AustralieFrV1, PascalFrancis, Curation, bibRecord, 001486

Allelic loss on chromosomes 2q21 and 19p13.2 in oxyphilic thyroid tumors

Identifieur interne : 001486 ( PascalFrancis/Curation ); précédent : 001485; suivant : 001487

Allelic loss on chromosomes 2q21 and 19p13.2 in oxyphilic thyroid tumors

Auteurs : Karmen Stankov [Italie] ; Alessandro Pastore [Italie] ; Luca Toschi [Italie] ; James Mckay [Australie] ; Fabienne Lesueur [Royaume-Uni] ; Jean Louis Kraimps [France] ; Dominique Bonneau [France] ; Hélène Gibelin [France] ; Pierre Levillain [France] ; Marco Volante [Italie] ; Mauro Papotti [Italie] ; Giovanni Romeo [Italie]

Source :

International journal of cancer [ 0020-7136 ] ; 2004.

RBID : Pascal:04-0586379

Descripteurs français

Pascal (Inist)
- Perte hétérozygotie, Délétion, Chromosome A2 anormal, Chromosome F19 anormal, Cancérologie, Cytogénétique, Homme, Tumeur oxyphile thyroïde.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Abnormal chromosome A2, Abnormal chromosome F19, Cancerology, Cytogenetics, Deletion, Human, Loss of heterozygosity.

Abstract

Hürthle thyroid tumors are characterized by frequent numerical chromosomal aberrations, including aneuploidy or polyploidy, losses and gains of some chromosomal regions and DNA fragmentation. In recent years, great attention has been paid to the combined analysis of morphologic and genetic features of oxyphilic tumors and to the elucidation of their pathogenesis. We analyzed for loss of heterozygosity (LOH) of the candidate regions for TCO (thyroid tumor with cell oxyphilia) and NMTCI (nonmedullary thyroid carcinoma I), 2 loci already mapped on chromosomes 19p13.2 and 2q21, respectively. Matched normal and tumor DNA samples from 70 patients with sporadic oxyphilic thyroid tumors and 20 with sporadic follicular tumors were subjected to microsatellite analysis using 10 markers on 19p13.2 and 6 markers on 2q21. This approach led us to the observation of a more significant LOH in oxyphilic than in follicular tumors. Allelic loss in tumor samples was evenly distributed in both 19p13.2 and 2q21 regions, in accordance with the established linkage of TCO and NMTCI for inherited tumors. In order to investigate the possible contribution of both susceptibility loci in oxyphilic tumors, the family that led to the original mapping of TCO locus was reanalyzed for the markers in the 2q21 region. This led to the exclusion of linkage with the NMTCI locus and to the refutation of the digenic inheritance hypothesis at least in this family.

