LymphedemaV1, France, Analysis, bibRecord, 000234

Alterations of p53 and PIK3CA/AKT/mTOR Pathways in Angiosarcomas: A Pattern Distinct from Other Sarcomas with Complex Genomics

Identifieur interne : 000234 ( France/Analysis ); précédent : 000233; suivant : 000235

Alterations of p53 and PIK3CA/AKT/mTOR Pathways in Angiosarcomas: A Pattern Distinct from Other Sarcomas with Complex Genomics

Auteurs : Antoine Italiano [États-Unis, France] ; Chun-Liang Chen [États-Unis] ; Rachael Thomas [États-Unis] ; Matthew Breen [États-Unis] ; Françoise Bonnet [France] ; Nicolas Sevenet [France] ; Michel Longy [France] ; Robert G. Maki [États-Unis] ; Jean-Michel Coindre [France] ; Cristina R. Antonescu [États-Unis]

Source :

Cancer [ 0008-543X ] ; 2012.

RBID : PMC:3434269

Abstract

Background

The p53 and the PIK3CA/AKT/mTOR pathways are frequently altered in sarcoma with complex genomics such as leiomyosarcoma (LMS) or undifferentiated pleomorphic sarcoma (UPS). The scale of genetic abnormalities in these pathways remains unknown in angiosarcoma.

Methods

We investigated the status of critical genes involved in the p53 and the PIK3CA/AKT/mTOR pathways in a series of 62 AS.

Results

The mutation and deletion rates of TP53 were 4% and 0, respectively. p53 overexpression was detected by immunohistochemistry in 49% of cases and was associated with inferior disease-free survival. Although p14 inactivation or HDM2 overexpression are frequent in LMS and UPS and could substitute for TP53 mutation or deletion, such alterations were rare in angiosarcomas. pS6K and/or p-4eBP1 overexpression was observed in 42% of cases suggesting frequent activation of the PIK3CA/AKT/mTOR pathway in angiosarcomas. Activation was not related to intragenic deletion of PTEN, an aberration that is frequent in LMS and UPS, but absent in angiosarcomas.

Conclusion

Angiosarcomas constitute a distinct subgroup among sarcomas with complex genomics. Although TP53 mutation and PTEN deletion are frequent in LMS and UPS, these aberrations are rarely involved in the pathogenesis of AS.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434269

DOI: 10.1002/cncr.27614
PubMed: 22648906
PubMed Central: 3434269

Affiliations:

