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1. Regional perturbation of gene transcription is associated with intrachromosomal rearrangements and gene fusion transcripts in high grade ovarian cancer.

Author

Krzyzanowski, Paul, Sircoulomb, Fabrice, Yousif, Fouad, Normand, Josee, La Rose, Jose, E Francis, Kyle, Suarez, Fernando, Beck, Tim, McPherson, John, Stein, Lincoln, and Rottapel, Robert

Abstract

Genomic rearrangements are a hallmark of cancer biology and progression, allowing cells to rapidly transform through alterations in regulatory structures, changes in expression patterns, reprogramming of signaling pathways, and creation of novel transcripts via gene fusion events. Though functional gene fusions encoding oncogenic proteins are the most dramatic outcomes of genomic rearrangements, we investigated the relationship between rearrangements evidenced by fusion transcripts and local expression changes in cancer using transcriptome data alone. 9,953 gene fusion predictions from 418 primary serious ovarian cancer tumors were analyzed, identifying depletions of gene fusion breakpoints within coding regions of fused genes as well as an N-terminal enrichment of breakpoints within fused genes. We identified 48 genes with significant fusion-associated upregulation and furthermore demonstrate that significant regional overexpression of intact genes in patient transcriptomes occurs within 1 megabase of 78 novel gene fusions that function as central markers of these regions. We reveal that cancer transcriptomes select for gene fusions that preserve protein and protein domain coding potential. The association of gene fusion transcripts with neighboring gene overexpression supports rearrangements as mechanism through which cancer cells remodel their transcriptomes and identifies a new way to utilize gene fusions as indicators of regional expression changes in diseased cells with only transcriptomic data.

Published
2019

2. Genotype B of deformed wing virus and related recombinant viruses become dominant in European honey bee colonies.

Author

Sircoulomb, Fabrice, Dubois, Eric, Schurr, Frank, Lucas, Pierrick, Meixner, Marina, Bertolotti, Alicia, Blanchard, Yannick, and Thiéry, Richard

Abstract

The Varroa destructor mite's transmission of deformed wing virus (DWV) to honey bees is responsible for most winter mortalities of colonies worldwide. Four DWV genotypes (A, B, C and D) and numerous recombinants have been described. The most recent studies have reported the greater prevalence of DWV-B over DWV-A in several countries, including European ones, while C and D genotypes appear rare or extinct. However, no global evaluation of DWV-A and DWV-B distribution was available at the European level to date. In this study, we quantified both DWV genotypes by real-time PCR from pools or individual honey bees and from V. destructor mites sampled in 15 European countries between 2010 and 2017. These data and the sequencing of the viral RNA provide a first insight into DWV diversity, with a clear dominance of DWV-B and recombinants (A/B) in Europe. Chimeric sequencing reads were used to locate the recombinant junctions along the DWV genome. These were not randomly distributed, but mainly clustered in three genomic areas: the 5'UTR, leader peptide and helicase coding sequences. In our study, the DWV recombinant genomes shared at least the VP1-VP3 coding sequences with the DWV-B. Further studies are needed to explore the apicultural context explaining these differences in DWV genotype dominance. [ABSTRACT FROM AUTHOR]

Published
2025
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7. Supplementary Table 5a from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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8. Supplementary Tables 1-7 from Comprehensive Profiling of 8p11-12 Amplification in Breast Cancer

Author

Gelsi-Boyer, Véronique, primary, Orsetti, Béatrice, primary, Cervera, Nathalie, primary, Finetti, Pascal, primary, Sircoulomb, Fabrice, primary, Rougé, Carole, primary, Lasorsa, Laurence, primary, Letessier, Anne, primary, Ginestier, Christophe, primary, Monville, Florence, primary, Esteyriès, Séverine, primary, Adélaïde, José, primary, Esterni, Benjamin, primary, Henry, Catherine, primary, Ethier, Stephen P., primary, Bibeau, Frédéric, primary, Mozziconacci, Marie-Joëlle, primary, Charafe-Jauffret, Emmanuelle, primary, Jacquemier, Jocelyne, primary, Bertucci, François, primary, Birnbaum, Daniel, primary, Theillet, Charles, primary, and Chaffanet, Max, primary

