0042-6822(88)90676-9

Cited by 73 publications

(51 citation statements)

References 23 publications

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“…O, ACTGT sequences (an arrow indicates the ACTGT sequence previously suggested to be important in silencer activity; Wu & Mounts, 1988). (a) 94 bp insertion relative to HPV-6b at nt 7350; (b) 24 bp insertion at nt 7323; (c) 58 bp insertion at nt 7350; (d) 49 bp deletion at nt 7350 (Kasher & Roman, 1988;Farr et al, 1991). Note that 57 nt of the 58 bp insertion (c) in HPV6-T70 are identical to the first 58 bp of the 94 bp insertion (a) of HPV6-W50.…”

Section: I Imentioning

confidence: 84%

“…HPV6-W50 and HPV6-T70 were cloned from a benign wart and an invasive carcinoma, respectively (Kasher & Roman, 1988;Farr et al, 1991). Sequence analysis of the LCRs, and the E5, E6 and E7 open reading frames indicated that only the LCR sequences differed (Farr et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

“…Fax +1 317 274 4090. e-mail aroman @indycms.iupui.edu Dollard et al, 1993;Kyo et al, 1993;Kyo et al, 1994;May et al, 1994). We have recently cloned and characterized an HPV-6 from a benign lesion, HPV6-W50, and one from a malignant lesion, HPV6-T70, in an effort to understand the relationship of the viral genomes to the type of lesion from which they were isolated (Kasher & Roman, 1988;Farr et al, 1991). The two viruses are identical in the genes implicated in oncogenesis (E5, E6 and E7), but differ in sequences in the 5' half of the LCR, upstream of the L1 polyadenylation signal.…”

Section: Introductionmentioning

confidence: 99%

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Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Farr

Pattison

Youn

et al. 1995

Journal of General Virology

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Human papillomavirus type 6 (HPV-6) DNA is the predominant HPV type found in condyloma acuminata: it is rarely found in carcinomas. We have previously reported cloning and characterizing an HPV-6 from a vulvar condyloma (HPV6-W50) and an HPV-6 from a vulvar carcinoma (HPV6-T70). The E5, E6 and E7 proteins encoded by the two genomes were identical, however, the two genomes differed in the long control region (LCR). Cloning of the entire LCR into the enhancerless plasmid pSVEcat showed that the two LCRs had comparable enhancer activity. Since the major differences between the two LCRs resided in the 5' end of the LCR, upstream of the L1 polyadenylation signal, we subcloned the two LCRs to analyse more closely their effect on cat gene expression. The data indicated that LCR subclones of the two genomes had comparable chloramphenicol acetyltransferase (CAT) activity. A negative regulatory region was detectable when the test plasmids were transfected into HeLa and C33A cells and in primary keratinocytes. A decrease in CAT activity was also detected when the SV40 early promoter was replaced with the putative HPV-6 E6 promoter. The negative regulatory region functioned in a position-and orientation-independent manner, thus fulfilling the definition of a silencer.

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Section: I Imentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Farr

Pattison

Youn

et al. 1995

Journal of General Virology

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“…Analysis of HPV genomes in human cancers have also demonstrated that replication by HPV E1 and E2 can result in rearranged HPV genomes. Viral genomes with deletions, insertions, or rearrangements (20,21,22,23,24) or parts of the viral genome integrated into the cellular genome (23,24) are commonly found and this is indicative of the instability of viral replication. A study using tonsillar cancer biopsies recently demonstrated that in three from eleven HPV16 episomal DNA positive samples there were episomal viral genomes with deletions, and two of these were coexistent with full-length episomal HPV DNA (24).…”

Section: Fidelity Of Hpv16 E1/e2-mediated Dna Replication 52228 Discumentioning

confidence: 99%

“…It is known that HPV E1/E2-mediated replication initiation can also occur more than once per cell cycle (19), however the fidelity of E1/E2-mediated replication is unknown. In many HPV lesions there are episomal genomes that either contain multiple insertions/deletions (20) or single deletions (21,22,23,24). The mechanisms responsible for these rearrangements could also lead to chromosomal integration of viral sequences resulting in progression to cancer.…”

