Evidence for a Turner syndrome locus or loci at Xp11.2-p22.1.
Identifieur interne : 004D90 ( PubMed/Curation ); précédent : 004D89; suivant : 004D91Evidence for a Turner syndrome locus or loci at Xp11.2-p22.1.
Auteurs : A R Zinn [États-Unis] ; V S Tonk ; Z. Chen ; W L Flejter ; H A Gardner ; R. Guerra ; H. Kushner ; S. Schwartz ; V P Sybert ; D L Van Dyke ; J L RossSource :
- American journal of human genetics [ 0002-9297 ] ; 1998.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Adulte d'âge moyen, Autoanticorps (analyse), Cartographie chromosomique, Centromère (génétique), Chromosome X (génétique), Compensation de dosage génétique, Coude (malformations), Délétion de segment de chromosome, Enfant, Enfant d'âge préscolaire, Femelle, Génotype, Humains, Insuffisance ovarienne primitive (génétique), Liaison génétique, Maladies de la thyroïde (génétique), Maladies de la thyroïde (immunologie), Marqueurs génétiques, Méthylation de l'ADN, Nourrisson, Palais (malformations), Syndrome de Turner (anatomopathologie), Syndrome de Turner (génétique), Syndrome de Turner (immunologie), Taille (génétique), Technique FISH, Études de cohortes.
- MESH :
- analyse : Autoanticorps.
- anatomopathologie : Syndrome de Turner.
- génétique : Centromère, Chromosome X, Insuffisance ovarienne primitive, Maladies de la thyroïde, Syndrome de Turner, Taille.
- immunologie : Maladies de la thyroïde, Syndrome de Turner.
- malformations : Coude, Palais.
- Adolescent, Adulte, Adulte d'âge moyen, Cartographie chromosomique, Compensation de dosage génétique, Délétion de segment de chromosome, Enfant, Enfant d'âge préscolaire, Femelle, Génotype, Humains, Liaison génétique, Marqueurs génétiques, Méthylation de l'ADN, Nourrisson, Technique FISH, Études de cohortes.
English descriptors
- KwdEn :
- Adolescent, Adult, Autoantibodies (analysis), Body Height (genetics), Centromere (genetics), Child, Child, Preschool, Chromosome Deletion, Chromosome Mapping, Cohort Studies, DNA Methylation, Dosage Compensation, Genetic, Elbow (abnormalities), Female, Genetic Linkage, Genetic Markers, Genotype, Humans, In Situ Hybridization, Fluorescence, Infant, Middle Aged, Palate (abnormalities), Primary Ovarian Insufficiency (genetics), Thyroid Diseases (genetics), Thyroid Diseases (immunology), Turner Syndrome (genetics), Turner Syndrome (immunology), Turner Syndrome (pathology), X Chromosome (genetics).
- MESH :
- chemical , analysis : Autoantibodies.
- abnormalities : Elbow, Palate.
- genetics : Body Height, Centromere, Primary Ovarian Insufficiency, Thyroid Diseases, Turner Syndrome, X Chromosome.
- immunology : Thyroid Diseases, Turner Syndrome.
- pathology : Turner Syndrome.
- Adolescent, Adult, Child, Child, Preschool, Chromosome Deletion, Chromosome Mapping, Cohort Studies, DNA Methylation, Dosage Compensation, Genetic, Female, Genetic Linkage, Genetic Markers, Genotype, Humans, In Situ Hybridization, Fluorescence, Infant, Middle Aged.
Abstract
Turner syndrome is the complex human phenotype associated with complete or partial monosomy X. Principle features of Turner syndrome include short stature, ovarian failure, and a variety of other anatomic and physiological abnormalities, such as webbed neck, lymphedema, cardiovascular and renal anomalies, hypertension, and autoimmune thyroid disease. We studied 28 apparently nonmosaic subjects with partial deletions of Xp, in order to map loci responsible for various components of the Turner syndrome phenotype. Subjects were carefully evaluated for the presence or absence of Turner syndrome features, and their deletions were mapped by FISH with a panel of Xp markers. Using a statistical method to examine genotype/phenotype correlations, we mapped one or more Turner syndrome traits to a critical region in Xp11.2-p22.1. These traits included short stature, ovarian failure, high-arched palate, and autoimmune thyroid disease. The results are useful for genetic counseling of individuals with partial monosomy X. Study of additional subjects should refine the localization of Turner syndrome loci and provide a rational basis for exploration of candidate genes.
