[{"article_processing_charge":"No","has_accepted_license":"1","day":"07","scopus_import":"1","date_published":"2018-02-07T00:00:00Z","citation":{"chicago":"Reiter, Johannes, Christian Hilbe, David Rand, Krishnendu Chatterjee, and Martin Nowak. “Crosstalk in Concurrent Repeated Games Impedes Direct Reciprocity and Requires Stronger Levels of Forgiveness.” Nature Communications. Nature Publishing Group, 2018. https://doi.org/10.1038/s41467-017-02721-8.","mla":"Reiter, Johannes, et al. “Crosstalk in Concurrent Repeated Games Impedes Direct Reciprocity and Requires Stronger Levels of Forgiveness.” Nature Communications, vol. 9, no. 1, 555, Nature Publishing Group, 2018, doi:10.1038/s41467-017-02721-8.","short":"J. Reiter, C. Hilbe, D. Rand, K. Chatterjee, M. Nowak, Nature Communications 9 (2018).","ista":"Reiter J, Hilbe C, Rand D, Chatterjee K, Nowak M. 2018. Crosstalk in concurrent repeated games impedes direct reciprocity and requires stronger levels of forgiveness. Nature Communications. 9(1), 555.","apa":"Reiter, J., Hilbe, C., Rand, D., Chatterjee, K., & Nowak, M. (2018). Crosstalk in concurrent repeated games impedes direct reciprocity and requires stronger levels of forgiveness. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-02721-8","ieee":"J. Reiter, C. Hilbe, D. Rand, K. Chatterjee, and M. Nowak, “Crosstalk in concurrent repeated games impedes direct reciprocity and requires stronger levels of forgiveness,” Nature Communications, vol. 9, no. 1. Nature Publishing Group, 2018.","ama":"Reiter J, Hilbe C, Rand D, Chatterjee K, Nowak M. Crosstalk in concurrent repeated games impedes direct reciprocity and requires stronger levels of forgiveness. Nature Communications. 2018;9(1). doi:10.1038/s41467-017-02721-8"},"publication":"Nature Communications","issue":"1","abstract":[{"lang":"eng","text":"Direct reciprocity is a mechanism for cooperation among humans. Many of our daily interactions are repeated. We interact repeatedly with our family, friends, colleagues, members of the local and even global community. In the theory of repeated games, it is a tacit assumption that the various games that a person plays simultaneously have no effect on each other. Here we introduce a general framework that allows us to analyze “crosstalk” between a player’s concurrent games. In the presence of crosstalk, the action a person experiences in one game can alter the person’s decision in another. We find that crosstalk impedes the maintenance of cooperation and requires stronger levels of forgiveness. The magnitude of the effect depends on the population structure. In more densely connected social groups, crosstalk has a stronger effect. A harsh retaliator, such as Tit-for-Tat, is unable to counteract crosstalk. The crosstalk framework provides a unified interpretation of direct and upstream reciprocity in the context of repeated games."}],"type":"journal_article","file":[{"date_updated":"2020-07-14T12:46:31Z","date_created":"2018-12-12T10:09:18Z","checksum":"b6b90367545b4c615891c960ab0567f1","file_id":"4741","relation":"main_file","creator":"system","content_type":"application/pdf","file_size":843646,"file_name":"IST-2018-964-v1+1_2018_Hilbe_Crosstalk_in.pdf","access_level":"open_access"}],"oa_version":"Published Version","pubrep_id":"964","intvolume":" 9","title":"Crosstalk in concurrent repeated games impedes direct reciprocity and requires stronger levels of forgiveness","status":"public","ddc":["004"],"_id":"454","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"02","language":[{"iso":"eng"}],"doi":"10.1038/s41467-017-02721-8","project":[{"call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307"},{"call_identifier":"FWF","name":"Modern Graph Algorithmic Techniques in Formal Verification","grant_number":"P 23499-N23","_id":"2584A770-B435-11E9-9278-68D0E5697425"},{"name":"Game Theory","call_identifier":"FWF","_id":"25863FF4-B435-11E9-9278-68D0E5697425","grant_number":"S11407"},{"call_identifier":"FP7","name":"International IST Postdoc Fellowship