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confidence: 99%

The Fidelity of HPV16 E1/E2-mediated DNA Replication

Taylor

Dornan

Boner

et al. 2003

Journal of Biological Chemistry

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Human papillomaviruses (HPV) are causative agents in a variety of human diseases; for example over 99% of cervical carcinomas contain HPV DNA sequences. Often in cervical carcinoma the HPV genome is integrated into the host genome resulting in unregulated expression of the viral transforming proteins E6 and E7. Therefore viral integration is a step toward HPV-induced carcinogenesis. Integration of the HPV genome could occur following double-strand DNA breaks that could arise during viral DNA replication. We investigated the fidelity of HPV 16 E1-and E2-mediated DNA replication of non-damaged and UVC-damaged templates in a variety of cell lines with different genetic backgrounds; C33a (derived from an HPV-negative cervical carcinoma), XP30RO (deficient in the by-pass polymerase (pol )), XP30 (expressing a restored wild-type pol ), XP12RO (nucleotide excision repair defective), and MRC5 (derived from a 14-week-old human fetus). The results demonstrate that the fidelity of E1-and E2-mediated DNA replication is reflective of the genetic background in which the assays are carried out. Human papilloma viruses (HPVs) 1 are small doublestranded DNA tumor viruses that are causative agents in a variety of human diseases. Over 99% of cervical carcinomas contain HPV sequences; these are of the high-risk type with HPV16 being the most common. The low risk HPVs are causative agents of genital warts, and HPV6/11 are the most commonly found in this disease (1). HPVs are maintained as episomal circular DNA molecules in infected cells and are replicated by the viral proteins E1 and E2 (2, 3). The E2 protein forms homodimers and recognizes and binds to 12bp palindromic DNA sequences in the transcriptional control region of HPV (4). E2 can then regulate transcription from the adjacent promoter that controls the expression of the HPV oncogenes E6 and E7; E2 can either activate or repress transcription depending upon E2 protein levels and the cell type (5, 6). As well as regulating transcription E2 is also essential for replication of the viral genome; there are three E2 DNA binding sequences surrounding the viral origin (ori) of replication and a physical interaction between E2 and E1 results in recruitment of E1 to the ori sequence (7,8,9). Following recruitment by E2 the E1 protein interacts with the ori DNA sequence and then forms a hexameric complex required for replication of the viral genome by virtue of its helicase activity (10). E1 is known to interact with subunits of DNA polymerase-␣ and with components of the Swi/Snf complex in order to activate DNA replication (11,12).In many HPV-induced cervical cancers the HPV genome is found integrated into the host genome. This integration usually deletes the coding sequence for the E2 protein and results in elevated expression of the viral oncoproteins E6 and E7 (13). It is proposed that increased E6 and E7 levels are involved in progression toward carcinoma. Therefore the loss of episomal status of the HPV genome is an important step on the way to carcinogenesis. The integration i...

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Nucleotide and amino acid sequence variations in the L1 open reading frame of human papillomavirus type 6

et al. 1997

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Human papillomavirus (HPV) type 6 induces benign tumors such as condyloma acuminata and laryngeal papilloma. The HPV-6 DNA has been thought to be a heterogeneous group of subtypes and variant-types. To examine sequence variations of the HPV-6 L1 ORF, we analyzed by single-strand conformation polymorphism (SSCP) and by DNA sequencing 21 specimens from condyloma acuminata and laryngeal papilloma that harbor HPV-6 DNA. PCR products of HPV-6 DNA were digested with 6 restriction enzymes yielding 8 fragments, which were then analyzed by SSCP. The resolution patterns showed that the L1 coding sequences were separated into three SSCP groups, I, II, and III, and two minor groups, (I) and (III). By sequencing the five representatives of each SSCP group and by comparing these sequences with those of HPV-6a [Hofmann et al., 1995] and HPV-6b [Schwarz et al., 1983], we identified base substitutions at 20 positions in the L1 coding region and an amino acid substitution in one case.

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Characterization of human papillomavirus type 6b DNA isolated from an invasive squamous carcinoma of the vulva

Cited by 73 publications

References 23 publications

Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

The Fidelity of HPV16 E1/E2-mediated DNA Replication

Nucleotide and amino acid sequence variations in the L1 open reading frame of human papillomavirus type 6

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