High frequency of a 30‐bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non‐Hodgkin's brain lymphomas
Identifieur interne : 002104 ( Istex/Corpus ); précédent : 002103; suivant : 002105High frequency of a 30‐bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non‐Hodgkin's brain lymphomas
Auteurs : A. Vallat-Decouvelaere ; M. Bretel ; I. Vassias ; J. Laplanche ; M. Polivka ; M. Wassef ; M. Brunet ; J. Thiebaut ; B. Gosselin ; F. Morinet ; J. MikolSource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 2002-12.
English descriptors
- Teeft :
- Activation domain, Amino, Amino acid, Base pairs, Blackwell publishing, Brain lymphomas, Deletion, Deletion variants, Different primers, High frequency, High prevalence, Knecht, Latent membrane oncogene deletions, Latent membrane protein, Leuk lymphoma, Lmp1, Lmp1 gene, Lmp1 oncogene, Lymphoma, Membrane, Membrane protein, Mutation, Mutational hotspots, Nasopharyngeal carcinoma, Nasopharyngeal carcinomas, Negative control, Neurobiology, Neuropathology, Oligonucleotide primers, Oncogene, Oncogenic, Pathol, Point mutations, Polymerase chain reaction, Primer, Reactive lymphoid tissue, Sequence results, Transformation effector sites, Virus strains, Virus type, Wild type.
Abstract
A characteristic 30‐base pair (bp) deletion (del) in the 3′ end of the Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) gene, coding for the C‐terminal NF‐kappaB activation domain, has been identified in various lymphoproliferative disorders and nasopharyngeal carcinomas. In the single report to date of human immunodeficiency virus primary brain lymphomas (HIV‐PBLs), del‐LMP1 was noted in seven cases out of nine. The present study was designed to identify this deletion in a series of 31 diffuse large B‐cell HIV‐PBLs, with the aim of determining its possible oncogenic action. The presence of EBV was confirmed by EBER mRNA in situ hybridization. After genomic extraction from frozen tissue, two 20‐base oligonucleotide primers flanking the site of the 30‐bp deletion were used. DNA sequencing of the polymerase chain reaction (PCR) products confirmed an identical segment spanning 30‐bp and 69‐bp, frequently associated with mutational hotspots in 19 cases (61%). A role for del‐LMP1 in the oncogenic potential of EBV in systemic proliferations is a matter of debate. Its high incidence suggests that the oncogenic mechanism of LMP1 in the brain might differ significantly from that in systemic lymphoid proliferations, and might be enhanced by HIV infection.
Url:
DOI: 10.1046/j.1365-2990.2002.t01-1-00418.x
Links to Exploration step
ISTEX:803A8F5A5E3434CCB7B5AEE330961ADD2B35DA60Le document en format XML
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Vallat-Decouvelaere</name><affiliation><mods:affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: a‐decouvelaere@chru‐lille.fr</mods:affiliation></affiliation></author><author><name sortKey="Bretel, M" sort="Bretel, M" uniqKey="Bretel M" first="M." last="Bretel">M. Bretel</name><affiliation><mods:affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Vassias, I" sort="Vassias, I" uniqKey="Vassias I" first="I." last="Vassias">I. Vassias</name><affiliation><mods:affiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Laplanche, J" sort="Laplanche, J" uniqKey="Laplanche J" first="J." last="Laplanche">J. Laplanche</name><affiliation><mods:affiliation>Department of Biochemistry and Molecular Biology, Lariboisière Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Polivka, M" sort="Polivka, M" uniqKey="Polivka M" first="M." last="Polivka">M. Polivka</name><affiliation><mods:affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Wassef, M" sort="Wassef, M" uniqKey="Wassef M" first="M." last="Wassef">M. Wassef</name><affiliation><mods:affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Brunet, M" sort="Brunet, M" uniqKey="Brunet M" first="M." last="Brunet">M. Brunet</name><affiliation><mods:affiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Thiebaut, J" sort="Thiebaut, J" uniqKey="Thiebaut J" first="J." last="Thiebaut">J. Thiebaut</name><affiliation><mods:affiliation>Department of Neurosurgery, Rothschild Foundation, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Gosselin, B" sort="Gosselin, B" uniqKey="Gosselin B" first="B." last="Gosselin">B. Gosselin</name><affiliation><mods:affiliation>Department of Pathology, Hôpital Calmette, Lille, France</mods:affiliation></affiliation></author><author><name sortKey="Morinet, F" sort="Morinet, F" uniqKey="Morinet F" first="F." last="Morinet">F. Morinet</name><affiliation><mods:affiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Mikol, J" sort="Mikol, J" uniqKey="Mikol