High frequency of allelic imbalance at regions of chromosome arm 8p in ovarian carcinoma
Identifieur interne : 00B915 ( Main/Exploration ); précédent : 00B914; suivant : 00B916High 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.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Allele, Allelic, Allelic imbalance, Anchor markers, Borderline tumors, Cancer genetics, Carcinoma, Chromosome, Chromosome C8, Cytogenetics, Deletion, Disease stage, Early stage, Early stage tumors, Elsevier science, Figo stages, Frequent loss, Gene, Gene frequency, Genes chromosom cancer, Genetic changes, Genetics, Gynecol oncol, Highest loss, Histological subtype, Histopathological parameters, Homozygous deletion, Homozygous deletions, Human, Imbalance, Imbalance factor, Locus, Marker, Molecular oncology group, Oncology, Oral cancer, Ovarian, Ovarian cancer, Ovary, Overall frequency, Pathogenesis, Pathology, Pathophysiology, Polymorphic, Polymorphic markers, Prostate, Prostate cancer, Short arm, Smallest regions, Stage tumors, Tumor, Tumor differentiation, Tumor progression, Tumor stage, Tumor suppressor genes, University hospital.
- Teeft :
- Allelic, Allelic imbalance, Anchor markers, Borderline tumors, Cancer genetics, Carcinoma, Chromosome, Cytogenetics, Deletion, Disease stage, Early stage, Early stage tumors, Elsevier science, Figo stages, Frequent loss, Genes chromosom cancer, Genetic changes, Genetics, Gynecol oncol, Highest loss, Histological subtype, Histopathological parameters, Homozygous deletion, Homozygous deletions, Imbalance, Imbalance factor, Locus, Marker, Molecular oncology group, Oncology, Oral cancer, Ovarian, Ovarian cancer, Overall frequency, Polymorphic, Polymorphic markers, Prostate, Prostate cancer, Smallest regions, Stage tumors, Tumor, Tumor differentiation, Tumor stage, Tumor suppressor genes, University hospital.
Abstract
Abstract: Progressive genetic changes such as the inactivation of tumor suppressor genes (TSG) are thought to play an important role in the initiation and progression of ovarian cancer. Frequent nonrandom allelic imbalance (AI) at 8p11∼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.
Url:
DOI: 10.1016/S0165-4608(01)00419-8
Affiliations:
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Hacker</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Gynaecological Cancer Centre, Royal Women Hospital, Randwick</wicri:regionArea><wicri:noRegion>Randwick</wicri:noRegion></affiliation></author><author><name sortKey="Friedlander, Michael L" sort="Friedlander, Michael L" uniqKey="Friedlander M" first="Michael L" last="Friedlander">Michael L. Friedlander</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department Medical Oncology, Prince of Wales Hospital, Randwick</wicri:regionArea><wicri:noRegion>Randwick</wicri:noRegion></affiliation></author><author><name sortKey="Birnbaum, Daniel" sort="Birnbaum, Daniel" uniqKey="Birnbaum D" first="Daniel" last="Birnbaum">Daniel Birnbaum</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Institut Paoli-Clamettes, U.119 Inserm, Marseille</wicri:regionArea><placeName><region type="region">Provence-Alpes-Côte d'Azur</region><region type="old region">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName></affiliation></author><author><name sortKey="Zeillinger, Robert" sort="Zeillinger, Robert" uniqKey="Zeillinger R" first="Robert" last="Zeillinger">Robert Zeillinger</name><affiliation wicri:level="1"><country wicri:rule="url">Autriche</country></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Gynecology and Obstetrics, University Hospital, Molecular Oncology Group, Währingergürtel 18-20, A-1090 Vienna</wicri:regionArea><wicri:noRegion>A-1090 Vienna</wicri:noRegion></affiliation></author><author><name sortKey="Krainer, Michael" sort="Krainer, Michael" uniqKey="Krainer M" first="Michael" last="Krainer">Michael Krainer</name><affiliation wicri:level="1"><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Medicine I, Clinical Division of Oncology, University Hospital, Molecular Oncology Group, Währingergürtel 18-20, A-1090 Vienna</wicri:regionArea><wicri:noRegion>A-1090 Vienna</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Cancer Genetics and Cytogenetics</title><title level="j" type="abbrev">CGC</title><idno type="ISSN">0165-4608</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">129</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="23">23</biblScope><biblScope unit="page" to="29">29</biblScope></imprint><idno type="ISSN">0165-4608</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-4608</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Allele</term><term>Allelic</term><term>Allelic imbalance</term><term>Anchor markers</term><term>Borderline tumors</term><term>Cancer genetics</term><term>Carcinoma</term><term>Chromosome</term><term>Chromosome C8</term><term>Cytogenetics</term><term>Deletion</term><term>Disease stage</term><term>Early