Programme","grant_number":"291734","_id":"25681D80-B435-11E9-9278-68D0E5697425"}],"isi":1,"quality_controlled":"1","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"external_id":{"isi":["000424318200001"]},"publist_id":"7368","ec_funded":1,"file_date_updated":"2020-07-14T12:46:31Z","article_number":"555","volume":9,"date_created":"2018-12-11T11:46:34Z","date_updated":"2023-09-11T12:51:03Z","author":[{"id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","first_name":"Johannes","last_name":"Reiter","full_name":"Reiter, Johannes"},{"last_name":"Hilbe","first_name":"Christian","orcid":"0000-0001-5116-955X","id":"2FDF8F3C-F248-11E8-B48F-1D18A9856A87","full_name":"Hilbe, Christian"},{"first_name":"David","last_name":"Rand","full_name":"Rand, David"},{"last_name":"Chatterjee","first_name":"Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","full_name":"Chatterjee, Krishnendu"},{"full_name":"Nowak, Martin","first_name":"Martin","last_name":"Nowak"}],"department":[{"_id":"KrCh"}],"publisher":"Nature Publishing Group","publication_status":"published","acknowledgement":"This work was supported by the European Research Council (ERC) start grant 279307: Graph Games (C.K.), Austrian Science Fund (FWF) grant no P23499-N23 (C.K.), FWF\r\nNFN grant no S11407-N23 RiSE/SHiNE (C.K.), Office of Naval Research grant N00014-16-1-2914 (M.A.N.), National Cancer Institute grant CA179991 (M.A.N.) and by the John Templeton Foundation. J.G.R. is supported by an Erwin Schrödinger fellowship\r\n(Austrian Science Fund FWF J-3996). C.H. acknowledges generous support from the\r\nISTFELLOW program. The Program for Evolutionary Dynamics is supported in part by\r\na gift from B Wu and Eric Larson.","year":"2018"},{"file_date_updated":"2020-07-14T12:47:33Z","ec_funded":1,"publist_id":"7092","author":[{"full_name":"Makohon Moore, Alvin","last_name":"Makohon Moore","first_name":"Alvin"},{"full_name":"Zhang, Ming","last_name":"Zhang","first_name":"Ming"},{"first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","full_name":"Reiter, Johannes"},{"last_name":"Božić","first_name":"Ivana","full_name":"Božić, Ivana"},{"full_name":"Allen, Benjamin","first_name":"Benjamin","last_name":"Allen"},{"full_name":"Kundu, Deepanjan","id":"1d4c0f4f-e8a3-11ec-a351-e36772758c45","last_name":"Kundu","first_name":"Deepanjan"},{"full_name":"Chatterjee, Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","last_name":"Chatterjee","first_name":"Krishnendu"},{"first_name":"Fay","last_name":"Wong","full_name":"Wong, Fay"},{"full_name":"Jiao, Yuchen","first_name":"Yuchen","last_name":"Jiao"},{"last_name":"Kohutek","first_name":"Zachary","full_name":"Kohutek, Zachary"},{"full_name":"Hong, Jungeui","last_name":"Hong","first_name":"Jungeui"},{"last_name":"Attiyeh","first_name":"Marc","full_name":"Attiyeh, Marc"},{"first_name":"Breanna","last_name":"Javier","full_name":"Javier, Breanna"},{"first_name":"Laura","last_name":"Wood","full_name":"Wood, Laura"},{"full_name":"Hruban, Ralph","last_name":"Hruban","first_name":"Ralph"},{"first_name":"Martin","last_name":"Nowak","full_name":"Nowak, Martin"},{"full_name":"Papadopoulos, Nickolas","last_name":"Papadopoulos","first_name":"Nickolas"},{"full_name":"Kinzler, Kenneth","last_name":"Kinzler","first_name":"Kenneth"},{"full_name":"Vogelstein, Bert","last_name":"Vogelstein","first_name":"Bert"},{"full_name":"Iacobuzio Donahue, Christine","first_name":"Christine","last_name":"Iacobuzio Donahue"}],"date_created":"2018-12-11T11:47:43Z","date_updated":"2022-06-10T09:55:08Z","volume":49,"year":"2017","acknowledgement":"We thank the Memorial Sloan Kettering Cancer Center Molecular Cytology core facility for immunohistochemistry staining. This work was supported by Office of Naval Research grant N00014-16-1-2914, the Bill and Melinda Gates Foundation (OPP1148627), and a gift from B. Wu and E. Larson (M.A.N.), National Institutes of Health grants CA179991 (C.A.I.-D. and I.B.), F31 CA180682 (A.P.M.