J" first="J." last="Mikol">J. Mikol</name><affiliation><mods:affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Neuropathology and Applied Neurobiology</title><title level="j" type="alt">NEUROPATHOLOGY APPLIED NEUROBIOLOGY</title><idno type="ISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><imprint><biblScope unit="vol">28</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="471">471</biblScope><biblScope unit="page" to="479">479</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-12">2002-12</date></imprint><idno type="ISSN">0305-1846</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1846</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Activation domain</term><term>Amino</term><term>Amino acid</term><term>Base pairs</term><term>Blackwell publishing</term><term>Brain lymphomas</term><term>Deletion</term><term>Deletion variants</term><term>Different primers</term><term>High frequency</term><term>High prevalence</term><term>Knecht</term><term>Latent membrane oncogene deletions</term><term>Latent membrane protein</term><term>Leuk lymphoma</term><term>Lmp1</term><term>Lmp1 gene</term><term>Lmp1 oncogene</term><term>Lymphoma</term><term>Membrane</term><term>Membrane protein</term><term>Mutation</term><term>Mutational hotspots</term><term>Nasopharyngeal carcinoma</term><term>Nasopharyngeal carcinomas</term><term>Negative control</term><term>Neurobiology</term><term>Neuropathology</term><term>Oligonucleotide primers</term><term>Oncogene</term><term>Oncogenic</term><term>Pathol</term><term>Point mutations</term><term>Polymerase chain reaction</term><term>Primer</term><term>Reactive lymphoid tissue</term><term>Sequence results</term><term>Transformation effector sites</term><term>Virus strains</term><term>Virus type</term><term>Wild type</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A characteristic 30‐base pair (bp) deletion (del) in the 3′ end of the Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) gene, coding for the C‐terminal NF‐kappaB activation domain, has been identified in various lymphoproliferative disorders and nasopharyngeal carcinomas. In the single report to date of human immunodeficiency virus primary brain lymphomas (HIV‐PBLs), del‐LMP1 was noted in seven cases out of nine. The present study was designed to identify this deletion in a series of 31 diffuse large B‐cell HIV‐PBLs, with the aim of determining its possible oncogenic action. The presence of EBV was confirmed by EBER mRNA in situ hybridization. After genomic extraction from frozen tissue, two 20‐base oligonucleotide primers flanking the site of the 30‐bp deletion were used. DNA sequencing of the polymerase chain reaction (PCR) products confirmed an identical segment spanning 30‐bp and 69‐bp, frequently associated with mutational hotspots in 19 cases (61%). A role for del‐LMP1 in the oncogenic potential of EBV in systemic proliferations is a matter of debate. Its high incidence suggests that the oncogenic mechanism of LMP1 in the brain might differ significantly from that in systemic lymphoid proliferations, and might be enhanced by HIV infection.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>deletion</json:string><json:string>lmp1</json:string><json:string>oncogene</json:string><json:string>lymphoma</json:string><json:string>neurobiology</json:string><json:string>blackwell publishing</json:string><json:string>primer</json:string><json:string>oncogenic</json:string><json:string>mutation</json:string><json:string>pathol</json:string><json:string>membrane protein</json:string><json:string>high frequency</json:string><json:string>latent membrane protein</json:string><json:string>brain lymphomas</json:string><json:string>lmp1 gene</json:string><json:string>neuropathology</json:string><json:string>wild type</json:string><json:string>activation domain</json:string><json:string>lmp1 oncogene</json:string><json:string>amino acid</json:string><json:string>knecht</json:string><json:string>amino</json:string><json:string>mutational hotspots</json:string><json:string>polymerase chain reaction</json:string><json:string>point mutations</json:string><json:string>nasopharyngeal carcinoma</json:string><json:string>deletion variants</json:string><json:string>reactive lymphoid tissue</json:string><json:string>high prevalence</json:string><json:string>sequence results</json:string><json:string>oligonucleotide primers</json:string><json:string>different primers</json:string><json:string>transformation effector sites</json:string><json:string>nasopharyngeal carcinomas</json:string><json:string>latent membrane oncogene deletions</json:string><json:string>leuk lymphoma</json:string><json:string>negative control</json:string><json:string>base pairs</json:string><json:string>virus strains</json:string><json:string>virus type</json:string><json:string>membrane</json:string></teeft></keywords><author><json:item><name>A.