Published
2023
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9. Supplementary Figures 1-8 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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10. Supplementary Table 2 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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11. Supplementary Table 1 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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12. Supplementary Table 6 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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13. Data from Comprehensive Profiling of 8p11-12 Amplification in Breast Cancer

Author

Gelsi-Boyer, Véronique, primary, Orsetti, Béatrice, primary, Cervera, Nathalie, primary, Finetti, Pascal, primary, Sircoulomb, Fabrice, primary, Rougé, Carole, primary, Lasorsa, Laurence, primary, Letessier, Anne, primary, Ginestier, Christophe, primary, Monville, Florence, primary, Esteyriès, Séverine, primary, Adélaïde, José, primary, Esterni, Benjamin, primary, Henry, Catherine, primary, Ethier, Stephen P., primary, Bibeau, Frédéric, primary, Mozziconacci, Marie-Joëlle, primary, Charafe-Jauffret, Emmanuelle, primary, Jacquemier, Jocelyne, primary, Bertucci, François, primary, Birnbaum, Daniel, primary, Theillet, Charles, primary, and Chaffanet, Max, primary

Published
2023
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14. Supplementary Table 3 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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15. Supplementary Methods from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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16. Supplementary Figures 1-4 from Comprehensive Profiling of 8p11-12 Amplification in Breast Cancer

Author

Gelsi-Boyer, Véronique, primary, Orsetti, Béatrice, primary, Cervera, Nathalie, primary, Finetti, Pascal, primary, Sircoulomb, Fabrice, primary, Rougé, Carole, primary, Lasorsa, Laurence, primary, Letessier, Anne, primary, Ginestier, Christophe, primary, Monville, Florence, primary, Esteyriès, Séverine, primary, Adélaïde, José, primary, Esterni, Benjamin, primary, Henry, Catherine, primary, Ethier, Stephen P., primary, Bibeau, Frédéric, primary, Mozziconacci, Marie-Joëlle, primary, Charafe-Jauffret, Emmanuelle, primary, Jacquemier, Jocelyne, primary, Bertucci, François, primary, Birnbaum, Daniel, primary, Theillet, Charles, primary, and Chaffanet, Max, primary

Published
2023
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17. Supplementary Table 7 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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18. Data from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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19. Supplementary Table 8 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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20. Supplementary Table 9 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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21. Supplementary Table 4 from Essential Gene Profiles in Breast, Pancreatic, and Ovarian Cancer Cells

Author

Marcotte, Richard, primary, Brown, Kevin R., primary, Suarez, Fernando, primary, Sayad, Azin, primary, Karamboulas, Konstantina, primary, Krzyzanowski, Paul M., primary, Sircoulomb, Fabrice, primary, Medrano, Mauricio, primary, Fedyshyn, Yaroslav, primary, Koh, Judice L.Y., primary, van Dyk, Dewald, primary, Fedyshyn, Bohdana, primary, Luhova, Marianna, primary, Brito, Glauber C., primary, Vizeacoumar, Franco J., primary, Vizeacoumar, Frederick S., primary, Datti, Alessandro, primary, Kasimer, Dahlia, primary, Buzina, Alla, primary, Mero, Patricia, primary, Misquitta, Christine, primary, Normand, Josee, primary, Haider, Maliha, primary, Ketela, Troy, primary, Wrana, Jeffrey L., primary, Rottapel, Robert, primary, Neel, Benjamin G., primary, and Moffat, Jason, primary

Published
2023
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24. Data from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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25. Supplementary Figure 2 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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26. Supplementary Figure 4 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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27. Supplementary Figure 8 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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28. Supplementary Figure 9 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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29. Supplementary Figure 3 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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30. Supplementary Figure 6 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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31. Supplementary Figure 1C from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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32. Supplementary Materials from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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33. Supplementary Tables 1-9 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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34. Supplementary Figure 5 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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35. Supplementary Figure 7 from Integrated Profiling of Basal and Luminal Breast Cancers

Author

Adélaïde, José, primary, Finetti, Pascal, primary, Bekhouche, Ismahane, primary, Repellini, Laetitia, primary, Geneix, Jeannine, primary, Sircoulomb, Fabrice, primary, Charafe-Jauffret, Emmanuelle, primary, Cervera, Nathalie, primary, Desplans, Jérôme, primary, Parzy, Daniel, primary, Schoenmakers, Eric, primary, Viens, Patrice, primary, Jacquemier, Jocelyne, primary, Birnbaum, Daniel, primary, Bertucci, François, primary, and Chaffanet, Max, primary

