Conservation of HPV‐16 E6/E7 ORF sequences in a cervical carcinoma
Identifieur interne : 001347 ( Istex/Curation ); précédent : 001346; suivant : 001348Conservation of HPV‐16 E6/E7 ORF sequences in a cervical carcinoma
Auteurs : Richard W. Cone [États-Unis] ; Anthony C. Minson [États-Unis, Royaume-Uni] ; Michael R. Smith [États-Unis] ; James K. Mcdougall [États-Unis]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 1992-06.
English descriptors
- Teeft :
- Bamhi, Bamhi fragment, Base changes, Base pairs, Binding site, Biological activity, Carcinoma, Cell line, Cell lines, Cervical, Cervical cancer, Cervical carcinoma, Cervical carcinomas, Clone, Deletion, Ecori, Fpol region, Fragment, Further study, Genomic, Homology, Human papillomavirus type, Hybridization, Hybridized, Iiii, Incomplete copy, Insertion, Integration site, Integration sites, Long control region, Metastatic, Metastatic tumor, National academy, Normal genomic, Oncogene, Open reading frame, Open reading frames, Opposite strand, Orfs, Original tumor, Papillomavirus, Prototype sequence, Radical hysterectomy, Repetitive element, Repetitive sequences, Restriction digests, Restriction fragments, Restriction sites, Right obturator, Seedorf, Sequence analysis, Sequencing, Sheared salmon sperm, Significant homology, Single band, Single base deletion, Single copy, Southern blot, Subclone, Tumor clone, Tumor subclone, Tumor tissue, Virology, Virology kaur.
Abstract
A cervical carcinoma that contained human papillomavirus (HPV)‐l6 homologous DNA was analyzed. Each tumor cell genome contained a single, incomplete copy of HPV‐16 DNA. The E6 and E7 open reading frames (ORFs) were com‐ pletely conserved relative to other published HPV‐I6 sequences. Much of the non‐coding region (NCR) was free of base changes, including complete conservation of several regulatory elements. Multiple mutations were identified in the remaining integrated HPV‐16 DNA, which was composed of parts of the L1 and E1 ORFs. The extraordinary conservation of the E6/E7 DNA sequence, as compared with other regions of the integrated HPV‐16 DNA, supports the role of E6/E7 in tumorigenesis. © 1992 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.1890370205
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Cone</name><affiliation wicri:level="4"><mods:affiliation>Department of Laboratory Medicine, University of washington, Pacific avenue NE, Seattle, WA and Children's Hospital, Virology Division, 4800 Sand Point way NE, Seattle, Wa 98105</mods:affiliation><orgName type="university">Université de Washington</orgName><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation><affiliation wicri:level="4"><mods:affiliation>Correspondence address: Department of Laboratory Medicine, University of washington, Pacific avenue NE, Seattle, WA and Children's Hospital, Virology Division, 4800 Sand Point way NE, Seattle, Wa 98105===</mods:affiliation><orgName type="university">Université de Washington</orgName><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Minson, Anthony C" sort="Minson, Anthony C" uniqKey="Minson A" first="Anthony C." last="Minson">Anthony C. Minson</name><affiliation wicri:level="2"><mods:affiliation>First Hill Women's Clinic, Seattle, Washington</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>First Hill Women's Clinic, Seattle</wicri:cityArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Current Address: Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, UK</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Current Address: Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge</wicri:regionArea></affiliation></author><author><name sortKey="Smith, Michael R" sort="Smith, Michael R" uniqKey="Smith M" first="Michael R." last="Smith">Michael R. 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Mcdougall</name><affiliation wicri:level="2"><mods:affiliation>Fred Hutchinson Cancer Research Center, Seattle, Washington</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Fred Hutchinson Cancer Research Center, Seattle</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">37</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="99">99</biblScope><biblScope unit="page" to="107">107</biblScope><biblScope unit="page-count">9</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="1992-06">1992-06</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Bamhi</term><term>Bamhi fragment</term><term>Base changes</term><term>Base pairs</term><term>Binding site</term><term>Biological activity</term><term>Carcinoma</term><term>Cell line</term><term>Cell lines</term><term>Cervical</term><term>Cervical cancer</term><term>Cervical carcinoma</term><term>Cervical carcinomas</term><term>Clone</term><term>Deletion</term><term>Ecori</term><term>Fpol region</term><term>Fragment</term><term>Further study</term><term>Genomic</term><term>Homology</term><term>Human papillomavirus type</term><term>Hybridization</term><term>Hybridized</term><term>Iiii</term><term>Incomplete copy</term><term>Insertion</term><term>Integration site</term><term>Integration sites</term><term>Long control region</term><term>Metastatic</term><term>Metastatic tumor</term><term>National academy</term><term>Normal genomic</term><term>Oncogene</term><term>Open reading frame</term><term>Open reading frames</term><term>Opposite strand</term><term>Orfs</term><term>Original tumor</term><term>Papillomavirus</term><term>Prototype sequence</term><term>Radical hysterectomy</term><term>Repetitive element</term><term>Repetitive sequences</term><term>Restriction digests</term><term>Restriction fragments</term><term>Restriction sites</term><term>Right obturator</term><term>Seedorf</term><term>Sequence analysis</term><term>Sequencing</term><term>Sheared salmon sperm</term><term>Significant homology</term><term>Single band</term><term>Single base deletion</term><term>Single copy</term><term>Southern blot</term><term>Subclone</term><term>Tumor clone</term><term>Tumor subclone</term><term>Tumor tissue</term><term>Virology</term><term>Virology kaur</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A cervical carcinoma that contained human papillomavirus (HPV)‐l6 homologous DNA was analyzed. Each tumor cell genome contained a single, incomplete copy of HPV‐16 DNA. The E6 and E7 open reading frames (ORFs) were com‐ pletely conserved relative to other published HPV‐I6 sequences. Much of the non‐coding region (NCR) was free of base changes, including complete conservation of several regulatory elements. Multiple mutations were identified in the remaining integrated HPV‐16 DNA, which was composed of parts of the L1 and E1 ORFs. The extraordinary conservation of the E6/E7 DNA sequence, as compared with other regions of the integrated HPV‐16 DNA, supports the role of E6/E7 in tumorigenesis. © 1992 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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