stage</term><term>Early stage tumors</term><term>Elsevier science</term><term>Figo stages</term><term>Frequent loss</term><term>Gene</term><term>Gene frequency</term><term>Genes chromosom cancer</term><term>Genetic changes</term><term>Genetics</term><term>Gynecol oncol</term><term>Highest loss</term><term>Histological subtype</term><term>Histopathological parameters</term><term>Homozygous deletion</term><term>Homozygous deletions</term><term>Human</term><term>Imbalance</term><term>Imbalance factor</term><term>Locus</term><term>Marker</term><term>Molecular oncology group</term><term>Oncology</term><term>Oral cancer</term><term>Ovarian</term><term>Ovarian cancer</term><term>Ovary</term><term>Overall frequency</term><term>Pathogenesis</term><term>Pathology</term><term>Pathophysiology</term><term>Polymorphic</term><term>Polymorphic markers</term><term>Prostate</term><term>Prostate cancer</term><term>Short arm</term><term>Smallest regions</term><term>Stage tumors</term><term>Tumor</term><term>Tumor differentiation</term><term>Tumor progression</term><term>Tumor stage</term><term>Tumor suppressor genes</term><term>University hospital</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Allèle</term><term>Anatomopathologie</term><term>Bras court</term><term>Carcinome</term><term>Chromosome C8</term><term>Fréquence génique</term><term>Gène</term><term>Homme</term><term>Ovaire</term><term>Pathogénie</term><term>Physiopathologie</term><term>Progression carcinogenèse</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Allelic</term><term>Allelic imbalance</term><term>Anchor markers</term><term>Borderline tumors</term><term>Cancer genetics</term><term>Carcinoma</term><term>Chromosome</term><term>Cytogenetics</term><term>Deletion</term><term>Disease stage</term><term>Early stage</term><term>Early stage tumors</term><term>Elsevier science</term><term>Figo stages</term><term>Frequent loss</term><term>Genes chromosom cancer</term><term>Genetic changes</term><term>Genetics</term><term>Gynecol oncol</term><term>Highest loss</term><term>Histological subtype</term><term>Histopathological parameters</term><term>Homozygous deletion</term><term>Homozygous deletions</term><term>Imbalance</term><term>Imbalance factor</term><term>Locus</term><term>Marker</term><term>Molecular oncology group</term><term>Oncology</term><term>Oral cancer</term><term>Ovarian</term><term>Ovarian cancer</term><term>Overall frequency</term><term>Polymorphic</term><term>Polymorphic markers</term><term>Prostate</term><term>Prostate cancer</term><term>Smallest regions</term><term>Stage tumors</term><term>Tumor</term><term>Tumor differentiation</term><term>Tumor stage</term><term>Tumor suppressor genes</term><term>University hospital</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Génétique</term><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Progressive genetic changes such as the inactivation of tumor suppressor genes (TSG) are thought to play an important role in the initiation and progression of ovarian cancer. Frequent nonrandom allelic imbalance (AI) at 8p11∼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></TEI><affiliations><list><country><li>Australie</li><li>Autriche</li><li>France</li></country><region><li>Provence-Alpes-Côte d'Azur</li></region><settlement><li>Marseille</li></settlement></list><tree><country name="Autriche"><noRegion><name sortKey="Pribill, Ingrid" sort="Pribill, Ingrid" uniqKey="Pribill I" first="Ingrid" last="Pribill">Ingrid Pribill</name></noRegion><name sortKey="Krainer, Michael" sort="Krainer, Michael" uniqKey="Krainer M" first="Michael" last="Krainer">Michael Krainer</name><name sortKey="Leodolter, Sepp" sort="Leodolter, Sepp" uniqKey="Leodolter S" first="Sepp" last="Leodolter">Sepp Leodolter</name><name sortKey="Speiser, Paul" sort="Speiser, Paul" uniqKey="Speiser P" first="Paul" last="Speiser">Paul Speiser</name><name sortKey="Zeillinger, Robert" sort="Zeillinger, Robert" uniqKey="Zeillinger R" first="Robert" last="Zeillinger">Robert Zeillinger</name><name sortKey="Zeillinger, Robert" sort="Zeillinger, Robert" uniqKey="Zeillinger R" first="Robert" last="Zeillinger">Robert Zeillinger</name></country><country name="Australie"><noRegion><name sortKey="Leary, Jennifer" sort="Leary, Jennifer" uniqKey="Leary J" first="Jennifer" last="Leary">Jennifer Leary</name></noRegion><name sortKey="Friedlander, Michael L" sort="Friedlander, Michael L" uniqKey="Friedlander M" first="Michael L" last="Friedlander">Michael L. Friedlander</name><name sortKey="Hacker, Neville F" sort="Hacker, Neville F" uniqKey="Hacker N" first="Neville F" last="Hacker">Neville F. Hacker</name></country><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Birnbaum, Daniel" sort="Birnbaum, Daniel" uniqKey="Birnbaum D" first="Daniel" last="Birnbaum">Daniel Birnbaum</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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