Human hepatocellular carcinomas with a periportal phenotype have the lowest potential for early recurrence after curative resection.
Identifieur interne : 000A60 ( Main/Exploration ); précédent : 000A59; suivant : 000A61Human hepatocellular carcinomas with a periportal phenotype have the lowest potential for early recurrence after curative resection.
Auteurs : Romain Désert [France] ; Florian Rohart [Australie] ; Frédéric Canal [France] ; Marie Sicard [France] ; Mireille Desille [France] ; Stéphanie Renaud [France] ; Bruno Turlin [France] ; Pascale Bellaud [France] ; Christine Perret [France] ; Bruno Clément [France] ; Kim-Anh Lê Cao [Australie] ; Orlando Musso [France]Source :
- Hepatology (Baltimore, Md.) [ 1527-3350 ] ; 2017.
Descripteurs français
- KwdFr :
- Carcinome hépatocellulaire (), Carcinome hépatocellulaire (anatomopathologie), Carcinome hépatocellulaire (génétique), Carcinome hépatocellulaire (mortalité), Facteur nucléaire hépatocytaire HNF-4 (métabolisme), Foie (anatomopathologie), France (épidémiologie), Humains, Mutation, Phénotype, Récidive tumorale locale (anatomopathologie), Récidive tumorale locale (génétique), Transcriptome, Tumeurs du foie (), Tumeurs du foie (anatomopathologie), Tumeurs du foie (génétique), Tumeurs du foie (mortalité), bêta-Caténine (génétique).
- MESH :
- anatomopathologie : Carcinome hépatocellulaire, Foie, Récidive tumorale locale, Tumeurs du foie.
- génétique : Carcinome hépatocellulaire, Récidive tumorale locale, Tumeurs du foie, bêta-Caténine.
- mortalité : Carcinome hépatocellulaire, Tumeurs du foie.
- métabolisme : Facteur nucléaire hépatocytaire HNF-4.
- épidémiologie : France.
- Carcinome hépatocellulaire, Humains, Mutation, Phénotype, Transcriptome, Tumeurs du foie.
English descriptors
- KwdEn :
- Carcinoma, Hepatocellular (genetics), Carcinoma, Hepatocellular (mortality), Carcinoma, Hepatocellular (pathology), Carcinoma, Hepatocellular (surgery), France (epidemiology), Hepatocyte Nuclear Factor 4 (metabolism), Humans, Liver (pathology), Liver Neoplasms (genetics), Liver Neoplasms (mortality), Liver Neoplasms (pathology), Liver Neoplasms (surgery), Mutation, Neoplasm Recurrence, Local (genetics), Neoplasm Recurrence, Local (pathology), Phenotype, Transcriptome, beta Catenin (genetics).
- MESH :
- chemical , genetics : beta Catenin.
- chemical , metabolism : Hepatocyte Nuclear Factor 4.
- epidemiology : France.
- genetics : Carcinoma, Hepatocellular, Liver Neoplasms, Neoplasm Recurrence, Local.
- mortality : Carcinoma, Hepatocellular, Liver Neoplasms.
- pathology : Carcinoma, Hepatocellular, Liver, Liver Neoplasms, Neoplasm Recurrence, Local.
- surgery : Carcinoma, Hepatocellular, Liver Neoplasms.
- Humans, Mutation, Phenotype, Transcriptome.