Published
2023
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37. Development and evaluation of a core genome multilocus sequence typing scheme for Paenibacillus larvae, the deadly American foulbrood pathogen of honeybees

Author

Bertolotti, Alicia C., Forsgren, Eva, Schäfer, Marc O., Sircoulomb, Fabrice, Gaïani, Nicolas, Ribière‐Chabert, Magali, Paris, Laurianne, Lucas, Pierrick, de Boisséson, Claire, Skarin, Joakim, Rivière, Marie‐Pierre, Laboratoire de Sophia Antipolis, Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES), Swedish University of Agricultural Sciences (SLU), Friedrich-Loeffler-Institut (FLI), Laboratoire de Ploufragan-Plouzané-Niort [ANSES], Statens Veterinarmedicinska Anstalt (SVA), and The financers of European-wide analysis of Paenibacillus larvae genetic diversity (EuroPlarva) were the European Commission, the Member States and the EU Reference Laboratory. Additional financial support was provided by the Swedish Research Council FORMAS (dnr 2017-01345)

Subjects
Whole Genome Sequencing, [SDV]Life Sciences [q-bio], [SDV.BA]Life Sciences [q-bio]/Animal biology, Paenibacillus larvae, Sharing data, Bees, Apis Mellifera, Core genome multilocus sequence typing, Standardization, Disease Outbreaks, MESH: Bees, Honeybees, MESH: Multilocus Sequence Typing, Microbiology (Microbiology in the medical area to be 30109), Animals, MESH: Paenibacillus larvae, MESH: Whole Genome Sequencing, Research Articles, Genome, Bacterial, Research Article, Multilocus Sequence Typing
Abstract

International audience; Paenibacillus larvae is the causative agent of the fatal American foulbrood disease in honeybees (Apis mellifera). Strain identification is vital for preventing the spread of the disease. To date, the most accessible and robust scheme to identify strains is the multilocus sequence typing (MLST) method. However, this approach has limited resolution, especially for epidemiological studies. As the cost of wholegenome sequencing has decreased and as it becomes increasingly available to most laboratories, an extended MLST based on the core genome (cgMLST) presents a valuable tool for high-resolution investigations. In this study, we present a standardized, robust cgMLST scheme for P. larvae typing using whole-genome sequencing. A total of 333 genomes were used to identify, validate and evaluate 2419 core genes. The cgMLST allowed finescale differentiation between samples that had the same profile using traditional MLST and allowed for the characterization of strains impossible by MLST. The scheme was successfully used to trace a localized Swedish outbreak, where a cluster of 38 isolates was linked to a country-wide beekeeping operation. cgMLST greatly enhances the power of a traditional typing scheme, while preserving the same stability and standardization for sharing results and methods across different laboratories.

Published
2021
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38. ZNF703 gene amplification at 8p12 specifies luminal B breast cancer

Author

Sircoulomb, Fabrice, Nicolas, Nathalie, Ferrari, Anthony, Finetti, Pascal, Bekhouche, Ismahane, Rousselet, Estelle, Lonigro, Aurélie, Adélaïde, José, Baudelet, Emilie, Esteyriès, Séverine, Wicinski, Julien, Audebert, Stéphane, Charafe‐Jauffret, Emmanuelle, Jacquemier, Jocelyne, Lopez, Marc, Borg, Jean‐Paul, Sotiriou, Christos, Popovici, Cornel, Bertucci, François, Birnbaum, Daniel, Chaffanet, Max, and Ginestier, Christophe

Published
2011
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40. CaPSID: A bioinformatics platform for computational pathogen sequence identification in human genomes and transcriptomes

Author

Borozan Ivan, Wilson Shane, Blanchette Paola, Laflamme Philippe, Watt Stuart N, Krzyzanowski Paul M, Sircoulomb Fabrice, Rottapel Robert, Branton Philip E, and Ferretti Vincent

Subjects
Computer applications to medicine. Medical informatics, R858-859.7, Biology (General), QH301-705.5
Abstract

