AustralieFrV1, PascalFrancis, Curation, bibRecord, 000695

High frequency of allelic imbalance at regions of chromosome arm 8p in ovarian carcinoma

Identifieur interne : 000695 ( PascalFrancis/Curation ); précédent : 000694; suivant : 000696

High frequency of allelic imbalance at regions of chromosome arm 8p in ovarian carcinoma

Auteurs : Ingrid Pribill [Autriche] ; Paul Speiser [Autriche] ; Jennifer Leary [Australie] ; Sepp Leodolter [Autriche] ; Neville F. Hacker [Australie] ; Michael L. Friedlander [Australie] ; Daniel Birnbaum [France] ; Robert Zeillinger [Autriche] ; Michael Krainer [Autriche]

Source :

Cancer genetics and cytogenetics [ 0165-4608 ] ; 2001.

RBID : Pascal:02-0000349

Descripteurs français

Pascal (Inist)
- Carcinome, Ovaire, Chromosome C8, Bras court, Allèle, Physiopathologie, Homme, Fréquence génique, Anatomopathologie, Progression carcinogenèse, Pathogénie, Gène.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Allele, Carcinoma, Chromosome C8, Gene, Gene frequency, Human, Ovary, Pathogenesis, Pathology, Pathophysiology, Short arm, Tumor progression.

Abstract

Progressive genetic changes such as the inactivation of tumor suppressor genes (TSG) are though to play an important role in the initiation and progression of ovarian cancer. Frequent nonrandom allelic imbalance (Al) at Spl 1∼p21 and 8p22∼pter suggests the existence of TSGs that may be involved in the carcinogenesis of several human malignancies. We investigated 70 ovarian tumors with 11 highly polymorphic markers spanning 8p12∼p21 and 8p22∼pter to produce an AI map of 8p in epithelial ovarian cancer. Allelic imbalance was demonstrated in 54 tumors (77%) most frequently occurring at D8S136 (54%) and at D8S1992 (55%). Poorly differentiated and advanced stage cancers were more often affected by AI (G1+G2 vs G3; 20% vs. 66%; stage I+II vs. III+IV 36% vs 54%, P<.001; Kruskal-Wallis test) than well differentiated and early stage tumors. There was no relationship between histological subtype and AI Smallest regions of overlap (SRO) were delineated by analyzing 38 tumors with partial AI. This study provides compelling evidence for the involvement of TSGs on the short arm of chromosome 8, at 8p12∼p21 and at 8p23 in the development and progression of epithelial ovarian cancer.