‐V. Vallat‐Decouvelaere</name><affiliations><json:string>Department of Pathology, Lariboisière Hospital, Paris, France</json:string><json:string>E-mail: a‐decouvelaere@chru‐lille.fr</json:string></affiliations></json:item><json:item><name>M.‐A. Bretel</name><affiliations><json:string>Department of Pathology, Lariboisière Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>I. Vassias</name><affiliations><json:string>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>J.‐L. Laplanche</name><affiliations><json:string>Department of Biochemistry and Molecular Biology, Lariboisière Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>M. Polivka</name><affiliations><json:string>Department of Pathology, Lariboisière Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>M. Wassef</name><affiliations><json:string>Department of Pathology, Lariboisière Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>M. Brunet</name><affiliations><json:string>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>J.‐B. Thiebaut</name><affiliations><json:string>Department of Neurosurgery, Rothschild Foundation, Paris, France</json:string></affiliations></json:item><json:item><name>B. Gosselin</name><affiliations><json:string>Department of Pathology, Hôpital Calmette, Lille, France</json:string></affiliations></json:item><json:item><name>F. Morinet</name><affiliations><json:string>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>J. Mikol</name><affiliations><json:string>Department of Pathology, Lariboisière Hospital, Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Epstein–Barr virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HIV</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>central nervous system</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>lymphoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deletion</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mutation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>NF‐kappaB</value></json:item></subject><articleId><json:string>NAN418</json:string></articleId><arkIstex>ark:/67375/WNG-2K7TWJ6T-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>A characteristic 30‐base pair (bp) deletion (del) in the 3′ end of the Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) gene, coding for the C‐terminal NF‐kappaB activation domain, has been identified in various lymphoproliferative disorders and nasopharyngeal carcinomas. In the single report to date of human immunodeficiency virus primary brain lymphomas (HIV‐PBLs), del‐LMP1 was noted in seven cases out of nine. The present study was designed to identify this deletion in a series of 31 diffuse large B‐cell HIV‐PBLs, with the aim of determining its possible oncogenic action. The presence of EBV was confirmed by EBER mRNA in situ hybridization. After genomic extraction from frozen tissue, two 20‐base oligonucleotide primers flanking the site of the 30‐bp deletion were used. DNA sequencing of the polymerase chain reaction (PCR) products confirmed an identical segment spanning 30‐bp and 69‐bp, frequently associated with mutational hotspots in 19 cases (61%). A role for del‐LMP1 in the oncogenic potential of EBV in systemic proliferations is a matter of debate. 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Vallat‐Decouvelaere, Department of Pathology, Hôpital Calmette, Bv du Pr. J. Leclerc, 59037 Lille Cedex, France. Tel.: + 33 3 20 44 49 85; Fax: + 33 3 20 44 47 27; E‐mail: a‐decouvelaere@chru‐lille.fr</affiliation></author><author xml:id="author-0001"><persName><forename type="first">M.‐A.</forename><surname>Bretel</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><address><addrLine>Lariboisière Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">I.</forename><surname>Vassias</surname></persName><affiliation><orgName type="department">Department of Bacteriology and Virology</orgName><address><addrLine>Saint‐Louis Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">J.‐L.</forename><surname>Laplanche</surname></persName><affiliation><orgName type="department">Department of Biochemistry and Molecular Biology</orgName><address><addrLine>Lariboisière Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">M.</forename><surname>Polivka</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><address><addrLine>Lariboisière Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">M.</forename><surname>Wassef</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><address><addrLine>Lariboisière Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first"> M.