Abstract Background It is now well established that nearly 20% of human cancers are caused by infectious agents, and the list of human oncogenic pathogens will grow in the future for a variety of cancer types. Whole tumor transcriptome and genome sequencing by next-generation sequencing technologies presents an unparalleled opportunity for pathogen detection and discovery in human tissues but requires development of new genome-wide bioinformatics tools. Results Here we present CaPSID (Computational Pathogen Sequence IDentification), a comprehensive bioinformatics platform for identifying, querying and visualizing both exogenous and endogenous pathogen nucleotide sequences in tumor genomes and transcriptomes. CaPSID includes a scalable, high performance database for data storage and a web application that integrates the genome browser JBrowse. CaPSID also provides useful metrics for sequence analysis of pre-aligned BAM files, such as gene and genome coverage, and is optimized to run efficiently on multiprocessor computers with low memory usage. Conclusions To demonstrate the usefulness and efficiency of CaPSID, we carried out a comprehensive analysis of both a simulated dataset and transcriptome samples from ovarian cancer. CaPSID correctly identified all of the human and pathogen sequences in the simulated dataset, while in the ovarian dataset CaPSID’s predictions were successfully validated in vitro.

Published
2012
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43. Genome profiling of ERBB2-amplified breast cancers

Author

Ayed Farhat, Tarpin Carole, Charafe-Jauffret Emmanuelle, Innocenti Charlène, Raynaud Stéphane, Bonansea Julien, Hamida Azza, Adélaïde José, Finetti Pascal, Bekhouche Ismahane, Sircoulomb Fabrice, Viens Patrice, Jacquemier Jocelyne, Bertucci François, Birnbaum Daniel, and Chaffanet Max

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Around 20% of breast cancers (BC) show ERBB2 gene amplification and overexpression of the ERBB2 tyrosine kinase receptor. They are associated with a poor prognosis but can benefit from targeted therapy. A better knowledge of these BCs, genomically and biologically heterogeneous, may help understand their behavior and design new therapeutic strategies. Methods We defined the high resolution genome and gene expression profiles of 54 ERBB2-amplified BCs using 244K oligonucleotide array-comparative genomic hybridization and whole-genome DNA microarrays. Expression of ERBB2, phosphorylated ERBB2, EGFR, IGF1R and FOXA1 proteins was assessed by immunohistochemistry to evaluate the functional ERBB2 status and identify co-expressions. Results First, we identified the ERBB2-C17orf37-GRB7 genomic segment as the minimal common 17q12-q21 amplicon, and CRKRS and IKZF3 as the most frequent centromeric and telomeric amplicon borders, respectively. Second, GISTIC analysis identified 17 other genome regions affected by copy number aberration (CNA) (amplifications, gains, losses). The expression of 37 genes of these regions was deregulated. Third, two types of heterogeneity were observed in ERBB2-amplified BCs. The genomic profiles of estrogen receptor-postive (ER+) and negative (ER-) ERBB2-amplified BCs were different. The WNT/β-catenin signaling pathway was involved in ER- ERBB2-amplified BCs, and PVT1 and TRPS1 were candidate oncogenes associated with ER+ ERBB2-amplified BCs. The size of the ERBB2 amplicon was different in inflammatory (IBC) and non-inflammatory BCs. ERBB2-amplified IBCs were characterized by the downregulated and upregulated mRNA expression of ten and two genes in proportion to CNA, respectively. IHC results showed (i) a linear relationship between ERBB2 gene amplification and its gene and protein expressions with a good correlation between ERBB2 expression and phosphorylation status; (ii) a potential signaling cross-talk between EGFR or IGF1R and ERBB2, which could influence response of ERBB2-positive BCs to inhibitors. FOXA1 was frequently coexpressed with ERBB2 but its expression did not impact on the outcome of patients with ERBB2-amplified tumors. Conclusion We have shown that ER+ and ER- ERBB2-amplified BCs are different, distinguished ERBB2 amplicons in IBC and non-IBC, and identified genomic features that may be useful in the design of alternative therapeutical strategies.