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A08	`01`	`1`	`ENG`	`@1 Allelic loss on chromosomes 2q21 and 19p13.2 in oxyphilic thyroid tumors`
A11	`01`	`1`		`@1 STANKOV (Karmen)`
A11	`02`	`1`		`@1 PASTORE (Alessandro)`
A11	`03`	`1`		`@1 TOSCHI (Luca)`
A11	`04`	`1`		`@1 MCKAY (James)`
A11	`05`	`1`		`@1 LESUEUR (Fabienne)`
A11	`06`	`1`		`@1 KRAIMPS (Jean Louis)`
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A11	`11`	`1`		`@1 PAPOTTI (Mauro)`
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A14	`01`			`@1 Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia, Unità Operativa di Genetica Medica, Policlinico S. Orsola-Malpighi @2 Bologna @3 ITA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 12 aut.`
A14	`02`			`@1 Menzies Centre for Population Health Research, Royal Hobart Hospital @2 Hobart, Tasmania @3 AUS @Z 4 aut.`
A14	`03`			`@1 Strangeways Research Laboratory, Worts Causeway @2 Cambridge @3 GBR @Z 5 aut.`
A14	`04`			`@1 Department of Endocrine Surgery, Jean Bernard Hospital, Groupe de Recherche en Endocrinologie Experimentale et Clinique @2 Poitiers @3 FRA @Z 6 aut. @Z 8 aut. @Z 9 aut.`
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C01	`01`		`ENG`	@0 Hürthle thyroid tumors are characterized by frequent numerical chromosomal aberrations, including aneuploidy or polyploidy, losses and gains of some chromosomal regions and DNA fragmentation. In recent years, great attention has been paid to the combined analysis of morphologic and genetic features of oxyphilic tumors and to the elucidation of their pathogenesis. We analyzed for loss of heterozygosity (LOH) of the candidate regions for TCO (thyroid tumor with cell oxyphilia) and NMTCI (nonmedullary thyroid carcinoma I), 2 loci already mapped on chromosomes 19p13.2 and 2q21, respectively. Matched normal and tumor DNA samples from 70 patients with sporadic oxyphilic thyroid tumors and 20 with sporadic follicular tumors were subjected to microsatellite analysis using 10 markers on 19p13.2 and 6 markers on 2q21. This approach led us to the observation of a more significant LOH in oxyphilic than in follicular tumors. Allelic loss in tumor samples was evenly distributed in both 19p13.2 and 2q21 regions, in accordance with the established linkage of TCO and NMTCI for inherited tumors. In order to investigate the possible contribution of both susceptibility loci in oxyphilic tumors, the family that led to the original mapping of TCO locus was reanalyzed for the markers in the 2q21 region. This led to the exclusion of linkage with the NMTCI locus and to the refutation of the digenic inheritance hypothesis at least in this family.
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C03	`01`	`X`	`FRE`	`@0 Perte hétérozygotie @5 01`
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C03	`01`	`X`	`SPA`	`@0 Pérdida heterozigosis @5 01`
C03	`02`	`X`	`FRE`	`@0 Délétion @5 02`
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C03	`03`	`X`	`FRE`	`@0 Chromosome A2 anormal @5 03`
C03	`03`	`X`	`ENG`	`@0 Abnormal chromosome A2 @5 03`
C03	`03`	`X`	`SPA`	`@0 Cromosoma A2 anormal @5 03`
C03	`04`	`X`	`FRE`	`@0 Chromosome F19 anormal @5 04`
C03	`04`	`X`	`ENG`	`@0 Abnormal chromosome F19 @5 04`
C03	`04`	`X`	`SPA`	`@0 Cromosoma F19 anormal @5 04`
C03	`05`	`X`	`FRE`	`@0 Cancérologie @5 05`
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C03	`08`	`X`	`FRE`	`@0 Tumeur oxyphile thyroïde @4 INC @5 86`
C07	`01`	`X`	`FRE`	`@0 Chromosome anormal`
C07	`01`	`X`	`ENG`	`@0 Abnormal chromosome`
C07	`01`	`X`	`SPA`	`@0 Cromosoma anormal`
C07	`02`	`X`	`FRE`	`@0 Aberration chromosomique`
C07	`02`	`X`	`ENG`	`@0 Chromosomal aberration`
C07	`02`	`X`	`SPA`	`@0 Aberración cromosómica`
C07	`03`	`X`	`FRE`	`@0 Thyroïde pathologie @5 37`
C07	`03`	`X`	`ENG`	`@0 Thyroid diseases @5 37`
C07	`03`	`X`	`SPA`	`@0 Tiroides patología @5 37`
C07	`04`	`X`	`FRE`	`@0 Tumeur maligne @5 38`
C07	`04`	`X`	`ENG`	`@0 Malignant tumor @5 38`
C07	`04`	`X`	`SPA`	`@0 Tumor maligno @5 38`
C07	`05`	`X`	`FRE`	`@0 Tumeur bénigne @5 39`
C07	`05`	`X`	`ENG`	`@0 Benign neoplasm @5 39`
C07	`05`	`X`	`SPA`	`@0 Tumor benigno @5 39`
C07	`06`	`X`	`FRE`	`@0 Endocrinopathie @5 40`
C07	`06`	`X`	`ENG`	`@0 Endocrinopathy @5 40`
C07	`06`	`X`	`SPA`	`@0 Endocrinopatía @5 40`
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N44	`01`			`@1 PSI`
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Pascal:04-0586379