</forename><surname>Brunet</surname></persName><affiliation><orgName type="department">Department of Bacteriology and Virology</orgName><address><addrLine>Saint‐Louis Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">J.‐B.</forename><surname>Thiebaut</surname></persName><affiliation><orgName type="department">Department of Neurosurgery</orgName><address><addrLine>Rothschild Foundation</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">B.</forename><surname>Gosselin</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><address><addrLine>Hôpital Calmette</addrLine><addrLine>Lille</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0009"><persName><forename type="first">F.</forename><surname>Morinet</surname></persName><affiliation><orgName type="department">Department of Bacteriology and Virology</orgName><address><addrLine>Saint‐Louis Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><author xml:id="author-0010"><persName><forename type="first">J.</forename><surname>Mikol</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><address><addrLine>Lariboisière Hospital</addrLine><addrLine>Paris</addrLine><country key="FR">FRANCE</country><country key="FR"></country></address></affiliation></author><idno type="istex">803A8F5A5E3434CCB7B5AEE330961ADD2B35DA60</idno><idno type="ark">ark:/67375/WNG-2K7TWJ6T-V</idno><idno type="DOI">10.1046/j.1365-2990.2002.t01-1-00418.x</idno><idno type="unit">NAN418</idno><idno type="toTypesetVersion">file:NAN.NAN418.pdf</idno></analytic><monogr><title level="j" type="main">Neuropathology and Applied Neurobiology</title><title level="j" type="alt">NEUROPATHOLOGY APPLIED NEUROBIOLOGY</title><idno type="pISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><idno type="book-DOI">10.1111/(ISSN)1365-2990</idno><idno type="book-part-DOI">10.1111/nan.2002.28.issue-6</idno><idno type="product">NAN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">28</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="471">471</biblScope><biblScope unit="page" to="479">479</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-12"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p>A characteristic 30‐base pair (bp) deletion (del) in the 3′ end of the Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) gene, coding for the C‐terminal NF‐kappaB activation domain, has been identified in various lymphoproliferative disorders and nasopharyngeal carcinomas. In the single report to date of human immunodeficiency virus primary brain lymphomas (HIV‐PBLs), del‐LMP1 was noted in seven cases out of nine. The present study was designed to identify this deletion in a series of 31 diffuse large B‐cell HIV‐PBLs, with the aim of determining its possible oncogenic action. The presence of EBV was confirmed by EBER mRNA <hi rend="italic">in situ</hi> hybridization. After genomic extraction from frozen tissue, two 20‐base oligonucleotide primers flanking the site of the 30‐bp deletion were used. DNA sequencing of the polymerase chain reaction (PCR) products confirmed an identical segment spanning 30‐bp and 69‐bp, frequently associated with mutational hotspots in 19 cases (61%). A role for del‐LMP1 in the oncogenic potential of EBV in systemic proliferations is a matter of debate. Its high incidence suggests that the oncogenic mechanism of LMP1 in the brain might differ significantly from that in systemic lymphoid proliferations, and might be enhanced by HIV infection.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">Epstein–Barr virus</term><term xml:id="k2">HIV</term><term xml:id="k3">central nervous system</term><term xml:id="k4">lymphoma</term><term xml:id="k5">deletion</term><term xml:id="k6">mutation</term><term xml:id="k7">NF‐kappaB </term></keywords><keywords rend="tocHeading1"><term>Original articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-2K7TWJ6T-V/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2990</doi><issn type="print">0305-1846</issn><issn type="electronic">1365-2990</issn><idGroup><id type="product" value="NAN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="NEUROPATHOLOGY APPLIED NEUROBIOLOGY">Neuropathology and Applied Neurobiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="12006"><doi origin="wiley">10.1111/nan.2002.28.issue-6</doi><numberingGroup><numbering type="journalVolume" number="28">28</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2002-12">December 2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0047100" status="forIssue"><doi origin="wiley">10.1046/j.1365-2990.2002.t01-1-00418.x</doi><idGroup><id type="unit" value="NAN418"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><eventGroup><event type="firstOnline" date="2002-11-24"></event><event type="publishedOnlineFinalForm" date="2002-11-24"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText source:FullText result:FullText" date="2010-07-19"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="471">471</numbering><numbering type="pageLast" number="479">479</numbering></numberingGroup><correspondenceTo>A.