DOI: 10.1086/302152
PubMed: 9837829
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Andrew.Zinn@email.swmed.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Eugene McDermott Center for Human Growth, Department of Internal Medicine, University of Texas, Dallas</wicri:regionArea></affiliation></author><author><name sortKey="Tonk, V S" sort="Tonk, V S" uniqKey="Tonk V" first="V S" last="Tonk">V S Tonk</name></author><author><name sortKey="Chen, Z" sort="Chen, Z" uniqKey="Chen Z" first="Z" last="Chen">Z. Chen</name></author><author><name sortKey="Flejter, W L" sort="Flejter, W L" uniqKey="Flejter W" first="W L" last="Flejter">W L Flejter</name></author><author><name sortKey="Gardner, H A" sort="Gardner, H A" uniqKey="Gardner H" first="H A" last="Gardner">H A Gardner</name></author><author><name sortKey="Guerra, R" sort="Guerra, R" uniqKey="Guerra R" first="R" last="Guerra">R. Guerra</name></author><author><name sortKey="Kushner, H" sort="Kushner, H" uniqKey="Kushner H" first="H" last="Kushner">H. 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Methylation</term><term>Dosage Compensation, Genetic</term><term>Elbow (abnormalities)</term><term>Female</term><term>Genetic Linkage</term><term>Genetic Markers</term><term>Genotype</term><term>Humans</term><term>In Situ Hybridization, Fluorescence</term><term>Infant</term><term>Middle Aged</term><term>Palate (abnormalities)</term><term>Primary Ovarian Insufficiency (genetics)</term><term>Thyroid Diseases (genetics)</term><term>Thyroid Diseases (immunology)</term><term>Turner Syndrome (genetics)</term><term>Turner Syndrome (immunology)</term><term>Turner Syndrome (pathology)</term><term>X Chromosome (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Autoanticorps (analyse)</term><term>Cartographie chromosomique</term><term>Centromère (génétique)</term><term>Chromosome X (génétique)</term><term>Compensation de dosage génétique</term><term>Coude (malformations)</term><term>Délétion de segment de chromosome</term><term>Enfant</term><term>Enfant d'âge préscolaire</term><term>Femelle</term><term>Génotype</term><term>Humains</term><term>Insuffisance ovarienne primitive (génétique)</term><term>Liaison génétique</term><term>Maladies de la thyroïde (génétique)</term><term>Maladies de la thyroïde (immunologie)</term><term>Marqueurs génétiques</term><term>Méthylation de l'ADN</term><term>Nourrisson</term><term>Palais (malformations)</term><term>Syndrome de Turner (anatomopathologie)</term><term>Syndrome de Turner (génétique)</term><term>Syndrome de Turner (immunologie)</term><term>Taille (génétique)</term><term>Technique FISH</term><term>Études de cohortes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Autoantibodies</term></keywords><keywords scheme="MESH" qualifier="abnormalities" xml:lang="en"><term>Elbow</term><term>Palate</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Autoanticorps</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Syndrome de Turner</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Body Height</term><term>Centromere</term><term>Primary Ovarian Insufficiency</term><term>Thyroid Diseases</term><term>Turner Syndrome</term><term>X Chromosome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Centromère</term><term>Chromosome X</term><term>Insuffisance ovarienne primitive</term><term>Maladies de la thyroïde</term><term>Syndrome de Turner</term><term>Taille</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Maladies de la thyroïde</term><term>Syndrome de Turner</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Thyroid Diseases</term><term>Turner Syndrome</term></keywords><keywords scheme="MESH" qualifier="malformations" xml:lang="fr"><term>Coude</term><term>Palais</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Turner Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Child</term><term>Child, Preschool</term><term>Chromosome Deletion</term><term>Chromosome Mapping</term><term>Cohort Studies</term><term>DNA Methylation</term><term>Dosage Compensation, Genetic</term><term>Female</term><term>Genetic Linkage</term><term>Genetic Markers</term><term>Genotype</term><term>Humans</term><term>In Situ Hybridization, Fluorescence</term><term>Infant</term><term>Middle Aged</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Cartographie chromosomique</term><term>Compensation de dosage génétique</term><term>Délétion de segment de chromosome</term><term>Enfant</term><term>Enfant d'âge préscolaire</term><term>Femelle</term><term>Génotype</term><term>Humains</term><term>Liaison génétique</term><term>Marqueurs génétiques</term><term>Méthylation de l'ADN</term><term>Nourrisson</term><term>Technique FISH</term><term>Études de cohortes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Turner syndrome is the complex human phenotype associated with complete or partial monosomy X. Principle