360 results on '"Pritchard, Antonia"'
Search Results
2. The Role of Histone Variants in Cancer
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Pritchard, Antonia L., Hesson, Luke B., editor, and Pritchard, Antonia L., editor
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- 2019
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3. The Clinical Utility of Epigenetics: A Case Study
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Hesson, Luke B., Sloane, Mathew A., Pritchard, Antonia L., Hesson, Luke B., editor, and Pritchard, Antonia L., editor
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- 2019
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4. FRAMe: Familial Risk Assessment of Melanoma—a risk prediction tool to guide CDKN2A germline mutation testing in Australian familial melanoma
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Holland, Elizabeth A., Lo, Serigne, Kelly, Blake, Schmid, Helen, Cust, Anne E., Palmer, Jane M., Drummond, Martin, Hayward, Nicholas K., Pritchard, Antonia L., and Mann, Graham J.
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- 2021
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5. Lymphoblastoid cell lines do not recapitulate physiological circulating B cell subtypes
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MacKinnon, Connie, primary, McLean, Ryan, additional, and Pritchard, Antonia L., additional
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- 2024
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6. The ATM Ser49Cys Variant Effects ATM Function as a Regulator of Oncogene-Induced Senescence.
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Atkinson, Caroline, McInerney-Leo, Aideen M., Proctor, Martina, Lanagan, Catherine, Stevenson, Alexander J., Dehkhoda, Farhad, Caole, Mary, Maas, Ellie, Ainger, Stephen, Pritchard, Antonia L., Johansson, Peter A., Leo, Paul, Hayward, Nicholas K., Sturm, Richard A., Duncan, Emma L., and Gabrielli, Brian
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DNA repair ,DNA damage ,ONCOGENES ,AUTOMATED teller machines ,PROTEIN kinases ,GENE frequency - Abstract
An apical component of the cell cycle checkpoint and DNA damage repair response is the ataxia-telangiectasia mutated (ATM) Ser/Thr protein kinase. A variant of ATM, Ser49Cys (rs1800054; minor allele frequency = 0.011), has been associated with an elevated risk of melanoma development; however, the functional consequence of this variant is not defined. ATM-dependent signalling in response to DNA damage has been assessed in a panel of patient-derived lymphoblastoid lines and primary human melanocytic cell strains heterozygous for the ATM Ser49Cys variant allele. The ATM Ser49Cys allele appears functional for acute p53-dependent signalling in response to DNA damage. Expression of the variant allele did reduce the efficacy of oncogene expression in inducing senescence. These findings demonstrate that the ATM 146C>G Ser49Cys allele has little discernible effect on the acute response to DNA damage but has reduced function observed in the chronic response to oncogene over-expression. Analysis of melanoma, naevus and skin colour genomics and GWAS analyses have demonstrated no association of this variant with any of these outcomes. The modest loss of function detected suggest that the variant may act as a modifier of other variants of ATM/p53-dependent signalling. [ABSTRACT FROM AUTHOR]
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- 2024
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7. Germline Variants in Childhood Cutaneous Melanoma
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Johansson, Peter A., primary, Palmer, Jane M., additional, Hamilton, Hayley R., additional, Whiteman, David C., additional, Pritchard, Antonia L., additional, and Hayward, Nicholas K., additional
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- 2023
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8. Bone marrow transplantation generates T cell-dependent control of myeloma in mice
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Vuckovic, Slavica, Minnie, Simone A., Smith, David, Gartlan, Kate H., Watkins, Thomas S., Markey, Kate A., Mukhopadhyay, Pamela, Guillerey, Camille, Kuns, Rachel D., Locke, Kelly R., Pritchard, Antonia L., Johansson, Peter A., Varelias, Antiopi, Zhang, Ping, Huntington, Nicholas D., Waddell, Nicola, Chesi, Marta, Miles, John J., Smyth, Mark J., and Hill, Geoffrey R.
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T cells -- Research ,Bone marrow transplantation -- Usage ,Multiple myeloma -- Control ,Laboratory rats -- Health aspects ,Health care industry - Abstract
Transplantation with autologous hematopoietic progenitors remains an important consolidation treatment for patients with multiple myeloma (MM) and is thought to prolong the disease plateau phase by providing intensive cytoreduction. However, transplantation induces inflammation in the context of profound lymphodepletion that may cause hitherto unexpected immunological effects. We developed preclinical models of bone marrow transplantation (BMT) for MM using Vk*MYC myeloma-bearing recipient mice and donor mice that were myeloma naive or myeloma experienced to simulate autologous transplantation. Surprisingly, we demonstrated broad induction of T cell-dependent myeloma control, most efficiently from memory T cells within myeloma-experienced grafts, but also through priming of naive T cells after BMT. [CD8.sup.+] T cells from mice with controlled myeloma had a distinct T cell receptor (TCR) repertoire and higher clonotype overlap relative to myeloma-free BMT recipients. Furthermore, T cell-dependent myeloma control could be adoptively transferred to secondary recipients and was myeloma cell clone specific. Interestingly, donor-derived IL-17A acted directly on myeloma cells expressing the IL-17 receptor to induce a transcriptional landscape that promoted tumor growth and immune escape. Conversely, donor IFN-[gamma] secretion and signaling were critical to protective immunity and were profoundly augmented by CD137 agonists. These data provide new insights into the mechanisms of action of transplantation in myeloma and provide rational approaches to improving clinical outcomes., IntroductionMultiple myeloma (MM) is a bone marrow-based (BM-based) plasma cell neoplasm that often evolves from a premalignant stage, known as monoclonal gammopathy of undetermined significance (MGUS), to present with characteristic [...]
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- 2019
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9. Prolonged stable disease in a uveal melanoma patient with germline MBD4 nonsense mutation treated with pembrolizumab and ipilimumab
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Johansson, Peter A., Stark, Andrew, Palmer, Jane M., Bigby, Kieron, Brooks, Kelly, Rolfe, Olivia, Pritchard, Antonia L., Whitehead, Kevin, Warrier, Sunil, Glasson, William, and Hayward, Nicholas K.