‐V. Vallat‐Decouvelaere, Department of Pathology, Hôpital Calmette, Bv du Pr. J. Leclerc, 59037 Lille Cedex, France. Tel.: + 33 3 20 44 49 85; Fax: + 33 3 20 44 47 27; E‐mail: <email normalForm="a-decouvelaere@chru-lille.fr">a‐decouvelaere@chru‐lille.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NAN.NAN418.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory><i>Received 21 January 2002</i> <i> Accepted after revision 12 May 2002</i></unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="2202"></count><count type="linksPubMed" number="35"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">High frequency of a 30‐bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non‐Hodgkin's brain lymphomas</title><title type="shortAuthors">A.‐V. Vallat‐Decouvelaere <i>et al</i>.</title><title type="short">A 30‐bp deletion of EBV‐LMP1 in HIV brain lymphomas</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>A.‐V.</givenNames><familyName>Vallat‐Decouvelaere</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>M.‐A.</givenNames><familyName>Bretel</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>I.</givenNames><familyName>Vassias</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>J.‐L.</givenNames><familyName>Laplanche</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>M.</givenNames><familyName>Polivka</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>M.</givenNames><familyName>Wassef</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a2"><personName><givenNames> M.</givenNames><familyName>Brunet</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a4"><personName><givenNames>J.‐B.</givenNames><familyName>Thiebaut</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a5"><personName><givenNames>B.</givenNames><familyName>Gosselin</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a2"><personName><givenNames>F.</givenNames><familyName>Morinet</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a1"><personName><givenNames>J.</givenNames><familyName>Mikol</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FR"><unparsedAffiliation>Department of Pathology, Lariboisière Hospital, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="FR"><unparsedAffiliation>Department of Biochemistry and Molecular Biology, Lariboisière Hospital, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="FR"><unparsedAffiliation>Department of Neurosurgery, Rothschild Foundation, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="FR"><unparsedAffiliation>Department of Pathology, Hôpital Calmette, Lille, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Epstein–Barr virus</keyword><keyword xml:id="k2">HIV</keyword><keyword xml:id="k3">central nervous system</keyword><keyword xml:id="k4">lymphoma</keyword><keyword xml:id="k5">deletion</keyword><keyword xml:id="k6">mutation</keyword><keyword xml:id="k7">NF‐kappaB </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!--
A.-V. Vallat-Decouvelaere, M.-A. Bretel, I. Vassias, J.-L. Laplanche, M. Polivka, M. Wassef, M. Brunet, J.-B. Thiebaut, B. Gosselin, F. Morinet and J. Mikol (2002) Neuropathology and Applied Neurobiology28, 471–479
High frequency of a 30-bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non-Hodgkin's brain lymphomas
--><p>A characteristic 30‐base pair (bp) deletion (del) in the 3′ end of the Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) gene, coding for the C‐terminal NF‐kappaB activation domain, has been identified in various lymphoproliferative disorders and nasopharyngeal carcinomas. In the single report to date of human immunodeficiency virus primary brain lymphomas (HIV‐PBLs), del‐LMP1 was noted in seven cases out of nine. The present study was designed to identify this deletion in a series of 31 diffuse large B‐cell HIV‐PBLs, with the aim of determining its possible oncogenic action. The presence of EBV was confirmed by EBER mRNA <i>in situ</i> hybridization. After genomic extraction from frozen tissue, two 20‐base oligonucleotide primers flanking the site of the 30‐bp deletion were used. DNA sequencing of the polymerase chain reaction (PCR) products confirmed an identical segment spanning 30‐bp and 69‐bp, frequently associated with mutational hotspots in 19 cases (61%). A role for del‐LMP1 in the oncogenic potential of EBV in systemic proliferations is a matter of debate. Its high incidence suggests that the oncogenic mechanism of LMP1 in the brain might differ significantly from that in systemic lymphoid proliferations, and might be enhanced by HIV infection.