Links to Exploration step

PMC:3434269

Le document en format XML

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<affiliation wicri:level="2"><nlm:aff id="A4">Center for Comparative Medicine and Translational Research, North Carolina State University, Raleigh, NC</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Caroline du Nord</region>
</placeName>
<wicri:cityArea>Center for Comparative Medicine and Translational Research, North Carolina State University, Raleigh</wicri:cityArea>
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<affiliation wicri:level="2"><nlm:aff id="A5">Cancer Genetics Program, UNC Lineberger Comprehensive Cancer Center, Chapel Hill, NC</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Caroline du Nord</region>
</placeName>
<wicri:cityArea>Cancer Genetics Program, UNC Lineberger Comprehensive Cancer Center, Chapel Hill</wicri:cityArea>
</affiliation>
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<author><name sortKey="Bonnet, Francoise" sort="Bonnet, Francoise" uniqKey="Bonnet F" first="Françoise" last="Bonnet">Françoise Bonnet</name>
<affiliation wicri:level="1"><nlm:aff id="A6">INSERM U916, University of Bordeaux, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>INSERM U916, University of Bordeaux</wicri:regionArea>
<wicri:noRegion>University of Bordeaux</wicri:noRegion>
<wicri:noRegion>University of Bordeaux</wicri:noRegion>
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<affiliation wicri:level="3"><nlm:aff id="A7">Cancer Genetics Unit, Institut Bergonié, Bordeaux, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Cancer Genetics Unit, Institut Bergonié, Bordeaux</wicri:regionArea>
<placeName><region type="region">Nouvelle-Aquitaine</region>
<region type="old region">Aquitaine</region>
<settlement type="city">Bordeaux</settlement>
</placeName>
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<author><name sortKey="Sevenet, Nicolas" sort="Sevenet, Nicolas" uniqKey="Sevenet N" first="Nicolas" last="Sevenet">Nicolas Sevenet</name>
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<affiliation wicri:level="3"><nlm:aff id="A7">Cancer Genetics Unit, Institut Bergonié, Bordeaux, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Cancer Genetics Unit, Institut Bergonié, Bordeaux</wicri:regionArea>
<placeName><region type="region">Nouvelle-Aquitaine</region>
<region type="old region">Aquitaine</region>
<settlement type="city">Bordeaux</settlement>
</placeName>
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<author><name sortKey="Longy, Michel" sort="Longy, Michel" uniqKey="Longy M" first="Michel" last="Longy">Michel Longy</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>INSERM U916, University of Bordeaux</wicri:regionArea>
<wicri:noRegion>University of Bordeaux</wicri:noRegion>
<wicri:noRegion>University of Bordeaux</wicri:noRegion>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Cancer Genetics Unit, Institut Bergonié, Bordeaux</wicri:regionArea>
<placeName><region type="region">Nouvelle-Aquitaine</region>
<region type="old region">Aquitaine</region>
<settlement type="city">Bordeaux</settlement>
</placeName>
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<author><name sortKey="Maki, Robert G" sort="Maki, Robert G" uniqKey="Maki R" first="Robert G." last="Maki">Robert G. Maki</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine/Pediatrics, Mount Sinai School of Medicine, New York, NY</wicri:regionArea>
<wicri:noRegion>NY</wicri:noRegion>
</affiliation>
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<author><name sortKey="Coindre, Jean Michel" sort="Coindre, Jean Michel" uniqKey="Coindre J" first="Jean-Michel" last="Coindre">Jean-Michel Coindre</name>
<affiliation wicri:level="3"><nlm:aff id="A9">Department of Pathology, Institut Bergonié, Bordeaux, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Department of Pathology, Institut Bergonié, Bordeaux</wicri:regionArea>
<placeName><region type="region">Nouvelle-Aquitaine</region>
<region type="old region">Aquitaine</region>
<settlement type="city">Bordeaux</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Antonescu, Cristina R" sort="Antonescu, Cristina R" uniqKey="Antonescu C" first="Cristina R." last="Antonescu">Cristina R. Antonescu</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">État de New York</region>
</placeName>
<wicri:cityArea>Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York</wicri:cityArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Cancer</title>
<idno type="ISSN">0008-543X</idno>
<idno type="eISSN">1097-0142</idno>
<imprint><date when="2012">2012</date>