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- 2019
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10. Identifying neoantigens for use in immunotherapy
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Hutchison, Sharon and Pritchard, Antonia L.
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- 2018
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11. Germline Variation at CDKN2A and Associations with Nevus Phenotypes among Members of Melanoma Families
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Taylor, Nicholas J., Mitra, Nandita, Goldstein, Alisa M., Tucker, Margaret A., Avril, Marie-Françoise, Azizi, Esther, Bergman, Wilma, Bishop, D. Timothy, Bressac-de Paillerets, Brigitte, Bruno, William, Calista, Donato, Cannon-Albright, Lisa A., Cuellar, Francisco, Cust, Anne E., Demenais, Florence, Elder, David E., Gerdes, Anne-Marie, Ghiorzo, Paola, Grazziotin, Thais C., Hansson, Johan, Harland, Mark, Hayward, Nicholas K., Hocevar, Marko, Höiom, Veronica, Ingvar, Christian, Landi, Maria Teresa, Landman, Gilles, Larre-Borges, Alejandra, Leachman, Sancy A., Mann, Graham J., Nagore, Eduardo, Olsson, Håkan, Palmer, Jane M., Perić, Barbara, Pjanova, Dace, Pritchard, Antonia, Puig, Susana, van der Stoep, Nienke, Wadt, Karin A.W., Whitaker, Linda, Yang, Xiaohong R., Newton Bishop, Julia A., Gruis, Nelleke A., and Kanetsky, Peter A.
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- 2017
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12. Microsimulation Model for Evaluating the Cost-Effectiveness of Surveillance in BAP1 Pathogenic Variant Carriers
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Walpole, Sebastian, Hayward, Nicholas K., Pritchard, Antonia L., and Johansson, Peter A.
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- 2021
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13. Whole genome landscapes of uveal melanoma show an ultraviolet radiation signature in iris tumours
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Johansson, Peter A., Brooks, Kelly, Newell, Felicity, Palmer, Jane M., Wilmott, James S., Pritchard, Antonia L., Broit, Natasa, Wood, Scott, Carlino, Matteo S., Leonard, Conrad, Koufariotis, Lambros T., Nathan, Vaishnavi, Beasley, Aaron B., Howlie, Madeleine, Dawson, Rebecca, Rizos, Helen, Schmidt, Chris W., Long, Georgina V., Hamilton, Hayley, Kiilgaard, Jens F., Isaacs, Timothy, Gray, Elin S., Rolfe, Olivia J., Park, John J., Stark, Andrew, Mann, Graham J., Scolyer, Richard A., Pearson, John V., van Baren, Nicolas, Waddell, Nicola, Wadt, Karin W., McGrath, Lindsay A., Warrier, Sunil K., Glasson, William, and Hayward, Nicholas K.
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- 2020
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14. Targeting Neoantigens for Personalised Immunotherapy
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Pritchard, Antonia L.
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- 2018
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15. Supplementary Data from Comparative Genomics Provides Etiologic and Biological Insight into Melanoma Subtypes
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Newell, Felicity, primary, Johansson, Peter A., primary, Wilmott, James S., primary, Nones, Katia, primary, Lakis, Vanessa, primary, Pritchard, Antonia L., primary, Lo, Serigne N., primary, Rawson, Robert V., primary, Kazakoff, Stephen H., primary, Colebatch, Andrew J., primary, Koufariotis, Lambros T., primary, Ferguson, Peter M., primary, Wood, Scott, primary, Leonard, Conrad, primary, Law, Matthew H., primary, Brooks, Kelly M., primary, Broit, Natasa, primary, Palmer, Jane M., primary, Couts, Kasey L., primary, Vergara, Ismael A., primary, Long, Georgina V., primary, Barbour, Andrew P., primary, Nieweg, Omgo E., primary, Shivalingam, Brindha, primary, Robinson, William A., primary, Stretch, Jonathan R., primary, Spillane, Andrew J., primary, Saw, Robyn P.M., primary, Shannon, Kerwin F., primary, Thompson, John F., primary, Mann, Graham J., primary, Pearson, John V., primary, Scolyer, Richard A., primary, Waddell, Nicola, primary, and Hayward, Nicholas K., primary
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- 2023
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16. Data from Comparative Genomics Provides Etiologic and Biological Insight into Melanoma Subtypes
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Newell, Felicity, primary, Johansson, Peter A., primary, Wilmott, James S., primary, Nones, Katia, primary, Lakis, Vanessa, primary, Pritchard, Antonia L., primary, Lo, Serigne N., primary, Rawson, Robert V., primary, Kazakoff, Stephen H., primary, Colebatch, Andrew J., primary, Koufariotis, Lambros T., primary, Ferguson, Peter M., primary, Wood, Scott, primary, Leonard, Conrad, primary, Law, Matthew H., primary, Brooks, Kelly M., primary, Broit, Natasa, primary, Palmer, Jane M., primary, Couts, Kasey L., primary, Vergara, Ismael A., primary, Long, Georgina V., primary, Barbour, Andrew P., primary, Nieweg, Omgo E., primary, Shivalingam, Brindha, primary, Robinson, William A., primary, Stretch, Jonathan R., primary, Spillane, Andrew J., primary, Saw, Robyn P.M., primary, Shannon, Kerwin F., primary, Thompson, John F., primary, Mann, Graham J., primary, Pearson, John V., primary, Scolyer, Richard A., primary, Waddell, Nicola, primary, and Hayward, Nicholas K., primary
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- 2023
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17. Supplementary Figure 1B from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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18. Supplementary Table S1 from Meta-Analysis and Systematic Review of the Genomics of Mucosal Melanoma
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Broit, Natasa, primary, Johansson, Peter A., primary, Rodgers, Chloe B., primary, Walpole, Sebastian T., primary, Newell, Felicity, primary, Hayward, Nicholas K., primary, and Pritchard, Antonia L., primary