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>High frequency of a 30‐bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non‐Hodgkin's brain lymphomas</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>A 30‐bp deletion of EBV‐LMP1 in HIV brain lymphomas</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>High frequency of a 30‐bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non‐Hodgkin's brain lymphomas</title></titleInfo><name type="personal"><namePart type="given">A.‐V.</namePart><namePart type="family">Vallat‐Decouvelaere</namePart><affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</affiliation><affiliation>E-mail: a‐decouvelaere@chru‐lille.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.‐A.</namePart><namePart type="family">Bretel</namePart><affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Vassias</namePart><affiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.‐L.</namePart><namePart type="family">Laplanche</namePart><affiliation>Department of Biochemistry and Molecular Biology, Lariboisière Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Polivka</namePart><affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Wassef</namePart><affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Brunet</namePart><affiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.‐B.</namePart><namePart type="family">Thiebaut</namePart><affiliation>Department of Neurosurgery, Rothschild Foundation, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Gosselin</namePart><affiliation>Department of Pathology, Hôpital Calmette, Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Morinet</namePart><affiliation>Department of Bacteriology and Virology, Saint‐Louis Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Mikol</namePart><affiliation>Department of Pathology, Lariboisière Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2002-12</dateIssued><edition>Received 21 January 2002 Accepted after revision 12 May 2002</edition><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">0</extent><extent unit="tables">0</extent><extent unit="formulas">0</extent><extent unit="references">38</extent><extent unit="linksCrossRef">0</extent><extent unit="words">2202</extent></physicalDescription><abstract lang="en">A characteristic 30‐base pair (bp) deletion (del) in the 3′ end of the Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) gene, coding for the C‐terminal NF‐kappaB activation domain, has been identified in various lymphoproliferative disorders and nasopharyngeal carcinomas. In the single report to date of human immunodeficiency virus primary brain lymphomas (HIV‐PBLs), del‐LMP1 was noted in seven cases out of nine. The present study was designed to identify this deletion in a series of 31 diffuse large B‐cell HIV‐PBLs, with the aim of determining its possible oncogenic action. The presence of EBV was confirmed by EBER mRNA in situ hybridization. After genomic extraction from frozen tissue, two 20‐base oligonucleotide primers flanking the site of the 30‐bp deletion were used. DNA sequencing of the polymerase chain reaction (PCR) products confirmed an identical segment spanning 30‐bp and 69‐bp, frequently associated with mutational hotspots in 19 cases (61%). A role for del‐LMP1 in the oncogenic potential of EBV in systemic proliferations is a matter of debate. Its high incidence suggests that the oncogenic mechanism of LMP1 in the brain might differ significantly from that in systemic lymphoid proliferations, and might be enhanced by HIV infection.</abstract><subject lang="en"><genre>keywords</genre><topic>Epstein–Barr virus</topic><topic>HIV</topic><topic>central nervous system</topic><topic>lymphoma</topic><topic>deletion</topic><topic>mutation</topic><topic>NF‐kappaB</topic></subject><relatedItem type="host"><titleInfo><title>Neuropathology and Applied Neurobiology</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0305-1846</identifier><identifier type="eISSN">1365-2990</identifier><identifier type="DOI">10.1111/(ISSN)1365-2990</identifier><identifier type="PublisherID">NAN</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>471</start><end>479</end><total>9</total></extent></part></relatedItem><identifier type="istex">803A8F5A5E3434CCB7B5AEE330961ADD2B35DA60</identifier><identifier type="ark">ark:/67375/WNG-2K7TWJ6T-V</identifier><identifier type="DOI">10.1046/j.1365-2990.2002.t01-1-00418.x</identifier><identifier type="ArticleID">NAN418</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-2K7TWJ6T-V/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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