Journal ArticleDOI
Chromosomal integration sites of human papillomavirus DNA in three cervical cancer cell lines mapped by in situ hybridization
TLDR
Metaphase chromosomes of three cervical cancer cell lines were subjected to in situ hybridizations with the DNA of human papillomaviruses (HPV) types 16 and 18 and indirectly support a trans-acting function of HPV-mediated cell transformation.Abstract:
Metaphase chromosomes of three cervical cancer cell lines (HeLa, CasKi, SiHa) were subjected to in situ hybridizations with the DNA of human papillomaviruses (HPV) types 16 and 18, respectively. Previous studies have demonstrated multiple copies of HPV 18 DNA in HeLa and of HPV 16 DNA in CasKi cells, but only 1-2 HPV 16 copies in cells of the SiHa line. The viral DNA persists in an integrated state (Schwarz et al 1985). Analysis of the integration sites revealed at least 11 chromosomal sites of HPV 16 integration in CasKi cells. SiHa cells contain integrated HPV 16 DNA in the region q21-q31 of chromosome No. 13. In HeLa cells integration of HPV 18 occurred in chromosome No. 8, band q24. Thus, no evidence was obtained for the existence of preferential chromosomal regions for HPV integration. The data indirectly support a trans-acting function of HPV-mediated cell transformation.read more
Citations
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The E6 and E7 genes of the human papillomavirus type 16 together are necessary and sufficient for transformation of primary human keratinocytes.
TL;DR: Both the full-length E6 and E7 genes were required for the induction of keratinocyte immortalization and resistance to terminal differentiation and mutation of either gene in the context of this recombinant plasmid eliminated the ability to induce stable differentiation-resistant transformants.
Journal ArticleDOI
Human papillomaviruses in the pathogenesis of anogenital cancer.
TL;DR: Virus infection and viral gene expression emerge as necessary but obviously not sufficient factors for cancer induction, and “endogenous” modifications seem to be most important in the pathogenesis of premalignant lesions and tumor progression.
Journal ArticleDOI
Cloning and expression of the cDNA for E6-AP, a protein that mediates the interaction of the human papillomavirus E6 oncoprotein with p53
TL;DR: The purification of E6-AP and the cloning of its corresponding cDNA, which contains a novel open reading frame encoding 865 amino acids, is reported, suggesting a model by which E6 deregulates cell growth control by the elimination of the p53 tumor suppressor protein.
Journal ArticleDOI
Systematic Review of Genomic Integration Sites of Human Papillomavirus Genomes in Epithelial Dysplasia and Invasive Cancer of the Female Lower Genital Tract
TL;DR: It is confirmed that HPV integration sites are randomly distributed over the whole genome with a clear predilection for genomic fragile sites, and no evidence for targeted disruption or functional alteration of critical cellular genes by the integrated viral sequences could be found.
Journal ArticleDOI
Localization of the E6-AP regions that direct human papillomavirus E6 binding, association with p53, and ubiquitination of associated proteins
TL;DR: Functional domains of E6-AP involved in binding E6, association with p53, and ubiquitination of p53 are mapped and it is shown that E 6-AP sequences in addition to those required for formation of a stable ternary complex with E6 and p 53 are necessary to stimulate the ubiquitinated p53.
References
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Journal ArticleDOI
A papillomavirus DNA from a cervical carcinoma and its prevalence in cancer biopsy samples from different geographic regions.
TL;DR: The data indicate that HPV 16 DNA prevails in malignant tumors, rendering an accidental contamination with papillomavirus DNA from adjacent papillomas rather unlikely, and suggests a dependence of HPV 16 replication on helper virus.
Journal ArticleDOI
Human c-myc onc gene is located on the region of chromosome 8 that is translocated in Burkitt lymphoma cells
Riccardo Dalla-Favera,Marco Bregni,Jan Erikson,David A. Patterson,Robert C. Gallo,Carlo M. Croce +5 more
TL;DR: Using a DNA probe that is specific for the complete gene (c-myc), different somatic cell hybrids possessing varying numbers of human chromosomes were analyzed by the Southern blotting technique and results indicate that the human c- myc gene is located on chromosome 8.
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Structure and transcription of human papillomavirus sequences in cervical carcinoma cells
Elisabeth Schwarz,U K Freese,Lutz Gissmann,Wolfgang Mayer,Birgit Roggenbuck,Armin Stremlau,Harald zur Hausen +6 more
TL;DR: It is found that the HPV 18 DNA is integrated into the cellular genome and is amplified in HeLa and 756 cells, and some of the transcripts are composed of HPV 18 and cellular sequences.
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Translocation of the c-myc gene into the immunoglobulin heavy chain locus in human Burkitt lymphoma and murine plasmacytoma cells
Rebecca Taub,Ilan R. Kirsch,Cynthia C. Morton,Gilbert M. Lenoir,D. Swan,Steven R. Tronick,Stuart A. Aaronson,Philip Leder +7 more
TL;DR: It is shown that transformation of human Burkitt lymphomas and murine plasmacytomas is frequently accompanied by the somatic rearrangement of a cellular analogue of an avian retrovirus transforming gene, c-myc, which provides a molecular basis for considering the role that specific translocations might play in malignant transformation.
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A new type of papillomavirus DNA, its presence in genital cancer biopsies and in cell lines derived from cervical cancer.
TL;DR: DNA of a new papillomavirus type was cloned from a cervical carcinoma biopsy and the data reveal that the DNA might be integrated into the host cell genome, which is tentatively proposed to be HPV 18.