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- 2023
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19. Supplementary Figure 4 from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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20. Data from Meta-Analysis and Systematic Review of the Genomics of Mucosal Melanoma
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Broit, Natasa, primary, Johansson, Peter A., primary, Rodgers, Chloe B., primary, Walpole, Sebastian T., primary, Newell, Felicity, primary, Hayward, Nicholas K., primary, and Pritchard, Antonia L., primary
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- 2023
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21. Supplementary Table 1 from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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22. Supplementary Figure 3 from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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23. Data from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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24. Supplementary Figure 5 from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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25. Supplementary Table 2 from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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26. Supplementary Methods from Meta-Analysis and Systematic Review of the Genomics of Mucosal Melanoma
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Broit, Natasa, primary, Johansson, Peter A., primary, Rodgers, Chloe B., primary, Walpole, Sebastian T., primary, Newell, Felicity, primary, Hayward, Nicholas K., primary, and Pritchard, Antonia L., primary
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- 2023
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27. Supplementary Figure 2 from Exome Sequencing to Predict Neoantigens in Melanoma
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Pritchard, Antonia L., primary, Burel, Julie G., primary, Neller, Michelle A., primary, Hayward, Nicholas K., primary, Lopez, J. Alejandro, primary, Fatho, Martina, primary, Lennerz, Volker, primary, Wölfel, Thomas, primary, and Schmidt, Christopher W., primary
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- 2023
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28. Supplementary Figures & Legends from Meta-Analysis and Systematic Review of the Genomics of Mucosal Melanoma
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Broit, Natasa, primary, Johansson, Peter A., primary, Rodgers, Chloe B., primary, Walpole, Sebastian T., primary, Newell, Felicity, primary, Hayward, Nicholas K., primary, and Pritchard, Antonia L., primary
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- 2023
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29. Supplementary Tables from G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma
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Kelly, Gregory M., primary, Al-Ejeh, Fares, primary, McCuaig, Robert, primary, Casciello, Francesco, primary, Ahmad Kamal, Nabilah, primary, Ferguson, Blake, primary, Pritchard, Antonia L., primary, Ali, Sayed, primary, Silva, Ines P., primary, Wilmott, James S., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rao, Sudha, primary, Hayward, Nicholas K., primary, Gannon, Frank, primary, and Lee, Jason S., primary
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- 2023
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30. Supplementary Figures from G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma
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Kelly, Gregory M., primary, Al-Ejeh, Fares, primary, McCuaig, Robert, primary, Casciello, Francesco, primary, Ahmad Kamal, Nabilah, primary, Ferguson, Blake, primary, Pritchard, Antonia L., primary, Ali, Sayed, primary, Silva, Ines P., primary, Wilmott, James S., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rao, Sudha, primary, Hayward, Nicholas K., primary, Gannon, Frank, primary, and Lee, Jason S., primary
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- 2023
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31. Evaluation of the contribution of germline variants in BRCA1 and BRCA2 to uveal and cutaneous melanoma
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Johansson, Peter A., Nathan, Vaishnavi, Bourke, Lauren M., Palmer, Jane M., Zhang, Tongwu, Symmons, Judith, Howlie, Madeleine, Patch, Ann-Marie, Read, Jazlyn, Holland, Elizabeth A., Schmid, Helen, Warrier, Sunil, Glasson, William, Höiom, Veronica, Wadt, Karin, Jönsson, Göran, Olsson, Håkan, Ingvar, Christian, Mann, Graham, Brown, Kevin M., Hayward, Nicholas K., and Pritchard, Antonia L.
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- 2019
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32. Immune signatures in cutaneous melanoma correlate with survival independently of immunotherapy treatment
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Johansson, Peter A., primary, Hayward, Nicholas K., additional, and Pritchard, Antonia L., additional
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- 2023
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33. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns
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Jiao, Wei, Atwal, Gurnit, Polak, Paz, Karlic, Rosa, Cuppen, Edwin, Al-Shahrour, Fatima, Bailey, Peter J, Biankin, Andrew V, Boutros, Paul C, Campbell, Peter J, Chang, David K, Cooke, Susanna L, Deshpande, Vikram, Faltas, Bishoy M, Faquin, William C, Garraway, Levi, Getz, Gad, Grimmond, Sean M, Haider, Syed, Hoadley, Katherine A, Kaiser, Vera B, Kato, Mamoru, Kübler, Kirsten, Lazar, Alexander J, Li, Constance H, Louis, David N, Margolin, Adam, Martin, Sancha, Nahal-Bose, Hardeep K, Nielsen, G Petur, Nik-Zainal, Serena, Omberg, Larsson, P’ng, Christine, Perry, Marc D, Rheinbay, Esther, Rubin, Mark A, Semple, Colin A, Sgroi, Dennis C, Shibata, Tatsuhiro, Siebert, Reiner, Smith, Jaclyn, Stein, Lincoln D, Stobbe, Miranda D, Sun, Ren X, Thai, Kevin, Wright, Derek W, Wu, Chin-Lee, Yuan, Ke, Zhang, Junjun, Danyi, Alexandra, de Ridder, Jeroen, van Herpen, Carla, Lolkema, Martijn P, Steeghs, Neeltje, Morris, Quaid D, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, Prashant, Baylin, Stephen B, Bazant, Wojciech, Beardsmore, Duncan, Beck, Timothy A, Behjati, Sam, Behren, Andreas, Niu, Beifang, Bell, Cindy, Beltran, Sergi, Benz, Christopher, Berchuck, Andrew, Bergmann, Anke K, Bergstrom, Erik N, Berman, Benjamin P, Berney, Daniel M, Bernhart, Stephan H, Beroukhim, Rameen, Berrios, Mario, Bersani, Samantha, Bertl, Johanna, Betancourt, Miguel, Bhandari, Vinayak, Bhosle, Shriram G, Bieg, Matthias, Bigner, Darell, Binder, Hans, Birney, Ewan, Birrer, Michael, Biswas, Nidhan K, Bjerkehagen, Bodil, Bodenheimer, Tom, Boice, Lori, Bonizzato, Giada, De Bono, Johann S, Boot, Arnoud, Bootwalla, Moiz S, Borg, Ake, Borkhardt, Arndt, Boroevich, Keith A, Borozan, Ivan, Borst, Christoph, Bosenberg, Marcus, Bosio, Mattia, Boultwood, Jacqueline, Bourque, Guillaume, Bova, G Steven, Bowen, David T, Bowlby, Reanne, Bowtell, David DL, Boyault, Sandrine, Boyce, Rich, Boyd, Jeffrey, Brazma, Alvis, Brennan, Paul, Brewer, Daniel S, Brinkman, Arie B, Bristow, Robert G, Broaddus, Russell R, Brock, Jane E, Brock, Malcolm, Broeks, Annegien, Brooks, Angela N, Brooks, Denise, Brors, Benedikt, Brunak, Søren, Bruxner, Timothy JC, Bruzos, Alicia L, Buchanan, Alex, Buchhalter, Ivo, Buchholz, Christiane, Bullman, Susan, Burke, Hazel, Burkhardt, Birgit, Burns, Kathleen H, Busanovich, John, Bustamante, Carlos D, Butler, Adam P, Butte, Atul J, Byrne, Niall J, Børresen-Dale, Anne-Lise, Caesar-Johnson, Samantha J, Cafferkey, Andy, Cahill, Declan, Calabrese, Claudia, Caldas, Carlos, Calvo, Fabien, Camacho, Niedzica, Campo, Elias, Cantù, Cinzia, Cao, Shaolong, Carey, Thomas E, Carlevaro-Fita, Joana, Carlsen, Rebecca, Cataldo, Ivana, Cazzola, Mario, Cebon, Jonathan, Cerfolio, Robert, Chadwick, Dianne E, Chakravarty, Dimple, Chalmers, Don, Chan, Calvin Wing Yiu, Chan, Kin, Chan-Seng-Yue, Michelle, Chandan, Vishal S, Chanock, Stephen J, Chantrill, Lorraine A, Chateigner, Aurélien, Chatterjee, Nilanjan, Chayama, Kazuaki, Chen, Hsiao-Wei, Chen, Jieming, Chen, Ken, Chen, Yiwen, Chen, Zhaohong, Cherniack, Andrew D, Chien, Jeremy, Chiew, Yoke-Eng, Chin, Suet-Feung, Cho, Juok, Cho, Sunghoon, Choi, Jung Kyoon, Choi, Wan, Chomienne, Christine, Chong, Zechen, Choo, Su Pin, Chou, Angela, Christ, Angelika N, Christie, Elizabeth L, Chuah, Eric, Cibulskis, Carrie, Cibulskis, Kristian, Cingarlini, Sara, Clapham, Peter, Claviez, Alexander, Cleary, Sean, Cloonan, Nicole, Cmero, Marek, Collins, Colin C, Connor, Ashton A, Cooper, Colin S, Cope, Leslie, Corbo, Vincenzo, Cordes, Matthew G, Cordner, Stephen M, Cortés-Ciriano, Isidro, Covington, Kyle, Cowin, Prue A, Craft, Brian, Craft, David, Creighton, Chad J, Cun, Yupeng, Curley, Erin, Cutcutache, Ioana, Czajka, Karolina, Czerniak, Bogdan, Dagg, Rebecca A, Danilova, Ludmila, Davi, Maria Vittoria, Davidson, Natalie R, Davies, Helen, Davis, Ian J, Davis-Dusenbery, Brandi N, Dawson, Kevin J, De La Vega, Francisco M, De Paoli-Iseppi, Ricardo, Defreitas, Timothy, Dei Tos, Angelo P, Delaneau, Olivier, Demchok, John A, Demeulemeester, Jonas, Demidov, German M, Demircioğlu, Deniz, Dennis, Nening M, Denroche, Robert E, Dentro, Stefan C, Desai, Nikita, Deshwar, Amit G, Desmedt, Christine, Deu-Pons, Jordi, Dhalla, Noreen, Dhani, Neesha C, Dhingra, Priyanka, Dhir, Rajiv, DiBiase, Anthony, Diamanti, Klev, Ding, Li, Ding, Shuai, Dinh, Huy Q, Dirix, Luc, Doddapaneni, HarshaVardhan, Donmez, Nilgun, Dow, Michelle T, Drapkin, Ronny, Drechsel, Oliver, Drews, Ruben M, Serge, Serge, Dudderidge, Tim, Dueso-Barroso, Ana, Dunford, Andrew J, Dunn, Michael, Dursi, Lewis Jonathan, Duthie, Fraser R, Dutton-Regester, Ken, Eagles, Jenna, Easton, Douglas F, Edmonds, Stuart, Edwards, Paul A, Edwards, Sandra E, Eeles, Rosalind A, Ehinger, Anna, Eils, Juergen, Eils, Roland, El-Naggar, Adel, Eldridge, Matthew, Ellrott, Kyle, Erkek, Serap, Escaramis, Georgia, Espiritu, Shadrielle MG, Estivill, Xavier, Etemadmoghadam, Dariush, Eyfjord, Jorunn E, Fan, Daiming, Fan, Yu, Farcas, Claudiu, Fassan, Matteo, Fatima, Aquila, Favero, Francesco, Fayzullaev, Nodirjon, Felau, Ina, Fereday, Sian, Ferguson, Martin L, Ferretti, Vincent, Feuerbach, Lars, Field, Matthew A, Fink, J Lynn, Finocchiaro, Gaetano, Fisher, Cyril, Fittall, Matthew W, Fitzgerald, Anna, Fitzgerald, Rebecca C, Flanagan, Adrienne M, Fleshner, Neil E, Flicek, Paul, Foekens, John A, Fong, Kwun M, Fonseca, Nuno A, Foster, Christopher S, Fox, Natalie S, Fraser, Michael, Frazer, Scott, Frenkel-Morgenstern, Milana, Friedman, William, Frigola, Joan, Fronick, Catrina C, Fujimoto, Akihiro, Fujita, Masashi, Fukayama, Masashi, Fulton, Lucinda A, Fulton, Robert S, Furuta, Mayuko, Futreal, P Andrew, Füllgrabe, Anja, Gabriel, Stacey B, Gallinger, Steven, Gambacorti-Passerini, Carlo, Gao, Jianjiong, Gao, Shengjie, Garred, Øystein, Garrison, Erik, Garsed, Dale W, Gehlenborg, Nils, Gelpi, Josep LL, George, Joshy, Gerhard, Daniela S, Gerhauser, Clarissa, Gershenwald, Jeffrey E, Gerstein, Mark, Gerstung, Moritz, Ghori, Mohammed, Ghossein, Ronald, Giama, Nasra H, Gibbs, 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Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