Published
2010
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44. Loss, mutation and deregulation of L3MBTL4 in breast cancers

Author

Addou-Klouche Lynda, Adélaïde José, Finetti Pascal, Cervera Nathalie, Ferrari Anthony, Bekhouche Ismahane, Sircoulomb Fabrice, Sotiriou Christos, Viens Patrice, Moulessehoul Soraya, Bertucci François, Birnbaum Daniel, and Chaffanet Max

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Many alterations are involved in mammary oncogenesis, including amplifications of oncogenes and losses of tumor suppressor genes (TSG). Losses may affect almost all chromosome arms and many TSGs remain to be identified. Results We studied 307 primary breast tumors and 47 breast cancer cell lines by high resolution array comparative genomic hybridization (aCGH). We identified a region on 18p11.31 lost in about 20% of the tumors and 40% of the cell lines. The minimal common region of loss (Chr18:6,366,938-6,375,929 bp) targeted the L3MBTL4 gene. This gene was also targeted by breakage in one tumor and in two cell lines. We studied the exon sequence of L3MBTL4 in 180 primary tumor samples and 47 cell lines and found six missense and one nonsense heterozygous mutations. Compared with normal breast tissue, L3MBTL4 mRNA expression was downregulated in 73% of the tumors notably in luminal, ERBB2 and normal-like subtypes. Losses of the 18p11 region were associated with low L3MBTL4 expression level. Integrated analysis combining genome and gene expression profiles of the same tumors pointed to 14 other potential 18p TSG candidates. Downregulated expression of ZFP161, PPP4R1 and YES1 was correlated with luminal B molecular subtype. Low ZFP161 gene expression was associated with adverse clinical outcome. Conclusion We have identified L3MBTL4 as a potential TSG of chromosome arm 18p. The gene is targeted by deletion, breakage and mutations and its mRNA is downregulated in breast tumors. Additional 18p TSG candidates might explain the aggressive phenotype associated with the loss of 18p in breast tumors.

Published
2010
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45. A reason why the ERBB2 gene is amplified and not mutated in breast cancer

Author

Sircoulomb Fabrice, Birnbaum Daniel, and Imbert Jean

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671
Abstract

Abstract Alterations of receptor-type tyrosine kinases (RTK) are frequent in human cancers. They can result from translocation, mutation or amplification. The ERBB2 RTK is encoded by a gene that is amplified in about 20% breast cancers. The question is: why is this RTK specifically subjected to this type of alteration? We propose that ERBB2 gene amplification is used to overcome repression of its expression by sequence-specific transcription factors.

Published
2009
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46. Regional perturbation of gene transcription is associated with intrachromosomal rearrangements and gene fusion transcripts in high grade ovarian cancer.

Author

Krzyzanowski, Paul M, Krzyzanowski, Paul M, Sircoulomb, Fabrice, Yousif, Fouad, Normand, Josee, La Rose, Jose, E Francis, Kyle, Suarez, Fernando, Beck, Tim, McPherson, John D, Stein, Lincoln D, Rottapel, Robert K, Krzyzanowski, Paul M, Krzyzanowski, Paul M, Sircoulomb, Fabrice, Yousif, Fouad, Normand, Josee, La Rose, Jose, E Francis, Kyle, Suarez, Fernando, Beck, Tim, McPherson, John D, Stein, Lincoln D, and Rottapel, Robert K

Abstract

Genomic rearrangements are a hallmark of cancer biology and progression, allowing cells to rapidly transform through alterations in regulatory structures, changes in expression patterns, reprogramming of signaling pathways, and creation of novel transcripts via gene fusion events. Though functional gene fusions encoding oncogenic proteins are the most dramatic outcomes of genomic rearrangements, we investigated the relationship between rearrangements evidenced by fusion transcripts and local expression changes in cancer using transcriptome data alone. 9,953 gene fusion predictions from 418 primary serious ovarian cancer tumors were analyzed, identifying depletions of gene fusion breakpoints within coding regions of fused genes as well as an N-terminal enrichment of breakpoints within fused genes. We identified 48 genes with significant fusion-associated upregulation and furthermore demonstrate that significant regional overexpression of intact genes in patient transcriptomes occurs within 1 megabase of 78 novel gene fusions that function as central markers of these regions. We reveal that cancer transcriptomes select for gene fusions that preserve protein and protein domain coding potential. The association of gene fusion transcripts with neighboring gene overexpression supports rearrangements as mechanism through which cancer cells remodel their transcriptomes and identifies a new way to utilize gene fusions as indicators of regional expression changes in diseased cells with only transcriptomic data.

