Integrated analysis of somatic mutations and focal copy-number changes identifies key genes and pathways in hepatocellular carcinoma
Jessica Zucman-Rossi and colleagues report exome sequencing of 24 hepatocellular carcinomas and non-tumor liver tissues and copy-number analysis of 125 tumors. They identify new recurrent mutations in ARID1A , RPS6KA3 , NFE2L2 and IRF2 in HCC. Hepatocellular carcinoma (HCC) is the most common primar...
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| Veröffentlicht in: | Nature genetics Jg. 44; H. 6; S. 694 - 698 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
New York
Nature Publishing Group US
01.06.2012
Nature Publishing Group Nature Pub. Co |
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| ISSN: | 1061-4036, 1546-1718, 1546-1718 |
| Online-Zugang: | Volltext |
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| Abstract | Jessica Zucman-Rossi and colleagues report exome sequencing of 24 hepatocellular carcinomas and non-tumor liver tissues and copy-number analysis of 125 tumors. They identify new recurrent mutations in
ARID1A
,
RPS6KA3
,
NFE2L2
and
IRF2
in HCC.
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes (
ARID1A
,
RPS6KA3
,
NFE2L2
and
IRF2
) not previously described in HCC. Functional analyses showed tumor suppressor properties for
IRF2
, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired
TP53
function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes (
RPS6KA3
-
AXIN1
and
NFE2L2
-
CTNNB1
) suggested that Wnt/β-catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors. |
|---|---|
| AbstractList | Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Functional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes (RPS6KA3-AXIN1 and NFE2L2-CTNNB1) suggested that Wnt/β-catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors.Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Functional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes (RPS6KA3-AXIN1 and NFE2L2-CTNNB1) suggested that Wnt/β-catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors. Jessica Zucman-Rossi and colleagues report exome sequencing of 24 hepatocellular carcinomas and non-tumor liver tissues and copy-number analysis of 125 tumors. They identify new recurrent mutations in ARID1A , RPS6KA3 , NFE2L2 and IRF2 in HCC. Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes ( ARID1A , RPS6KA3 , NFE2L2 and IRF2 ) not previously described in HCC. Functional analyses showed tumor suppressor properties for IRF2 , whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes ( RPS6KA3 - AXIN1 and NFE2L2 - CTNNB1 ) suggested that Wnt/β-catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors. Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Functional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes (RPS6KA3-AXIN1 and NFE2L2-CTNNB1) suggested that Wnt/ beta -catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors. Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Functional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes (RPS6KA3-AXIN1 and NFE2L2-CTNNB1) suggested that Wnt/β-catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors. Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. High-resolution copy number analysis of 125 tumors of which 24 were subjected to whole-exome sequencing identified 135 homozygous deletions and 994 somatic gene mutations with predicted functional consequences. We identified new recurrent alterations in 6 genes (ARID1A, RPS6KA3, NFE2L2, IRF2, CDH8 and PROKR2) not previously described in HCC. Functional analyses demonstrated tumor suppressor properties for IRF2 whose inactivation, exclusively found in hepatitis B virus related tumors, leads to impaired TP53 function. Alternatively, inactivation of proteins involved in chromatin remodeling was frequent and predominant in alcohol related tumors. Moreover, activation of the oxidative stress metabolism and inactivation of RPS6KA3 were new pathways associated with WNT/β-catenin activation, thereby suggesting a cooperative effect in tumorigenesis. This study shows the dramatic somatic genetic diversity in HCC, it reveals interactions between oncogene and tumor suppressor gene mutations markedly related to specific risk factors. Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional consequences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Functional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in alcohol-related tumors. Moreover, association of mutations in specific genes (RPS6KA3-AXIN1 and NFE2L2-CTNNB1) suggested that Wnt/β-catenin signaling might cooperate in liver carcinogenesis with both oxidative stress metabolism and Ras/mitogen-activated protein kinase (MAPK) pathways. This study provides insight into the somatic mutational landscape in HCC and identifies interactions between mutations in oncogene and tumor suppressor gene mutations related to specific risk factors. [PUBLICATION ABSTRACT] |
| Audience | Academic |
| Author | Imbeaud, Sandrine Bioulac-Sage, Paulette Letexier, Mélanie Degos, Françoise Clément, Bruno Calderaro, Julien Laurent, Alexis Ladeiro, Yannick Balabaud, Charles Calvo, Fabien Maad, Ichrafe Ben Pelletier, Laura Chevet, Eric Zucman-Rossi, Jessica Letouzé, Eric Amaddeo, Giuliana Couchy, Gabrielle Guichard, Cécile |
| AuthorAffiliation | 9 Service de Chirurgie Digestive Hôpital Henri Mondor - Assistance publique - Hôpitaux de Paris (AP-HP) 51, avenue du Maréchal de Lattre de Tassigny 94010 Créteil cedex,FR 10 CIT, Cartes d'Identité des Tumeurs Ligue Nationale Contre le Cancer (LNCC) 14 Rue Corvisart 75013 Paris, FR 3 Service de Pathologie [Créteil] Hôpital Henri Mondor - Assistance publique - Hôpitaux de Paris (AP-HP) 51, avenue du Maréchal de Lattre de Tassigny 94010 Créteil cedex, FR 12 Service d'Hépato-Gastro Entérologie et Oncologie Digestive Hôpital Européen Georges Pompidou - Assistance publique - Hôpitaux de Paris (AP-HP) 20, rue Leblanc 75908 Paris cedex 15, FR 7 Service d'Hépatologie Hôpital Beaujon - Assistance publique - Hôpitaux de Paris (AP-HP) Université Paris VII - Paris Diderot 100 Boulevard du Général Leclerc 92110 Clichy, FR 4 Service de Pathologie [Bordeaux] CHU Bordeaux Groupe hospitalier Pellegrin Université Victor Segalen - Bordeaux II 146 rue Léo-Saignat 33076 Bordeaux Cedex,FR 5 Physiopathologie du Ca |
| AuthorAffiliation_xml | – name: 3 Service de Pathologie [Créteil] Hôpital Henri Mondor - Assistance publique - Hôpitaux de Paris (AP-HP) 51, avenue du Maréchal de Lattre de Tassigny 94010 Créteil cedex, FR – name: 7 Service d'Hépatologie Hôpital Beaujon - Assistance publique - Hôpitaux de Paris (AP-HP) Université Paris VII - Paris Diderot 100 Boulevard du Général Leclerc 92110 Clichy, FR – name: 1 Genomique Fonctionnelle des Tumeurs Solides INSERM : U674 Université Paris VII - Paris Diderot - IFR 105 Hôpital Saint-Louis - Assistance publique - Hôpitaux de Paris (AP-HP) 27, Rue Juliette Dodu 75010 PARIS, FR – name: 9 Service de Chirurgie Digestive Hôpital Henri Mondor - Assistance publique - Hôpitaux de Paris (AP-HP) 51, avenue du Maréchal de Lattre de Tassigny 94010 Créteil cedex,FR – name: 12 Service d'Hépato-Gastro Entérologie et Oncologie Digestive Hôpital Européen Georges Pompidou - Assistance publique - Hôpitaux de Paris (AP-HP) 20, rue Leblanc 75908 Paris cedex 15, FR – name: 2 Labex Immuno-oncology Université Paris V - Paris Descartes PRES Sorbonne Paris Cité Faculté de Médecine Centre de Recherche des Cordeliers (CRC) 15 rue de l'école de Médecine 75006 PARIS, FR – name: 8 Foie, Métabolismes et Cancer INSERM : U991 Université de Rennes 1 Hôpital Pontchaillou - Biosit Rue Henri Le Guilloux 35033 Rennes Cedex, FR – name: 5 Physiopathologie du Cancer du Foie INSERM : U1053 Université Victor Segalen - Bordeaux II 146 rue Léo Saignat 33076 Bordeaux Cedex, FR – name: 4 Service de Pathologie [Bordeaux] CHU Bordeaux Groupe hospitalier Pellegrin Université Victor Segalen - Bordeaux II 146 rue Léo-Saignat 33076 Bordeaux Cedex,FR – name: 6 IntegraGen SA Genopole CAMPUS 1 bat G8 FR - 91030 Evry, FR – name: 10 CIT, Cartes d'Identité des Tumeurs Ligue Nationale Contre le Cancer (LNCC) 14 Rue Corvisart 75013 Paris, FR – name: 11 INCa, Institut National du Cancer Agence Nationale Sanitaire et Scientifique en Cancérologie 52, avenue André Morizet 92513 Boulogne Billancourt Cedex, FR |