In cancer, the primary tumour’s organ of origin and histopathology are the strongest determinants of its clinical behaviour, but in 3% of cases a patient presents with a metastatic tumour and no obvious primary. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we train a deep learning classifier to predict cancer type based on patterns of somatic passenger mutations detected in whole genome sequencing (WGS) of 2606 tumours representing 24 common cancer types produced by the PCAWG Consortium. Our classifier achieves an accuracy of 91% on held-out tumor samples and 88% and 83% respectively on independent primary and metastatic samples, roughly double the accuracy of trained pathologists when presented with a metastatic tumour without knowledge of the primary. Surprisingly, adding information on driver mutations reduced accuracy. Our results have clinical applicability, underscore how patterns of somatic passenger mutations encode the state of the cell of origin, and can inform future strategies to detect the source of circulating tumour DNA.
- Published
- 2023
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34. Combined burden and functional impact tests for cancer driver discovery using DriverPower
- Author
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
The discovery of driver mutations is one of the key motivations for cancer genome sequencing. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we describe DriverPower, a software package that uses mutational burden and functional impact evidence to identify driver mutations in coding and non-coding sites within cancer whole genomes. Using a total of 1373 genomic features derived from public sources, DriverPower’s background mutation model explains up to 93% of the regional variance in the mutation rate across multiple tumour types. By incorporating functional impact scores, we are able to further increase the accuracy of driver discovery. Testing across a collection of 2583 cancer genomes from the PCAWG project, DriverPower identifies 217 coding and 95 non-coding driver candidates. Comparing to six published methods used by the PCAWG Drivers and Functional Interpretation Working Group, DriverPower has the highest F1 score for both coding and non-coding driver discovery. This demonstrates that DriverPower is an effective framework for computational driver discovery.
- Published
- 2023
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35. Integrative pathway enrichment analysis of multivariate omics data
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Paczkowska, Marta, Barenboim, Jonathan, Sintupisut, Nardnisa, Fox, Natalie S, Zhu, Helen, Abd-Rabbo, Diala, Mee, Miles W, Boutros, Paul C, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Gonzalez-Perez, Abel, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, 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Vijver, Marc J, and Veer, L van’t
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Multi-omics datasets represent distinct aspects of the central dogma of molecular biology. Such high-dimensional molecular profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple datasets using statistical data fusion, rationalizes contributing evidence and highlights associated genes. As part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumor types, we integrated genes with coding and non-coding mutations and revealed frequently mutated pathways and additional cancer genes with infrequent mutations. We also analyzed prognostic molecular pathways by integrating genomic and transcriptomic features of 1780 breast cancers and highlighted associations with immune response and anti-apoptotic signaling. Integration of ChIP-seq and RNA-seq data for master regulators of the Hippo pathway across normal human tissues identified processes of tissue regeneration and stem cell regulation. ActivePathways is a versatile method that improves systems-level understanding of cellular organization in health and disease through integration of multiple molecular datasets and pathway annotations.
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- 2023
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36. Pathway and network analysis of more than 2500 whole cancer genomes
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
The catalog of cancer driver mutations in protein-coding genes has greatly expanded in the past decade. However, non-coding cancer driver mutations are less well-characterized and only a handful of recurrent non-coding mutations, most notably TERT promoter mutations, have been reported. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancer across 38 tumor types, we perform multi-faceted pathway and network analyses of non-coding mutations across 2583 whole cancer genomes from 27 tumor types compiled by the ICGC/TCGA PCAWG project that was motivated by the success of pathway and network analyses in prioritizing rare mutations in protein-coding genes. While few non-coding genomic elements are recurrently mutated in this cohort, we identify 93 genes harboring non-coding mutations that cluster into several modules of interacting proteins. Among these are promoter mutations associated with reduced mRNA expression in TP53, TLE4, and TCF4. We find that biological processes had variable proportions of coding and non-coding mutations, with chromatin remodeling and proliferation pathways altered primarily by coding mutations, while developmental pathways, including Wnt and Notch, altered by both coding and non-coding mutations. RNA splicing is primarily altered by non-coding mutations in this cohort, and samples containing non-coding mutations in well-known RNA splicing factors exhibit similar gene expression signatures as samples with coding mutations in these genes. These analyses contribute a new repertoire of possible cancer genes and mechanisms that are altered by non-coding mutations and offer insights into additional cancer vulnerabilities that can be investigated for potential therapeutic treatments.
- Published
- 2023
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37. Divergent mutational processes distinguish hypoxic and normoxic tumours
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.
