AustralieFrV1, PascalFrancis, Curation, bibRecord, 000D28

A case report in favor of a multistep adrenocortical tumorigenesis

Identifieur interne : 000D28 ( PascalFrancis/Curation ); précédent : 000D27; suivant : 000D29

A case report in favor of a multistep adrenocortical tumorigenesis

Auteurs : Marie-Hélène Bernard [France] ; Stan Sidhu [Australie] ; Nicole Berger [France] ; Jean-Louis Peix [France] ; Deborah J. Marsh [Australie] ; Bruce G. Robinson [Australie] ; Véronique Gaston [France] ; Yves Le Bouc [France] ; Christine Gicquel [France]

Source :

The Journal of clinical endocrinology and metabolism [ 0021-972X ] ; 2003.

RBID : Pascal:03-0195514

Descripteurs français

Pascal (Inist)
- Tumeur, Corticosurrénale, Transformation maligne, Etude cas, Carcinogenèse, Biologie moléculaire, Hybridation génomique comparative, Histopathologie, Adulte, Mâle.
Wicri :
- topic : Adulte.

English descriptors

KwdEn :
- Adrenal cortex, Adult, Carcinogenesis, Case study, Comparative genomic hybridization, Histopathology, Male, Malignant transformation, Molecular biology, Tumor.

Abstract

The mechanisms of adrenocortical tumorigenesis are still not fully understood. Data from clonal analysis, comparative genomic hybridization, and allelotyping suggest that it involves a multistep process during which several genetic defects are progressively acquired, leading to the malignant transformation. The events involved in the first steps of this process are not well known, and most of the abnormalities described in adrenocortical tumors to date are associated with the malignant phenotype. We report a case that suggests that adrenocortical tumorigenesis may be a multistep process. A 43-yr-old patient underwent surgery for an incidentally discovered adrenal mass. Pathological analysis showed that this tumor consisted of two parts: a central part with features of malignancy surrounded by another part with a strictly benign appearance. These data were confirmed by molecular analysis and comparative genomic hybridization that were consistent with either a malignant or benign presentation. The apparently malignant part of the tumor exhibited molecular abnormalities [17p13 loss of heterozygosity (LOH), 11p15 uniparental disomy and overexpression of the IGF-II gene] as well as chromosomal gains and losses (comparative genomic hybridization) that have been previously described in malignant tumors. No abnormalities were found in the surrounding benign tissues. Although this observation is not definitive proof that adrenocortical tumorigenesis occurs via a multistep process, it suggests that there is a progressive change from the benign to the malignant state in some adrenocortical tumors.

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The mechanisms of adrenocortical tumorigenesis are still not fully understood. Data from clonal analysis, comparative genomic hybridization, and allelotyping suggest that it involves a multistep process during which several genetic defects are progressively acquired, leading to the malignant transformation. The events involved in the first steps of this process are not well known, and most of the abnormalities described in adrenocortical tumors to date are associated with the malignant phenotype. We report a case that suggests that adrenocortical tumorigenesis may be a multistep process. A 43-yr-old patient underwent surgery for an incidentally discovered adrenal mass. Pathological analysis showed that this tumor consisted of two parts: a central part with features of malignancy surrounded by another part with a strictly benign appearance. These data were confirmed by molecular analysis and comparative genomic hybridization that were consistent with either a malignant or benign presentation. The apparently malignant part of the tumor exhibited molecular abnormalities [17p13 loss of heterozygosity (LOH), 11p15 uniparental disomy and overexpression of the IGF-II gene] as well as chromosomal gains and losses (comparative genomic hybridization) that have been previously described in malignant tumors. No abnormalities were found in the surrounding benign tissues. Although this observation is not definitive proof that adrenocortical tumorigenesis occurs via a multistep process, it suggests that there is a progressive change from the benign to the malignant state in some adrenocortical tumors.</div>
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<fA11 i1="07" i2="1"><s1>GASTON (Véronique)</s1>
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<fA11 i1="08" i2="1"><s1>LE BOUC (Yves)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>GICQUEL (Christine)</s1>
</fA11>
<fA14 i1="01"><s1>Service d'endocrinologie des Hôpitaux de Lyon</s1>
<s2>69321 Lyon</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Molecular Medicine, Kolling Institute of Medical Research and University of Sydney, St. Leonards</s1>
<s2>2065 NSW</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Service d'anatomopathologie des Hôpitaux de Lyon</s1>
<s2>69321 Lyon</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Service viscérale des Hôpitaux de Lyon</s1>
<s2>69321 Lyon</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Laboratoire d'Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, Assistance Publique-Hôpitaux de Paris</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>998-1001</s1>
</fA20>
<fA21><s1>2003</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>6022</s2>
<s5>354000103966210080</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2003 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>24 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>03-0195514</s0>
</fA47>
<fA60><s1>P</s1>
<s3>EC</s3>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>The Journal of clinical endocrinology and metabolism</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>The mechanisms of adrenocortical tumorigenesis are still not fully understood. Data from clonal analysis, comparative genomic hybridization, and allelotyping suggest that it involves a multistep process during which several genetic defects are progressively acquired, leading to the malignant transformation. The events involved in the first steps of this process are not well known, and most of the abnormalities described in adrenocortical tumors to date are associated with the malignant phenotype. We report a case that suggests that adrenocortical tumorigenesis may be a multistep process. A 43-yr-old patient underwent surgery for an incidentally discovered adrenal mass. Pathological analysis showed that this tumor consisted of two parts: a central part with features of malignancy surrounded by another part with a strictly benign appearance. These data were confirmed by molecular analysis and comparative genomic hybridization that were consistent with either a malignant or benign presentation. The apparently malignant part of the tumor exhibited molecular abnormalities [17p13 loss of heterozygosity (LOH), 11p15 uniparental disomy and overexpression of the IGF-II gene] as well as chromosomal gains and losses (comparative genomic hybridization) that have been previously described in malignant tumors. No abnormalities were found in the surrounding benign tissues. Although this observation is not definitive proof that adrenocortical tumorigenesis occurs via a multistep process, it suggests that there is a progressive change from the benign to the malignant state in some adrenocortical tumors.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B21B02</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Tumeur</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Tumor</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Tumor</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Corticosurrénale</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Adrenal cortex</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Corticosuprarrenal</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Transformation maligne</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Malignant transformation</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Transformación maligna</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Etude cas</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Case study</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Estudio caso</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Carcinogenèse</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Carcinogenesis</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Carcinogénesis</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Biologie moléculaire</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Molecular biology</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Biología molecular</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Hybridation génomique comparative</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Comparative genomic hybridization</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Hibridación genómica comparativa</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Histopathologie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Histopathology</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Histopatología</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Adulte</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Adult</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Adulto</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Mâle</s0>
<s5>21</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Male</s0>
<s5>21</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Macho</s0>
<s5>21</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Homme</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Human</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Hombre</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Endocrinopathie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Endocrinopathy</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Endocrinopatía</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Surrénale pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Adrenal gland diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Suprarrenal patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Corticosurrénale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Adrenal cortex diseases</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Corticosuprarrenal patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Génétique</s0>
<s5>53</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Genetics</s0>
<s5>53</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Genética</s0>
<s5>53</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Anatomopathologie</s0>
<s5>61</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Pathology</s0>
<s5>61</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Anatomía patológica</s0>
<s5>61</s5>
</fC07>
<fN21><s1>111</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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Serveur d'exploration sur les relations entre la France et l'Australie

A case report in favor of a multistep adrenocortical tumorigenesis

A case report in favor of a multistep adrenocortical tumorigenesis

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