features of Turner syndrome include short stature, ovarian failure, and a variety of other anatomic and physiological abnormalities, such as webbed neck, lymphedema, cardiovascular and renal anomalies, hypertension, and autoimmune thyroid disease. We studied 28 apparently nonmosaic subjects with partial deletions of Xp, in order to map loci responsible for various components of the Turner syndrome phenotype. Subjects were carefully evaluated for the presence or absence of Turner syndrome features, and their deletions were mapped by FISH with a panel of Xp markers. Using a statistical method to examine genotype/phenotype correlations, we mapped one or more Turner syndrome traits to a critical region in Xp11.2-p22.1. These traits included short stature, ovarian failure, high-arched palate, and autoimmune thyroid disease. The results are useful for genetic counseling of individuals with partial monosomy X. Study of additional subjects should refine the localization of Turner syndrome loci and provide a rational basis for exploration of candidate genes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9837829</PMID><DateCreated><Year>1999</Year><Month>02</Month><Day>01</Day></DateCreated><DateCompleted><Year>1999</Year><Month>02</Month><Day>01</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0002-9297</ISSN><JournalIssue CitedMedium="Print"><Volume>63</Volume><Issue>6</Issue><PubDate><Year>1998</Year><Month>Dec</Month></PubDate></JournalIssue><Title>American journal of human genetics</Title><ISOAbbreviation>Am. J. Hum. Genet.</ISOAbbreviation></Journal><ArticleTitle>Evidence for a Turner syndrome locus or loci at Xp11.2-p22.1.</ArticleTitle><Pagination><MedlinePgn>1757-66</MedlinePgn></Pagination><Abstract><AbstractText>Turner syndrome is the complex human phenotype associated with complete or partial monosomy X. Principle features of Turner syndrome include short stature, ovarian failure, and a variety of other anatomic and physiological abnormalities, such as webbed neck, lymphedema, cardiovascular and renal anomalies, hypertension, and autoimmune thyroid disease. We studied 28 apparently nonmosaic subjects with partial deletions of Xp, in order to map loci responsible for various components of the Turner syndrome phenotype. Subjects were carefully evaluated for the presence or absence of Turner syndrome features, and their deletions were mapped by FISH with a panel of Xp markers. Using a statistical method to examine genotype/phenotype correlations, we mapped one or more Turner syndrome traits to a critical region in Xp11.2-p22.1. These traits included short stature, ovarian failure, high-arched palate, and autoimmune thyroid disease. The results are useful for genetic counseling of individuals with partial monosomy X. Study of additional subjects should refine the localization of Turner syndrome loci and provide a rational basis for exploration of candidate genes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zinn</LastName><ForeName>A R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>Eugene McDermott Center for Human Growth, Department of Internal Medicine, University of Texas, Dallas, USA. Andrew.Zinn@email.swmed.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tonk</LastName><ForeName>V S</ForeName><Initials>VS</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Z</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Flejter</LastName><ForeName>W L</ForeName><Initials>WL</Initials></Author><Author ValidYN="Y"><LastName>Gardner</LastName><ForeName>H A</ForeName><Initials>HA</Initials></Author><Author ValidYN="Y"><LastName>Guerra</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Kushner</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Schwartz</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Sybert</LastName><ForeName>V P</ForeName><Initials>VP</Initials></Author><Author ValidYN="Y"><LastName>Van Dyke</LastName><ForeName>D L</ForeName><Initials>DL</Initials></Author><Author ValidYN="Y"><LastName>Ross</LastName><ForeName>J L</ForeName><Initials>JL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS35554</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Hum Genet</MedlineTA><NlmUniqueID>0370475</NlmUniqueID><ISSNLinking>0002-9297</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001323">Autoantibodies</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005819">Genetic 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Version="1">2221825</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001323" MajorTopicYN="N">Autoantibodies</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001827" MajorTopicYN="N">Body Height</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002503" MajorTopicYN="N">Centromere</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, 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