- Published
- 2023
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38. Genomic footprints of activated telomere maintenance mechanisms in cancer
- Author
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Sieverling, Lina, Hong, Chen, Koser, Sandra D, Ginsbach, Philip, Kleinheinz, Kortine, Hutter, Barbara, Braun, Delia M, Cortés-Ciriano, Isidro, Xi, Ruibin, Kabbe, Rolf, Park, Peter J, Eils, Roland, Schlesner, Matthias, Akdemir, Kadir C, Alvarez, Eva G, Baez-Ortega, Adrian, Beroukhim, Rameen, Boutros, Paul C, Bowtell, David DL, Brors, Benedikt, Burns, Kathleen H, Campbell, Peter J, Chan, Kin, Chen, Ken, Dueso-Barroso, Ana, Dunford, Andrew J, Edwards, Paul A, Estivill, Xavier, Etemadmoghadam, Dariush, Feuerbach, Lars, Fink, J Lynn, Frenkel-Morgenstern, Milana, Garsed, Dale W, Gerstein, Mark, Gordenin, Dmitry A, Haan, David, Haber, James E, Hess, Julian M, Imielinski, Marcin, Jones, David TW, Ju, Young Seok, Kazanov, Marat D, Klimczak, Leszek J, Koh, Youngil, Korbel, Jan O, Kumar, Kiran, Lee, Eunjung Alice, Lee, Jake June-Koo, Li, Yilong, Lynch, Andy G, Macintyre, Geoff, Markowetz, Florian, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Meyerson, Matthew, Miyano, Satoru, Nakagawa, 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Staaf, Johan, Stadler, Peter F, Staib, Peter, Stark, Stefan G, Stebbings, Lucy, Stefánsson, Ólafur Andri, Stegle, Oliver, Stein, Lincoln D, Stenhouse, Alasdair, Stilgenbauer, Stephan, Stobbe, Miranda D, Stratton, Michael R, Stretch, Jonathan R, Struck, Adam J, Stuart, Joshua M, Stunnenberg, Henk G, Su, Hong, Su, Xiaoping, Sun, Ren X, Sungalee, Stephanie, Susak, Hana, Suzuki, Akihiro, Sweep, Fred, Szczepanowski, Monika, Sültmann, Holger, Yugawa, Takashi, Tam, Angela, Tamborero, David, Tan, Benita Kiat Tee, Tan, Donghui, Tan, Patrick, Tanaka, Hiroko, Taniguchi, Hirokazu, Tanskanen, Tomas J, Tarabichi, Maxime, Tarnuzzer, Roy, Tarpey, Patrick, Taschuk, Morgan L, Tatsuno, Kenji, Tavaré, Simon, Taylor, Darrin F, Taylor-Weiner, Amaro, Teague, Jon W, Teh, Bin Tean, Tembe, Varsha, Temes, Javier, Thai, Kevin, Thayer, Sarah P, Thiessen, Nina, Thomas, Gilles, Thomas, Sarah, Thompson, Alan, Thompson, Alastair M, Thompson, John FF, Thompson, R Houston, Thorne, Heather, Thorne, Leigh B, Thorogood, Adrian, Tiao, Grace, Tijanic, Nebojsa, Timms, Lee E, Tirabosco, Roberto, Tojo, Marta, Tommasi, Stefania, Toon, Christopher W, Toprak, Umut H, Tortora, Giampaolo, Tost, Jörg, Totoki, Yasushi, Townend, David, Traficante, Nadia, Treilleux, Isabelle, Trotta, Jean-Rémi, Trümper, Lorenz HP, Tsao, Ming, Tsunoda, Tatsuhiko, Tucker, Olga, Turkington, Richard, Turner, Daniel J, Tutt, Andrew, Ueno, Masaki, Ueno, Naoto T, Umbricht, Christopher, Umer, Husen M, Underwood, Timothy J, Urban, Lara, Urushidate, Tomoko, Ushiku, Tetsuo, Uusküla-Reimand, Liis, Valencia, Alfonso, Van Den Berg, David J, Van Laere, Steven, Van Loo, Peter, Van Meir, Erwin G, Van den Eynden, Gert G, Van der Kwast, Theodorus, Vasudev, Naveen, Vazquez, Miguel, Vedururu, Ravikiran, Veluvolu, Umadevi, Vembu, Shankar, Verbeke, Lieven PC, Vermeulen, Peter, Verrill, Clare, Viari, Alain, Vicente, David, Vicentini, Caterina, VijayRaghavan, K, Viksna, Juris, Vilain, Ricardo E, Vincent-Salomon, Anne, Visakorpi, Tapio, Voet, Douglas, Vyas, Paresh, Vázquez-García, Ignacio, Waddell, Nick M, Wadelius, Claes, Wadi, Lina, Wagener, Rabea, Wang, Jian, Wang, Jiayin, Wang, Linghua, Wang, Qi, Wang, Wenyi, Wang, Yumeng, Wang, Zhining, Waring, Paul M, Warnatz, Hans-Jörg, Warrell, Jonathan, Warren, Anne Y, Waszak, Sebastian M, Wedge, David C, Weichenhan, Dieter, Weinberger, Paul, Weinstein, John N, Weisenberger, Daniel J, Welch, Ian, Wendl, Michael C, Werner, Johannes, Whalley, Justin P, Wheeler, David A, Whitaker, Hayley C, Wigle, Dennis, Wilkerson, Matthew D, Williams, Ashley, Wilmott, James S, Wilson, Gavin W, Wilson, Julie M, Wilson, Richard K, Winterhoff, Boris, Wintersinger, Jeffrey A, Wiznerowicz, Maciej, Wolf, Stephan, Wong, Bernice H, Wong, Tina, Wong, Winghing, Woo, Youngchoon, Wood, Scott, Wouters, Bradly G, Wright, Adam J, Wright, Derek W, Wright, Mark H, Wu, Chin-Lee, Wu, Dai-Ying, Wu, Guanming, Wu, Jianmin, Wu, Kui, Wu, Yang, Wu, Zhenggang, Xi, Liu, Xia, Tian, Xiang, Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
- Subjects
Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Cancers require telomere maintenance mechanisms for unlimited replicative potential. They achieve this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we dissect whole-genome sequencing data of over 2500 matched tumor-control samples from 36 different tumor types aggregated within the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium to characterize the genomic footprints of these mechanisms. While the telomere content of tumors with ATRX or DAXX mutations (ATRX/DAXXtrunc) is increased, tumors with TERT modifications show a moderate decrease of telomere content. One quarter of all tumor samples contain somatic integrations of telomeric sequences into non-telomeric DNA. This fraction is increased to 80% prevalence in ATRX/DAXXtrunc tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker. The latter feature includes enrichment or depletion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively. Our systematic analysis provides new insight into the recurrent genomic alterations associated with telomere maintenance mechanisms in cancer.