Le document en format XML

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<author><name sortKey="Stankov, Karmen" sort="Stankov, Karmen" uniqKey="Stankov K" first="Karmen" last="Stankov">Karmen Stankov</name>
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<author><name sortKey="Bonneau, Dominique" sort="Bonneau, Dominique" uniqKey="Bonneau D" first="Dominique" last="Bonneau">Dominique Bonneau</name>
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<author><name sortKey="Gibelin, Helene" sort="Gibelin, Helene" uniqKey="Gibelin H" first="Hélène" last="Gibelin">Hélène Gibelin</name>
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<author><name sortKey="Levillain, Pierre" sort="Levillain, Pierre" uniqKey="Levillain P" first="Pierre" last="Levillain">Pierre Levillain</name>
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<author><name sortKey="Volante, Marco" sort="Volante, Marco" uniqKey="Volante M" first="Marco" last="Volante">Marco Volante</name>
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<author><name sortKey="Papotti, Mauro" sort="Papotti, Mauro" uniqKey="Papotti M" first="Mauro" last="Papotti">Mauro Papotti</name>
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<author><name sortKey="Romeo, Giovanni" sort="Romeo, Giovanni" uniqKey="Romeo G" first="Giovanni" last="Romeo">Giovanni Romeo</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Allelic loss on chromosomes 2q21 and 19p13.2 in oxyphilic thyroid tumors</title>
<author><name sortKey="Stankov, Karmen" sort="Stankov, Karmen" uniqKey="Stankov K" first="Karmen" last="Stankov">Karmen Stankov</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia, Unità Operativa di Genetica Medica, Policlinico S. Orsola-Malpighi</s1>
<s2>Bologna</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
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<sZ>3 aut.</sZ>
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<author><name sortKey="Pastore, Alessandro" sort="Pastore, Alessandro" uniqKey="Pastore A" first="Alessandro" last="Pastore">Alessandro Pastore</name>
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<s2>Bologna</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
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</author>
<author><name sortKey="Toschi, Luca" sort="Toschi, Luca" uniqKey="Toschi L" first="Luca" last="Toschi">Luca Toschi</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia, Unità Operativa di Genetica Medica, Policlinico S. Orsola-Malpighi</s1>
<s2>Bologna</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
<country>Italie</country>
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</author>
<author><name sortKey="Mckay, James" sort="Mckay, James" uniqKey="Mckay J" first="James" last="Mckay">James Mckay</name>
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<author><name sortKey="Lesueur, Fabienne" sort="Lesueur, Fabienne" uniqKey="Lesueur F" first="Fabienne" last="Lesueur">Fabienne Lesueur</name>
<affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Strangeways Research Laboratory, Worts Causeway</s1>
<s2>Cambridge</s2>
<s3>GBR</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
<country>Royaume-Uni</country>
</affiliation>
</author>
<author><name sortKey="Kraimps, Jean Louis" sort="Kraimps, Jean Louis" uniqKey="Kraimps J" first="Jean Louis" last="Kraimps">Jean Louis Kraimps</name>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Endocrine Surgery, Jean Bernard Hospital, Groupe de Recherche en Endocrinologie Experimentale et Clinique</s1>
<s2>Poitiers</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Bonneau, Dominique" sort="Bonneau, Dominique" uniqKey="Bonneau D" first="Dominique" last="Bonneau">Dominique Bonneau</name>
<affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Service de Génétique Médicale, Centre Hospitalier Universitaire d'Angers</s1>
<s2>Angers</s2>
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</inist:fA14>
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</affiliation>
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<author><name sortKey="Gibelin, Helene" sort="Gibelin, Helene" uniqKey="Gibelin H" first="Hélène" last="Gibelin">Hélène Gibelin</name>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Endocrine Surgery, Jean Bernard Hospital, Groupe de Recherche en Endocrinologie Experimentale et Clinique</s1>
<s2>Poitiers</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Levillain, Pierre" sort="Levillain, Pierre" uniqKey="Levillain P" first="Pierre" last="Levillain">Pierre Levillain</name>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Endocrine Surgery, Jean Bernard Hospital, Groupe de Recherche en Endocrinologie Experimentale et Clinique</s1>
<s2>Poitiers</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Volante, Marco" sort="Volante, Marco" uniqKey="Volante M" first="Marco" last="Volante">Marco Volante</name>
<affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Department of Biomedical Sciences and Oncology, University of Turin</s1>
<s2>Turin</s2>
<s3>ITA</s3>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
<country>Italie</country>
</affiliation>
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<author><name sortKey="Papotti, Mauro" sort="Papotti, Mauro" uniqKey="Papotti M" first="Mauro" last="Papotti">Mauro Papotti</name>
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<affiliation wicri:level="1"><inist:fA14 i1="07"><s1>San Luigi Hospital</s1>
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<author><name sortKey="Romeo, Giovanni" sort="Romeo, Giovanni" uniqKey="Romeo G" first="Giovanni" last="Romeo">Giovanni Romeo</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia, Unità Operativa di Genetica Medica, Policlinico S. Orsola-Malpighi</s1>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abnormal chromosome A2</term>
<term>Abnormal chromosome F19</term>
<term>Cancerology</term>
<term>Cytogenetics</term>
<term>Deletion</term>
<term>Human</term>
<term>Loss of heterozygosity</term>
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<front><div type="abstract" xml:lang="en">Hürthle thyroid tumors are characterized by frequent numerical chromosomal aberrations, including aneuploidy or polyploidy, losses and gains of some chromosomal regions and DNA fragmentation. In recent years, great attention has been paid to the combined analysis of morphologic and genetic features of oxyphilic tumors and to the elucidation of their pathogenesis. We analyzed for loss of heterozygosity (LOH) of the candidate regions for TCO (thyroid tumor with cell oxyphilia) and NMTCI (nonmedullary thyroid carcinoma I), 2 loci already mapped on chromosomes 19p13.2 and 2q21, respectively. Matched normal and tumor DNA samples from 70 patients with sporadic oxyphilic thyroid tumors and 20 with sporadic follicular tumors were subjected to microsatellite analysis using 10 markers on 19p13.2 and 6 markers on 2q21. This approach led us to the observation of a more significant LOH in oxyphilic than in follicular tumors. Allelic loss in tumor samples was evenly distributed in both 19p13.2 and 2q21 regions, in accordance with the established linkage of TCO and NMTCI for inherited tumors. In order to investigate the possible contribution of both susceptibility loci in oxyphilic tumors, the family that led to the original mapping of TCO locus was reanalyzed for the markers in the 2q21 region. This led to the exclusion of linkage with the NMTCI locus and to the refutation of the digenic inheritance hypothesis at least in this family.</div>
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Allelic loss on chromosomes 2q21 and 19p13.2 in oxyphilic thyroid tumors

Allelic loss on chromosomes 2q21 and 19p13.2 in oxyphilic thyroid tumors

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