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Pascal:02-0000349

Le document en format XML

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<author><name sortKey="Hacker, Neville F" sort="Hacker, Neville F" uniqKey="Hacker N" first="Neville F." last="Hacker">Neville F. Hacker</name>
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<author><name sortKey="Friedlander, Michael L" sort="Friedlander, Michael L" uniqKey="Friedlander M" first="Michael L." last="Friedlander">Michael L. Friedlander</name>
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<author><name sortKey="Birnbaum, Daniel" sort="Birnbaum, Daniel" uniqKey="Birnbaum D" first="Daniel" last="Birnbaum">Daniel Birnbaum</name>
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<s2>Marseille</s2>
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<author><name sortKey="Zeillinger, Robert" sort="Zeillinger, Robert" uniqKey="Zeillinger R" first="Robert" last="Zeillinger">Robert Zeillinger</name>
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<s2>1090 Vienna</s2>
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<author><name sortKey="Krainer, Michael" sort="Krainer, Michael" uniqKey="Krainer M" first="Michael" last="Krainer">Michael Krainer</name>
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<s2>1090 Vienna</s2>
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<series><title level="j" type="main">Cancer genetics and cytogenetics</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Allele</term>
<term>Carcinoma</term>
<term>Chromosome C8</term>
<term>Gene</term>
<term>Gene frequency</term>
<term>Human</term>
<term>Ovary</term>
<term>Pathogenesis</term>
<term>Pathology</term>
<term>Pathophysiology</term>
<term>Short arm</term>
<term>Tumor progression</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Carcinome</term>
<term>Ovaire</term>
<term>Chromosome C8</term>
<term>Bras court</term>
<term>Allèle</term>
<term>Physiopathologie</term>
<term>Homme</term>
<term>Fréquence génique</term>
<term>Anatomopathologie</term>
<term>Progression carcinogenèse</term>
<term>Pathogénie</term>
<term>Gène</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term>
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<front><div type="abstract" xml:lang="en">Progressive genetic changes such as the inactivation of tumor suppressor genes (TSG) are though to play an important role in the initiation and progression of ovarian cancer. Frequent nonrandom allelic imbalance (Al) at Spl 1∼p21 and 8p22∼pter suggests the existence of TSGs that may be involved in the carcinogenesis of several human malignancies. We investigated 70 ovarian tumors with 11 highly polymorphic markers spanning 8p12∼p21 and 8p22∼pter to produce an AI map of 8p in epithelial ovarian cancer. Allelic imbalance was demonstrated in 54 tumors (77%) most frequently occurring at D8S136 (54%) and at D8S1992 (55%). Poorly differentiated and advanced stage cancers were more often affected by AI (G1+G2 vs G3; 20% vs. 66%; stage I+II vs. III+IV 36% vs 54%, P<.001; Kruskal-Wallis test) than well differentiated and early stage tumors. There was no relationship between histological subtype and AI Smallest regions of overlap (SRO) were delineated by analyzing 38 tumors with partial AI. This study provides compelling evidence for the involvement of TSGs on the short arm of chromosome 8, at 8p12∼p21 and at 8p23 in the development and progression of epithelial ovarian cancer.</div>
</front>
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<fA11 i1="04" i2="1"><s1>LEODOLTER (Sepp)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>HACKER (Neville F.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>FRIEDLANDER (Michael L.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>BIRNBAUM (Daniel)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>ZEILLINGER (Robert)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>KRAINER (Michael)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Medicine 1, Clinical Division of Oncology. University Hospital. Molecular Oncology Group, Währingergürtel 18-20</s1>
<s2>1090 Vienna</s2>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Gynecology and Obstetries, University Hospital, Molecular Oncology Group. Währingergürtel 18-20</s1>
<s2>1090 Vienna</s2>
<s3>AUT</s3>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Medical Oncology, Westmead Hospital</s1>
<s2>Westmead</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Ludwig Boltzmann Institute for Gynecologic Oncology and Reproductive Medicine, University Hospital, Molecular Oncology Group. Währingergürtel 18-20</s1>
<s2>1090 Vienna</s2>
<s3>AUT</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Gynaecological Cancer Centre, Royal Women Hospital</s1>
<s2>Randwick</s2>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department Medical Oncology. Prince of Wales Hospital</s1>
<s2>Randwick</s2>
<s3>AUS</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Institut Paoli-Clamettes, U. 119 Inserm</s1>
<s2>Marseille</s2>
<s3>FRA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>23-29</s1>
</fA20>
<fA21><s1>2001</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>18350</s2>
<s5>354000099392820040</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2002 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>20 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>02-0000349</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Cancer genetics and cytogenetics</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Progressive genetic changes such as the inactivation of tumor suppressor genes (TSG) are though to play an important role in the initiation and progression of ovarian cancer. Frequent nonrandom allelic imbalance (Al) at Spl 1∼p21 and 8p22∼pter suggests the existence of TSGs that may be involved in the carcinogenesis of several human malignancies. We investigated 70 ovarian tumors with 11 highly polymorphic markers spanning 8p12∼p21 and 8p22∼pter to produce an AI map of 8p in epithelial ovarian cancer. Allelic imbalance was demonstrated in 54 tumors (77%) most frequently occurring at D8S136 (54%) and at D8S1992 (55%). Poorly differentiated and advanced stage cancers were more often affected by AI (G1+G2 vs G3; 20% vs. 66%; stage I+II vs. III+IV 36% vs 54%, P<.001; Kruskal-Wallis test) than well differentiated and early stage tumors. There was no relationship between histological subtype and AI Smallest regions of overlap (SRO) were delineated by analyzing 38 tumors with partial AI. This study provides compelling evidence for the involvement of TSGs on the short arm of chromosome 8, at 8p12∼p21 and at 8p23 in the development and progression of epithelial ovarian cancer.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B20C02</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>235</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Carcinome</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Carcinoma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Carcinoma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Ovaire</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Ovary</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Ovario</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Chromosome C8</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Chromosome C8</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Cromosoma C8</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Bras court</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Short arm</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Brazo corto</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Allèle</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Allele</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Alelo</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Physiopathologie</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Pathophysiology</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Fisiopatología</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Homme</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Human</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Hombre</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Fréquence génique</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Gene frequency</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Frecuencia génica</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Anatomopathologie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Pathology</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Anatomía patológica</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Progression carcinogenèse</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Tumor progression</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Progresión carcinogénesis</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Pathogénie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Pathogenesis</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Patogenia</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Gène</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Gene</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Gen</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Tumeur maligne</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Malignant tumor</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Tumor maligno</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Appareil génital femelle pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Female genital diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Aparato genital hembra patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Ovaire pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Ovarian diseases</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Ovario patología</s0>
<s5>39</s5>
</fC07>
<fN21><s1>001</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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High frequency of allelic imbalance at regions of chromosome arm 8p in ovarian carcinoma

High frequency of allelic imbalance at regions of chromosome arm 8p in ovarian carcinoma

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