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- 2023
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39. The Role of 5-HT2C Polymorphisms in Behavioral and Psychological Symptoms of Alzheimer Disease
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Pritchard, Antonia, Di Giovanni, Giuseppe, editor, Esposito, Ennio, editor, and Di Matteo, Vincenzo, editor
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- 2011
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40. Comparative Genomics Provides Etiologic and Biological Insight into Melanoma Subtypes
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Newell, Felicity, primary, Johansson, Peter A., additional, Wilmott, James S., additional, Nones, Katia, additional, Lakis, Vanessa, additional, Pritchard, Antonia L., additional, Lo, Serigne N., additional, Rawson, Robert V., additional, Kazakoff, Stephen H., additional, Colebatch, Andrew J., additional, Koufariotis, Lambros T., additional, Ferguson, Peter M., additional, Wood, Scott, additional, Leonard, Conrad, additional, Law, Matthew H., additional, Brooks, Kelly M., additional, Broit, Natasa, additional, Palmer, Jane M., additional, Couts, Kasey L., additional, Vergara, Ismael A., additional, Long, Georgina V., additional, Barbour, Andrew P., additional, Nieweg, Omgo E., additional, Shivalingam, Brindha, additional, Robinson, William A., additional, Stretch, Jonathan R., additional, Spillane, Andrew J., additional, Saw, Robyn P.M., additional, Shannon, Kerwin F., additional, Thompson, John F., additional, Mann, Graham J., additional, Pearson, John V., additional, Scolyer, Richard A., additional, Waddell, Nicola, additional, and Hayward, Nicholas K., additional
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- 2022
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41. POLE mutations in families predisposed to cutaneous melanoma
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Aoude, Lauren G., Heitzer, Ellen, Johansson, Peter, Gartside, Michael, Wadt, Karin, Pritchard, Antonia L., Palmer, Jane M., Symmons, Judith, Gerdes, Anne-Marie, Montgomery, Grant W., Martin, Nicholas G., Tomlinson, Ian, Kearsey, Stephen, and Hayward, Nicholas K.
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- 2015
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42. Medical and Surgical Care of Patients With Mesothelioma and Their Relatives Carrying Germline BAP1 Mutations
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Carbone, Michele, primary, Pass, Harvey I., additional, Ak, Guntulu, additional, Alexander, H. Richard, additional, Baas, Paul, additional, Baumann, Francine, additional, Blakely, Andrew M., additional, Bueno, Raphael, additional, Bzura, Aleksandra, additional, Cardillo, Giuseppe, additional, Churpek, Jane E., additional, Dianzani, Irma, additional, De Rienzo, Assunta, additional, Emi, Mitsuru, additional, Emri, Salih, additional, Felley-Bosco, Emanuela, additional, Fennell, Dean A., additional, Flores, Raja M., additional, Grosso, Federica, additional, Hayward, Nicholas K., additional, Hesdorffer, Mary, additional, Hoang, Chuong D., additional, Johansson, Peter A., additional, Kindler, Hedy L., additional, Kittaneh, Muaiad, additional, Krausz, Thomas, additional, Mansfield, Aaron, additional, Metintas, Muzaffer, additional, Minaai, Michael, additional, Mutti, Luciano, additional, Nielsen, Maartje, additional, O’Byrne, Kenneth, additional, Opitz, Isabelle, additional, Pastorino, Sandra, additional, Pentimalli, Francesca, additional, de Perrot, Marc, additional, Pritchard, Antonia, additional, Ripley, Robert Taylor, additional, Robinson, Bruce, additional, Rusch, Valerie, additional, Taioli, Emanuela, additional, Takinishi, Yasutaka, additional, Tanji, Mika, additional, Tsao, Anne S., additional, Tuncer, A. Murat, additional, Walpole, Sebastian, additional, Wolf, Andrea, additional, Yang, Haining, additional, Yoshikawa, Yoshie, additional, Zolondick, Alicia, additional, Schrump, David S., additional, and Hassan, Raffit, additional
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- 2022
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43. Medical and Surgical Care of Patients With Mesothelioma and Their Relatives Carrying Germline BAP1 Mutations
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Carbone, Michele, Pass, Harvey I., Ak, Guntulu, Alexander, H. Richard, Baas, Paul, Baumann, Francine, Blakely, Andrew M., Bueno, Raphael, Bzura, Aleksandra, Cardillo, Giuseppe, Churpek, Jane E., Dianzani, Irma, De Rienzo, Assunta, Emi, Mitsuru, Emri, Salih, Felley-Bosco, Emanuela, Fennell, Dean A., Flores, Raja M., Grosso, Federica, Hayward, Nicholas K., Hesdorffer, Mary, Hoang, Chuong D., Johansson, Peter A., Kindler, Hedy L., Kittaneh, Muaiad, Krausz, Thomas, Mansfield, Aaron, Metintas, Muzaffer, Minaai, Michael, Mutti, Luciano, Nielsen, Maartje, O'Byrne, Kenneth, Opitz, Isabelle, Pastorino, Sandra, Pentimalli, Francesca, de Perrot, Marc, Pritchard, Antonia, Ripley, Robert Taylor, Robinson, Bruce, Rusch, Valerie, Taioli, Emanuela, Takinishi, Yasutaka, Tanji, Mika, Tsao, Anne S., Tuncer, A. Murat, Walpole, Sebastian, Wolf, Andrea, Yang, Haining, Yoshikawa, Yoshie, Zolondick, Alicia, Schrump, David S., Hassan, Raffit, Carbone, Michele, Pass, Harvey I., Ak, Guntulu, Alexander, H. Richard, Baas, Paul, Baumann, Francine, Blakely, Andrew M., Bueno, Raphael, Bzura, Aleksandra, Cardillo, Giuseppe, Churpek, Jane E., Dianzani, Irma, De Rienzo, Assunta, Emi, Mitsuru, Emri, Salih, Felley-Bosco, Emanuela, Fennell, Dean A., Flores, Raja M., Grosso, Federica, Hayward, Nicholas K., Hesdorffer, Mary, Hoang, Chuong D., Johansson, Peter A., Kindler, Hedy L., Kittaneh, Muaiad, Krausz, Thomas, Mansfield, Aaron, Metintas, Muzaffer, Minaai, Michael, Mutti, Luciano, Nielsen, Maartje, O'Byrne, Kenneth, Opitz, Isabelle, Pastorino, Sandra, Pentimalli, Francesca, de Perrot, Marc, Pritchard, Antonia, Ripley, Robert Taylor, Robinson, Bruce, Rusch, Valerie, Taioli, Emanuela, Takinishi, Yasutaka, Tanji, Mika, Tsao, Anne S., Tuncer, A. Murat, Walpole, Sebastian, Wolf, Andrea, Yang, Haining, Yoshikawa, Yoshie, Zolondick, Alicia, Schrump, David S., and Hassan, Raffit