| Author_xml | – sequence: 1 givenname: Cécile surname: Guichard fullname: Guichard, Cécile organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 2 givenname: Giuliana surname: Amaddeo fullname: Amaddeo, Giuliana organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 3 givenname: Sandrine surname: Imbeaud fullname: Imbeaud, Sandrine organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 4 givenname: Yannick surname: Ladeiro fullname: Ladeiro, Yannick organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 5 givenname: Laura surname: Pelletier fullname: Pelletier, Laura organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 6 givenname: Ichrafe Ben surname: Maad fullname: Maad, Ichrafe Ben organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 7 givenname: Julien surname: Calderaro fullname: Calderaro, Julien organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine, Department of Pathology, Assistance Publique–Hôpitaux de Paris (AP-HP), Centre Hospitalier Universitaire (CHU) Henri Mondor – sequence: 8 givenname: Paulette surname: Bioulac-Sage fullname: Bioulac-Sage, Paulette organization: INSERM, UMR-1053, Université Victor Segalen Bordeaux 2, Department of Pathology, CHU de Bordeaux, Pellegrin Hospital – sequence: 9 givenname: Mélanie surname: Letexier fullname: Letexier, Mélanie organization: IntegraGen – sequence: 10 givenname: Françoise surname: Degos fullname: Degos, Françoise organization: Department of Hepatology, AP-HP, Beaujon Hospital, Université Paris Diderot – sequence: 11 givenname: Bruno surname: Clément fullname: Clément, Bruno organization: INSERM, UMR-991, Université de Rennes 1 – sequence: 12 givenname: Charles surname: Balabaud fullname: Balabaud, Charles organization: INSERM, UMR-1053, Université Victor Segalen Bordeaux 2, Department of Pathology, CHU de Bordeaux, Pellegrin Hospital – sequence: 13 givenname: Eric surname: Chevet fullname: Chevet, Eric organization: INSERM, UMR-1053, Université Victor Segalen Bordeaux 2 – sequence: 14 givenname: Alexis surname: Laurent fullname: Laurent, Alexis organization: AP-HP, CHU Henri Mondor, Digestive, Hepatobiliary and Liver Transplantation, INSERM, U955 – sequence: 15 givenname: Gabrielle surname: Couchy fullname: Couchy, Gabrielle organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine – sequence: 16 givenname: Eric surname: Letouzé fullname: Letouzé, Eric organization: Programme Cartes d'Identité des Tumeurs, Ligue Nationale Contre le Cancer – sequence: 17 givenname: Fabien surname: Calvo fullname: Calvo, Fabien organization: Institut National du Cancer (INCa) – sequence: 18 givenname: Jessica surname: Zucman-Rossi fullname: Zucman-Rossi, Jessica email: zucman@cephb.fr organization: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR)-674, Génomique Fonctionnelle des Tumeurs Solides, Institut Universitaire d'Hematologie (IUH), Université Paris Descartes, Labex Immuno-oncology, Sorbonne Paris Cité, Faculté de Médecine, AP-HP, Hopital Europeen Georges Pompidou |
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| Snippet | Jessica Zucman-Rossi and colleagues report exome sequencing of 24 hepatocellular carcinomas and non-tumor liver tissues and copy-number analysis of 125 tumors.... Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. Here, we performed high-resolution copy-number analysis on 125 HCC tumors and... Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. High-resolution copy number analysis of 125 tumors of which 24 were subjected to... |
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| SubjectTerms | 631/208/2489/144 631/208/69 Agriculture Alcohol use Animal Genetics and Genomics Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Cancer Research Carcinogenesis Carcinoma, Hepatocellular - genetics Chromosomes Copy number variations DNA Copy Number Variations Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gene expression Gene Function Gene mutations Genetic aspects Genetics of eukaryotes. Biological and molecular evolution Genomes Health aspects Hepatitis B virus Hepatoma Human Genetics Humans Inactivation Interferon Regulatory Factor-2 - genetics letter Liver cancer Liver Neoplasms - genetics Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Mutation Oxidative stress Risk factors Signal Transduction - genetics Tumors |
| Title | Integrated analysis of somatic mutations and focal copy-number changes identifies key genes and pathways in hepatocellular carcinoma |
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