Published
2019

47. Frequency, prognostic impact, and subtype association of 8p12, 8q24, 11q13, 12p13, 17q12, and 20q13 amplifications in breast cancers

Author

Viens Patrice, Zemmour Christophe, Finetti Pascal, Geneix Jeannine, Esterni Benjamin, Gelsi-Boyer Véronique, Monville Florence, Cervera Nathalie, Ginestier Christophe, Sircoulomb Fabrice, Letessier Anne, Charafe-Jauffret Emmanuelle, Jacquemier Jocelyne, Birnbaum Daniel, and Chaffanet Max

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Oncogene amplification and overexpression occur in tumor cells. Amplification status may provide diagnostic and prognostic information and may lead to new treatment strategies. Chromosomal regions 8p12, 8q24, 11q13, 17q12 and 20q13 are recurrently amplified in breast cancers. Methods To assess the frequencies and clinical impact of amplifications, we analyzed 547 invasive breast tumors organized in a tissue microarray (TMA) by fluorescence in situ hybridization (FISH) and calculated correlations with histoclinical features and prognosis. BAC probes were designed for: (i) two 8p12 subregions centered on RAB11FIP1 and FGFR1 loci, respectively; (ii) 11q13 region centered on CCND1; (iii) 12p13 region spanning NOL1; and (iv) three 20q13 subregions centered on MYBL2, ZNF217 and AURKA, respectively. Regions 8q24 and 17q12 were analyzed with MYC and ERBB2 commercial probes, respectively. Results We observed amplification of 8p12 (amplified at RAB11FIP1 and/or FGFR1) in 22.8%, 8q24 in 6.1%, 11q13 in 19.6%, 12p13 in 4.1%, 17q12 in 9.9%, 20q13Z (amplified at ZNF217 only) in 9.9%, and 20q13Co (co-amplification of two or three 20q13 loci) in 8.5% of cases. The 8q24, 12p13, and 17q12 amplifications were correlated with high grade. The most frequent single amplifications were 8p12 (9.8%), 8q24 (3.3%) and 12p13 (3.3%), 20q13Z and 20q13Co (1.6%) regions. The 17q12 and 11q13 regions were never found amplified alone. The most frequent co-amplification was 8p12/11q13. Amplifications of 8p12 and 17q12 were associated with poor outcome. Amplification of 12p13 was associated with basal molecular subtype. Conclusion Our results establish the frequencies, prognostic impacts and subtype associations of various amplifications and co-amplifications in breast cancers.

Published
2006
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48. Correction to:ZNF703 gene amplification at 8p12 specifies luminal B breast cancer

Author

Sircoulomb, Fabrice, Nicolas, Nathalie, Ferrari, Anthony, Finetti, Pascal, Bekhouche, Ismahane, Rousselet, Estelle, Lonigro, Aurélie, Adélaïde, José, Baudelet, Emilie, Esteyriès, Séverine, Wicinski, Julien, Audebert, Stéphane, Charafe‐Jauffret, Emmanuelle, Jacquemier, Jocelyne, Lopez, Marc, Borg, Jean‐Paul, Sotiriou, Christos, Popovici, Cornel, Bertucci, François, Birnbaum, Daniel, Chaffanet, Max, and Ginestier, Christophe

Published
2011
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49. Interrogation of Functional Cell-Surface Markers Identifies CD151 Dependency in High-Grade Serous Ovarian Cancer

Author

Medrano, Mauricio, primary, Communal, Laudine, additional, Brown, Kevin R., additional, Iwanicki, Marcin, additional, Normand, Josee, additional, Paterson, Joshua, additional, Sircoulomb, Fabrice, additional, Krzyzanowski, Paul, additional, Novak, Marian, additional, Doodnauth, Sasha A., additional, Saiz, Fernando Suarez, additional, Cullis, Jane, additional, Al-awar, Rima, additional, Neel, Benjamin G., additional, McPherson, John, additional, Drapkin, Ronny, additional, Ailles, Laurie, additional, Mes-Massons, Anne-Marie, additional, and Rottapel, Robert, additional

Published
2017
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50. ZNF703: a novel oncogene involved in breast cancer

Author

Ginestier, Christophe, Sircoulomb, Fabrice, Charafe-Jauffret, Emmanuelle, Chaffanet, Max, Birnbaum, Daniel, Centre de Recherche en Cancérologie de Marseille (CRCM / U891 Inserm), Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Cancérologie (Inserm U599/IPC), Université de la Méditerranée - Aix-Marseille 2-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)

Subjects
[SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2011
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