- Abstract
The most common malignancies that develop in carriers of BAP1 germline mutations include diffuse malignant mesothelioma, uveal and cutaneous melanoma, renal cell carcinoma, and less frequently, breast cancer, several types of skin carcinomas, and other tumor types. Mesotheliomas in these patients are significantly less aggressive, and patients require a multidisciplinary approach that involves genetic counseling, medical genetics, pathology, surgical, medical, and radiation oncology expertise. Some BAP1 carriers have asymptomatic mesothelioma that can be followed by close clinical observation without apparent adverse outcomes: they may survive many years without therapy. Others may grow aggressively but very often respond to therapy. Detecting BAP1 germline mutations has, therefore, substantial medical, social, and economic impact. Close monitoring of these patients and their relatives is expected to result in prolonged life expectancy, improved quality of life, and being cost-effective. The co-authors of this paper are those who have published the vast majority of cases of mesothelioma occurring in patients carrying inactivating germline BAP1 mutations and who have studied the families affected by the BAP1 cancer syndrome for many years. This paper reports our experience. It is intended to be a source of information for all physicians who care for patients carrying germline BAP1 mutations. We discuss the clinical presentation, diagnostic and treatment challenges, and our recommendations of how to best care for these patients and their family members, including the potential economic and psychosocial impact.
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- 2022
44. Mutation load in melanoma is affected by MC1R genotype
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Johansson, Peter A., Pritchard, Antonia L., Patch, Ann‐Marie, Wilmott, James S., Pearson, John V., Waddell, Nicola, Scolyer, Richard A., Mann, Graham J., and Hayward, Nicholas K.
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- 2017
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45. Correction to: Prolonged stable disease in a uveal melanoma patient with germline MBD4 nonsense mutation treated with pembrolizumab and ipilimumab
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Johansson, Peter A., Stark, Andrew, Palmer, Jane M., Bigby, Kieron, Brooks, Kelly, Rolfe, Olivia, Pritchard, Antonia L., Whitehead, Kevin, Warrier, Sunil, Glasson, William, and Hayward, Nicholas K.
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- 2019
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46. Systematic review and meta‐analysis of genomic alterations in acral melanoma
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Broit, Natasa, primary, Johansson, Peter A., additional, Rodgers, Chloe B., additional, Walpole, Sebastian T., additional, Hayward, Nicholas K., additional, and Pritchard, Antonia L., additional
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- 2022
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47. A B‐cell or a key player? The different roles of B‐cells and antibodies in melanoma
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Rodgers, Chloe B., primary, Mustard, Colette J., additional, McLean, Ryan T., additional, Hutchison, Sharon, additional, and Pritchard, Antonia L., additional
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- 2022
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48. Nonsense Mutations in the Shelterin Complex Genes ACD and TERF2IP in Familial Melanoma
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Aoude, Lauren G., Pritchard, Antonia L., Robles-Espinoza, Carla Daniela, Wadt, Karin, Harland, Mark, Choi, Jiyeon, Gartside, Michael, Quesada, Víctor, Johansson, Peter, Palmer, Jane M., Ramsay, Andrew J., Zhang, Xijun, Jones, Kristine, Symmons, Judith, Holland, Elizabeth A., Schmid, Helen, Bonazzi, Vanessa, Woods, Susan, Dutton-Regester, Ken, Stark, Mitchell S., Snowden, Helen, van Doorn, Remco, Montgomery, Grant W., Martin, Nicholas G., Keane, Thomas M., López-Otín, Carlos, Gerdes, Anne-Marie, Olsson, Håkan, Ingvar, Christian, Borg, Åke, Gruis, Nelleke A., Trent, Jeffrey M., Jönsson, Göran, Bishop, D. Timothy, Mann, Graham J., Newton-Bishop, Julia A., Brown, Kevin M., Adams, David J., and Hayward, Nicholas K.
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- 2015
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49. Exploration of peptides bound to MHC class I molecules in melanoma
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Pritchard, Antonia L., Hastie, Marcus L., Neller, Michelle, Gorman, Jeffrey J., Schmidt, Chris W., and Hayward, Nicholas K.
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- 2015
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50. Genetics of familial melanoma: 20 years after CDKN2A
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Aoude, Lauren G., Wadt, Karin A. W., Pritchard, Antonia L., and Hayward, Nicholas K.
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- 2015
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