LymphedemaV1, France, Analysis, bibRecord, 000238

The miR‐17‐92 cluster and its target THBS1 are differentially expressed in angiosarcomas dependent on MYC amplification

Identifieur interne : 000238 ( France/Analysis ); précédent : 000237; suivant : 000239

The miR‐17‐92 cluster and its target THBS1 are differentially expressed in angiosarcomas dependent on MYC amplification

Auteurs : Antoine Italiano [États-Unis, France] ; Rachael Thomas [États-Unis] ; Matthew Breen [États-Unis] ; Lei Zhang [États-Unis] ; Aimee M. Crago [États-Unis] ; Samuel Singer [États-Unis] ; Raya Khanin [États-Unis] ; Robert G. Maki [États-Unis] ; Aleksandra Mihailovic [États-Unis] ; Markus Hafner [États-Unis] ; Tom Tuschl [États-Unis] ; Cristina R. Antonescu [États-Unis]

Source :

Genes, Chromosomes and Cancer [ 1045-2257 ] ; 2012-06.

RBID : ISTEX:F4EBB3667DCC0A4F77C6596D4BD56FA5213B3203

Descripteurs français

English descriptors

KwdEn :
- Adult, Aged, Aged, 80 and over, Comparative Genomic Hybridization, DNA-Binding Proteins (biosynthesis), DNA-Binding Proteins (genetics), Female, Gene Amplification, Gene Expression Regulation, Neoplastic, Genes, myc, Hemangiosarcoma (chemistry), Hemangiosarcoma (genetics), Hemangiosarcoma (metabolism), Humans, In Situ Hybridization, Fluorescence, Male, MicroRNAs (biosynthesis), MicroRNAs (genetics), Middle Aged, Proto-Oncogene Proteins c-myc (biosynthesis), Proto-Oncogene Proteins c-myc (genetics), Sequence Analysis, RNA, Thrombospondin 1 (biosynthesis), Thrombospondin 1 (genetics), Transcription Factors (biosynthesis), Transcription Factors (genetics), Vascular Neoplasms (chemistry), Vascular Neoplasms (genetics), Vascular Neoplasms (metabolism).
MESH :
- chemical , biosynthesis : DNA-Binding Proteins, MicroRNAs, Proto-Oncogene Proteins c-myc, Thrombospondin 1, Transcription Factors.
- chemical , genetics : DNA-Binding Proteins, MicroRNAs, Proto-Oncogene Proteins c-myc, Thrombospondin 1, Transcription Factors.
- chemistry : Hemangiosarcoma, Vascular Neoplasms.
- genetics : Hemangiosarcoma, Vascular Neoplasms.
- metabolism : Hemangiosarcoma, Vascular Neoplasms.
- Adult, Aged, Aged, 80 and over, Comparative Genomic Hybridization, Female, Gene Amplification, Gene Expression Regulation, Neoplastic, Genes, myc, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Sequence Analysis, RNA.

Abstract

Angiosarcomas (ASs) represent a heterogeneous group of malignant vascular tumors that may occur spontaneously as primary tumors or secondarily after radiation therapy or in the context of chronic lymphedema. Most secondary ASs have been associated with MYC oncogene amplification, whereas the role of MYC abnormalities in primary AS is not well defined. Twenty‐two primary and secondary ASs were analyzed by array‐comparative genomic hybridization (aCGH) and by deep sequencing of small RNA libraries. By aCGH and subsequently confirmed by fluorescence in situ hybridization, MYC amplification was identified in three out of six primary tumors and in 8 out of 12 secondary AS. We have also found MAML1 as a new potential oncogene in MYC‐amplified AS. Significant upregulation of the miR‐17‐92 cluster was observed in MYC‐amplified AS compared to AS lacking MYC amplification and the control group (other vascular tumors, nonvascular sarcomas). Moreover, MYC‐amplified ASs were associated with a significantly lower expression of thrombospondin‐1 (THBS1) than AS without MYC amplification or controls. Altogether, our study implicates MYC amplification not only in the pathogenesis of secondary AS but also in a subset of primary AS. Thus, MYC amplification may play a crucial role in the angiogenic phenotype of AS through upregulation of the miR‐17‐92 cluster, which subsequently downregulates THBS1, a potent endogenous inhibitor of angiogenesis. © 2012 Wiley Periodicals, Inc.

Url:

DOI: 10.1002/gcc.21943

Affiliations:

Links to Exploration step

ISTEX:F4EBB3667DCC0A4F77C6596D4BD56FA5213B3203

Le document en format XML

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<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Comparative Genomic Hybridization</term>
<term>DNA-Binding Proteins (biosynthesis)</term>
<term>DNA-Binding Proteins (genetics)</term>
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<term>Gene Amplification</term>
<term>Gene Expression Regulation, Neoplastic</term>
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<term>Vascular Neoplasms (genetics)</term>
<term>Vascular Neoplasms (metabolism)</term>
</keywords>
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<term>Adulte d'âge moyen</term>
<term>Amplification de gène</term>
<term>Analyse de séquence d'ARN</term>
<term>Facteurs de transcription (biosynthèse)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Femelle</term>
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<term>Humains</term>
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<term>Hémangiosarcome ()</term>
<term>Hémangiosarcome (génétique)</term>
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<term>Mâle</term>
<term>Protéines de liaison à l'ADN (biosynthèse)</term>
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<term>Protéines proto-oncogènes c-myc (génétique)</term>
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<term>Sujet âgé de 80 ans ou plus</term>
<term>Technique FISH</term>
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<term>Thrombospondine-1 (génétique)</term>
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<term>Tumeurs vasculaires (métabolisme)</term>
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<term>MicroRNAs</term>
<term>Proto-Oncogene Proteins c-myc</term>
<term>Thrombospondin 1</term>
<term>Transcription Factors</term>
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<term>Protéines de liaison à l'ADN</term>
<term>Protéines proto-oncogènes c-myc</term>
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<term>microARN</term>
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<term>Vascular Neoplasms</term>
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<term>Hémangiosarcome</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines proto-oncogènes c-myc</term>
<term>Thrombospondine-1</term>
<term>Tumeurs vasculaires</term>
<term>microARN</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hemangiosarcoma</term>
<term>Vascular Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Hémangiosarcome</term>
<term>Tumeurs vasculaires</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Comparative Genomic Hybridization</term>
<term>Female</term>
<term>Gene Amplification</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Genes, myc</term>
<term>Humans</term>
<term>In Situ Hybridization, Fluorescence</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Sequence Analysis, RNA</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Amplification de gène</term>
<term>Analyse de séquence d'ARN</term>
<term>Femelle</term>
<term>Gènes myc</term>
<term>Humains</term>
<term>Hybridation génomique comparative</term>
<term>Hémangiosarcome</term>
<term>Mâle</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Sujet âgé</term>
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<front><div type="abstract" xml:lang="en">Angiosarcomas (ASs) represent a heterogeneous group of malignant vascular tumors that may occur spontaneously as primary tumors or secondarily after radiation therapy or in the context of chronic lymphedema. Most secondary ASs have been associated with MYC oncogene amplification, whereas the role of MYC abnormalities in primary AS is not well defined. Twenty‐two primary and secondary ASs were analyzed by array‐comparative genomic hybridization (aCGH) and by deep sequencing of small RNA libraries. By aCGH and subsequently confirmed by fluorescence in situ hybridization, MYC amplification was identified in three out of six primary tumors and in 8 out of 12 secondary AS. We have also found MAML1 as a new potential oncogene in MYC‐amplified AS. Significant upregulation of the miR‐17‐92 cluster was observed in MYC‐amplified AS compared to AS lacking MYC amplification and the control group (other vascular tumors, nonvascular sarcomas). Moreover, MYC‐amplified ASs were associated with a significantly lower expression of thrombospondin‐1 (THBS1) than AS without MYC amplification or controls. Altogether, our study implicates MYC amplification not only in the pathogenesis of secondary AS but also in a subset of primary AS. Thus, MYC amplification may play a crucial role in the angiogenic phenotype of AS through upregulation of the miR‐17‐92 cluster, which subsequently downregulates THBS1, a potent endogenous inhibitor of angiogenesis. © 2012 Wiley Periodicals, Inc.</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
<li>États-Unis</li>
</country>
<region><li>Aquitaine</li>
<li>Caroline du Nord</li>
<li>Nouvelle-Aquitaine</li>
<li>État de New York</li>
</region>
<settlement><li>Bordeaux</li>
</settlement>
</list>
<tree><country name="États-Unis"><region name="État de New York"><name sortKey="Italiano, Antoine" sort="Italiano, Antoine" uniqKey="Italiano A" first="Antoine" last="Italiano">Antoine Italiano</name>
</region>
<name sortKey="Antonescu, Cristina R" sort="Antonescu, Cristina R" uniqKey="Antonescu C" first="Cristina R." last="Antonescu">Cristina R. Antonescu</name>
<name sortKey="Antonescu, Cristina R" sort="Antonescu, Cristina R" uniqKey="Antonescu C" first="Cristina R." last="Antonescu">Cristina R. Antonescu</name>
<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>
<name sortKey="Breen, Matthew" sort="Breen, Matthew" uniqKey="Breen M" first="Matthew" last="Breen">Matthew Breen</name>
<name sortKey="Crago, Aimee M" sort="Crago, Aimee M" uniqKey="Crago A" first="Aimee M." last="Crago">Aimee M. Crago</name>
<name sortKey="Hafner, Markus" sort="Hafner, Markus" uniqKey="Hafner M" first="Markus" last="Hafner">Markus Hafner</name>
<name sortKey="Italiano, Antoine" sort="Italiano, Antoine" uniqKey="Italiano A" first="Antoine" last="Italiano">Antoine Italiano</name>
<name sortKey="Khanin, Raya" sort="Khanin, Raya" uniqKey="Khanin R" first="Raya" last="Khanin">Raya Khanin</name>
<name sortKey="Maki, Robert G" sort="Maki, Robert G" uniqKey="Maki R" first="Robert G." last="Maki">Robert G. Maki</name>
<name sortKey="Mihailovic, Aleksandra" sort="Mihailovic, Aleksandra" uniqKey="Mihailovic A" first="Aleksandra" last="Mihailovic">Aleksandra Mihailovic</name>
<name sortKey="Singer, Samuel" sort="Singer, Samuel" uniqKey="Singer S" first="Samuel" last="Singer">Samuel Singer</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>
<name sortKey="Tuschl, Tom" sort="Tuschl, Tom" uniqKey="Tuschl T" first="Tom" last="Tuschl">Tom Tuschl</name>
<name sortKey="Zhang, Lei" sort="Zhang, Lei" uniqKey="Zhang L" first="Lei" last="Zhang">Lei Zhang</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>
</country>
</tree>
</affiliations>
</record>

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   |texte=   The miR‐17‐92 cluster and its target THBS1 are differentially expressed in angiosarcomas dependent on MYC amplification
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The miR‐17‐92 cluster and its target THBS1 are differentially expressed in angiosarcomas dependent on MYC amplification

The miR‐17‐92 cluster and its target THBS1 are differentially expressed in angiosarcomas dependent on MYC amplification

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