</imprint>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P3">The p53 and the PIK3CA/AKT/mTOR pathways are frequently altered in sarcoma with complex genomics such as leiomyosarcoma (LMS) or undifferentiated pleomorphic sarcoma (UPS). The scale of genetic abnormalities in these pathways remains unknown in angiosarcoma.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P4">We investigated the status of critical genes involved in the p53 and the PIK3CA/AKT/mTOR pathways in a series of 62 AS.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P5">The mutation and deletion rates of <italic>TP53</italic>
 were 4% and 0, respectively. p53 overexpression was detected by immunohistochemistry in 49% of cases and was associated with inferior disease-free survival. Although p14 inactivation or HDM2 overexpression are frequent in LMS and UPS and could substitute for <italic>TP53</italic>
 mutation or deletion, such alterations were rare in angiosarcomas. pS6K and/or p-4eBP1 overexpression was observed in 42% of cases suggesting frequent activation of the PIK3CA/AKT/mTOR pathway in angiosarcomas. Activation was not related to intragenic deletion of <italic>PTEN</italic>
, an aberration that is frequent in LMS and UPS, but absent in angiosarcomas.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P6">Angiosarcomas constitute a distinct subgroup among sarcomas with complex genomics. Although <italic>TP53</italic>
 mutation and <italic>PTEN</italic>
 deletion are frequent in LMS and UPS, these aberrations are rarely involved in the pathogenesis of AS.</p>
</sec>
</div>
</front>
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<name sortKey="Antonescu, Cristina R" sort="Antonescu, Cristina R" uniqKey="Antonescu C" first="Cristina R." last="Antonescu">Cristina R. Antonescu</name>
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<name sortKey="Breen, Matthew" sort="Breen, Matthew" uniqKey="Breen M" first="Matthew" last="Breen">Matthew Breen</name>
<name sortKey="Breen, Matthew" sort="Breen, Matthew" uniqKey="Breen M" first="Matthew" last="Breen">Matthew Breen</name>
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<name sortKey="Maki, Robert G" sort="Maki, Robert G" uniqKey="Maki R" first="Robert G." last="Maki">Robert G. Maki</name>
<name sortKey="Thomas, Rachael" sort="Thomas, Rachael" uniqKey="Thomas R" first="Rachael" last="Thomas">Rachael Thomas</name>
<name sortKey="Thomas, Rachael" sort="Thomas, Rachael" uniqKey="Thomas R" first="Rachael" last="Thomas">Rachael Thomas</name>
</country>
<country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Italiano, Antoine" sort="Italiano, Antoine" uniqKey="Italiano A" first="Antoine" last="Italiano">Antoine Italiano</name>
</region>
<name sortKey="Bonnet, Francoise" sort="Bonnet, Francoise" uniqKey="Bonnet F" first="Françoise" last="Bonnet">Françoise Bonnet</name>
<name sortKey="Bonnet, Francoise" sort="Bonnet, Francoise" uniqKey="Bonnet F" first="Françoise" last="Bonnet">Françoise Bonnet</name>
<name sortKey="Coindre, Jean Michel" sort="Coindre, Jean Michel" uniqKey="Coindre J" first="Jean-Michel" last="Coindre">Jean-Michel Coindre</name>
<name sortKey="Longy, Michel" sort="Longy, Michel" uniqKey="Longy M" first="Michel" last="Longy">Michel Longy</name>
<name sortKey="Longy, Michel" sort="Longy, Michel" uniqKey="Longy M" first="Michel" last="Longy">Michel Longy</name>
<name sortKey="Sevenet, Nicolas" sort="Sevenet, Nicolas" uniqKey="Sevenet N" first="Nicolas" last="Sevenet">Nicolas Sevenet</name>
<name sortKey="Sevenet, Nicolas" sort="Sevenet, Nicolas" uniqKey="Sevenet N" first="Nicolas" last="Sevenet">Nicolas Sevenet</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/France/Analysis

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000234 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/France/Analysis/biblio.hfd -nk 000234 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    LymphedemaV1
   |flux=    France
   |étape=   Analysis
   |type=    RBID
   |clé=     PMC:3434269
   |texte=   Alterations of p53 and PIK3CA/AKT/mTOR Pathways in Angiosarcomas: A Pattern Distinct from Other Sarcomas with Complex Genomics
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/France/Analysis/RBID.i   -Sk "pubmed:22648906" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/France/Analysis/biblio.hfd   \
       | NlmPubMed2Wicri -a LymphedemaV1

This area was generated with Dilib version V0.6.31.
Data generation: Sat Nov 4 17:40:35 2017. Site generation: Tue Feb 13 16:42:16 2024

Serveur d'exploration sur le lymphœdème

Alterations of p53 and PIK3CA/AKT/mTOR Pathways in Angiosarcomas: A Pattern Distinct from Other Sarcomas with Complex Genomics

Alterations of p53 and PIK3CA/AKT/mTOR Pathways in Angiosarcomas: A Pattern Distinct from Other Sarcomas with Complex Genomics

Source :

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki

	Serveur d'exploration sur le lymphœdème
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.