Abstract
Hepatocellular carcinomas (HCCs) exhibit a diversity of molecular phenotypes, raising major challenges in clinical management. HCCs detected by surveillance programs at an early stage are candidates for potentially curative therapies (local ablation, resection, or transplantation). In the long term, transplantation provides the lowest recurrence rates. Treatment allocation is based on tumor number, size, vascular invasion, performance status, functional liver reserve, and the prediction of early (<2 years) recurrence, which reflects the intrinsic aggressiveness of the tumor. Well-differentiated, potentially low-aggressiveness tumors form the heterogeneous molecular class of nonproliferative HCCs, characterized by an approximate 50% β-catenin mutation rate. To define the clinical, pathological, and molecular features and the outcome of nonproliferative HCCs, we constructed a 1,133-HCC transcriptomic metadata set and validated findings in a publically available 210-HCC RNA sequencing set. We show that nonproliferative HCCs preserve the zonation program that distributes metabolic functions along the portocentral axis in normal liver. More precisely, we identified two well-differentiated, nonproliferation subclasses, namely periportal-type (wild-type β-catenin) and perivenous-type (mutant β-catenin), which expressed negatively correlated gene networks. The new periportal-type subclass represented 29% of all HCCs; expressed a hepatocyte nuclear factor 4A-driven gene network, which was down-regulated in mouse hepatocyte nuclear factor 4A knockout mice; were early-stage tumors by Barcelona Clinic Liver Cancer, Cancer of the Liver Italian Program, and tumor-node-metastasis staging systems; had no macrovascular invasion; and showed the lowest metastasis-specific gene expression levels and TP53 mutation rates. Also, we identified an eight-gene periportal-type HCC signature, which was independently associated with the highest 2-year recurrence-free survival by multivariate analyses in two independent cohorts of 247 and 210 patients.
DOI: 10.1002/hep.29254
PubMed: 28498607
Affiliations:
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Le document en format XML
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<author><name sortKey="Renaud, Stephanie" sort="Renaud, Stephanie" uniqKey="Renaud S" first="Stéphanie" last="Renaud">Stéphanie Renaud</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Carcinoma, Hepatocellular (genetics)</term>
<term>Carcinoma, Hepatocellular (mortality)</term>
<term>Carcinoma, Hepatocellular (pathology)</term>
<term>Carcinoma, Hepatocellular (surgery)</term>
<term>France (epidemiology)</term>
<term>Hepatocyte Nuclear Factor 4 (metabolism)</term>
<term>Humans</term>
<term>Liver (pathology)</term>
<term>Liver Neoplasms (genetics)</term>
<term>Liver Neoplasms (mortality)</term>
<term>Liver Neoplasms (pathology)</term>
<term>Liver Neoplasms (surgery)</term>
<term>Mutation</term>
<term>Neoplasm Recurrence, Local (genetics)</term>
<term>Neoplasm Recurrence, Local (pathology)</term>
<term>Phenotype</term>
<term>Transcriptome</term>
<term>beta Catenin (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Carcinome hépatocellulaire ()</term>
<term>Carcinome hépatocellulaire (anatomopathologie)</term>
<term>Carcinome hépatocellulaire (génétique)</term>
<term>Carcinome hépatocellulaire (mortalité)</term>
<term>Facteur nucléaire hépatocytaire HNF-4 (métabolisme)</term>
<term>Foie (anatomopathologie)</term>
<term>France (épidémiologie)</term>
<term>Humains</term>
<term>Mutation</term>
<term>Phénotype</term>
<term>Récidive tumorale locale (anatomopathologie)</term>
<term>Récidive tumorale locale (génétique)</term>
<term>Transcriptome</term>
<term>Tumeurs du foie ()</term>
<term>Tumeurs du foie (anatomopathologie)</term>
<term>Tumeurs du foie (génétique)</term>
<term>Tumeurs du foie (mortalité)</term>
<term>bêta-Caténine (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>beta Catenin</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hepatocyte Nuclear Factor 4</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Foie</term>
<term>Récidive tumorale locale</term>
<term>Tumeurs du foie</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>France</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver Neoplasms</term>
<term>Neoplasm Recurrence, Local</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Récidive tumorale locale</term>
<term>Tumeurs du foie</term>
<term>bêta-Caténine</term>
</keywords>
<keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="mortalité" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Tumeurs du foie</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur nucléaire hépatocytaire HNF-4</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver</term>
<term>Liver Neoplasms</term>
<term>Neoplasm Recurrence, Local</term>
</keywords>
<keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>France</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Humans</term>
<term>Mutation</term>
<term>Phenotype</term>
<term>Transcriptome</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Humains</term>
<term>Mutation</term>
<term>Phénotype</term>
<term>Transcriptome</term>
<term>Tumeurs du foie</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Hepatocellular carcinomas (HCCs) exhibit a diversity of molecular phenotypes, raising major challenges in clinical management. HCCs detected by surveillance programs at an early stage are candidates for potentially curative therapies (local ablation, resection, or transplantation). In the long term, transplantation provides the lowest recurrence rates. Treatment allocation is based on tumor number, size, vascular invasion, performance status, functional liver reserve, and the prediction of early (<2 years) recurrence, which reflects the intrinsic aggressiveness of the tumor. Well-differentiated, potentially low-aggressiveness tumors form the heterogeneous molecular class of nonproliferative HCCs, characterized by an approximate 50% β-catenin mutation rate. To define the clinical, pathological, and molecular features and the outcome of nonproliferative HCCs, we constructed a 1,133-HCC transcriptomic metadata set and validated findings in a publically available 210-HCC RNA sequencing set. We show that nonproliferative HCCs preserve the zonation program that distributes metabolic functions along the portocentral axis in normal liver. More precisely, we identified two well-differentiated, nonproliferation subclasses, namely periportal-type (wild-type β-catenin) and perivenous-type (mutant β-catenin), which expressed negatively correlated gene networks. The new periportal-type subclass represented 29% of all HCCs; expressed a hepatocyte nuclear factor 4A-driven gene network, which was down-regulated in mouse hepatocyte nuclear factor 4A knockout mice; were early-stage tumors by Barcelona Clinic Liver Cancer, Cancer of the Liver Italian Program, and tumor-node-metastasis staging systems; had no macrovascular invasion; and showed the lowest metastasis-specific gene expression levels and TP53 mutation rates. Also, we identified an eight-gene periportal-type HCC signature, which was independently associated with the highest 2-year recurrence-free survival by multivariate analyses in two independent cohorts of 247 and 210 patients.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
<region><li>Région Bretagne</li>
<li>Île-de-France</li>
</region>
<settlement><li>Paris</li>
<li>Rennes</li>
</settlement>
</list>
<tree><country name="France"><region name="Région Bretagne"><name sortKey="Desert, Romain" sort="Desert, Romain" uniqKey="Desert R" first="Romain" last="Désert">Romain Désert</name>
</region>
<name sortKey="Bellaud, Pascale" sort="Bellaud, Pascale" uniqKey="Bellaud P" first="Pascale" last="Bellaud">Pascale Bellaud</name>
<name sortKey="Canal, Frederic" sort="Canal, Frederic" uniqKey="Canal F" first="Frédéric" last="Canal">Frédéric Canal</name>
<name sortKey="Clement, Bruno" sort="Clement, Bruno" uniqKey="Clement B" first="Bruno" last="Clément">Bruno Clément</name>
<name sortKey="Desille, Mireille" sort="Desille, Mireille" uniqKey="Desille M" first="Mireille" last="Desille">Mireille Desille</name>
<name sortKey="Musso, Orlando" sort="Musso, Orlando" uniqKey="Musso O" first="Orlando" last="Musso">Orlando Musso</name>
<name sortKey="Perret, Christine" sort="Perret, Christine" uniqKey="Perret C" first="Christine" last="Perret">Christine Perret</name>
<name sortKey="Renaud, Stephanie" sort="Renaud, Stephanie" uniqKey="Renaud S" first="Stéphanie" last="Renaud">Stéphanie Renaud</name>
<name sortKey="Sicard, Marie" sort="Sicard, Marie" uniqKey="Sicard M" first="Marie" last="Sicard">Marie Sicard</name>
<name sortKey="Turlin, Bruno" sort="Turlin, Bruno" uniqKey="Turlin B" first="Bruno" last="Turlin">Bruno Turlin</name>
</country>
<country name="Australie"><noRegion><name sortKey="Rohart, Florian" sort="Rohart, Florian" uniqKey="Rohart F" first="Florian" last="Rohart">Florian Rohart</name>
</noRegion>
<name sortKey="Le Cao, Kim Anh" sort="Le Cao, Kim Anh" uniqKey="Le Cao K" first="Kim-Anh" last="Lê Cao">Kim-Anh Lê Cao</name>
</country>
</tree>
</affiliations>
</record>
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