-M.), CA43460 (B.V.), and P50 CA62924, the Monastra Foundation, the Virginia and D.K. Ludwig Fund for Cancer Research, the Lustgarten Foundation for Pancreatic Cancer Research, the Sol Goldman Center for Pancreatic Cancer Research, the Sol Goldman Sequencing Center, ERC Start grant 279307: Graph Games (J.G.R., D.K., and C.K.), Austrian Science Fund (FWF) grant P23499-N23 (J.G.R., D.K., and C.K.), and FWF NFN grant S11407-N23 RiSE/SHiNE (J.G.R., D.K., and C.K.).","pmid":1,"publication_status":"published","publisher":"Nature Publishing Group","department":[{"_id":"KrCh"}],"month":"03","publication_identifier":{"issn":["10614036"]},"doi":"10.1038/ng.3764","language":[{"iso":"eng"}],"oa":1,"external_id":{"pmid":["28092682"]},"quality_controlled":"1","project":[{"grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425","name":"Quantitative Graph Games: Theory and Applications","call_identifier":"FP7"},{"call_identifier":"FWF","name":"Modern Graph Algorithmic Techniques in Formal Verification","_id":"2584A770-B435-11E9-9278-68D0E5697425","grant_number":"P 23499-N23"},{"call_identifier":"FWF","name":"Game Theory","grant_number":"S11407","_id":"25863FF4-B435-11E9-9278-68D0E5697425"}],"abstract":[{"text":"The extent of heterogeneity among driver gene mutations present in naturally occurring metastases - that is, treatment-naive metastatic disease - is largely unknown. To address this issue, we carried out 60× whole-genome sequencing of 26 metastases from four patients with pancreatic cancer. We found that identical mutations in known driver genes were present in every metastatic lesion for each patient studied. Passenger gene mutations, which do not have known or predicted functional consequences, accounted for all intratumoral heterogeneity. Even with respect to these passenger mutations, our analysis suggests that the genetic similarity among the founding cells of metastases was higher than that expected for any two cells randomly taken from a normal tissue. The uniformity of known driver gene mutations among metastases in the same patient has critical and encouraging implications for the success of future targeted therapies in advanced-stage disease.","lang":"eng"}],"issue":"3","type":"journal_article","file":[{"checksum":"e442dc3b7420a36ec805e9bb45cc1a2e","date_created":"2019-11-19T08:13:50Z","date_updated":"2020-07-14T12:47:33Z","relation":"main_file","file_id":"7050","file_size":908099,"content_type":"application/pdf","creator":"dernst","access_level":"open_access","file_name":"2017_NatureGenetics_Makohon.pdf"}],"oa_version":"Submitted Version","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"653","ddc":["000"],"title":"Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer","status":"public","intvolume":" 49","day":"01","article_processing_charge":"No","has_accepted_license":"1","scopus_import":"1","date_published":"2017-03-01T00:00:00Z","publication":"Nature Genetics","citation":{"short":"A. Makohon Moore, M. Zhang, J. Reiter, I. Božić, B. Allen, D. Kundu, K. Chatterjee, F. Wong, Y. Jiao, Z. Kohutek, J. Hong, M. Attiyeh, B. Javier, L. Wood, R. Hruban, M. Nowak, N. Papadopoulos, K. Kinzler, B. Vogelstein, C. Iacobuzio Donahue, Nature Genetics 49 (2017) 358–366.","mla":"Makohon Moore, Alvin, et al. “Limited Heterogeneity of Known Driver Gene Mutations among the Metastases of Individual Patients with Pancreatic Cancer.” Nature Genetics, vol. 49, no. 3, Nature Publishing Group, 2017, pp. 358–66, doi:10.1038/ng.3764.","chicago":"Makohon Moore, Alvin, Ming Zhang, Johannes Reiter, Ivana Božić, Benjamin Allen, Deepanjan Kundu, Krishnendu Chatterjee, et al. “Limited Heterogeneity of Known Driver Gene Mutations among the Metastases of Individual Patients with Pancreatic Cancer.” Nature Genetics. Nature Publishing Group, 2017. https://doi.org/10.1038/ng.3764.","ama":"Makohon Moore A, Zhang M, Reiter J, et al. Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. 2017;49(3):358-366. doi:10.1038/ng.3764","apa":"Makohon Moore, A., Zhang, M., Reiter, J., Božić, I., Allen, B., Kundu, D., … Iacobuzio Donahue, C. (2017). Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. Nature Publishing Group. https://doi.org/10.1038/ng.3764","ieee":"A. Makohon Moore et al., “Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer,” Nature Genetics, vol. 49, no. 3. Nature Publishing Group, pp. 358–366, 2017.","ista":"Makohon Moore A, Zhang M, Reiter J, Božić I, Allen B, Kundu D, Chatterjee K, Wong F, Jiao Y, Kohutek Z, Hong J, Attiyeh M, Javier B, Wood L, Hruban R, Nowak M, Papadopoulos N, Kinzler K, Vogelstein B, Iacobuzio Donahue C. 2017. Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. 49(3), 358–366."},"article_type":"original","page":"358 - 366"},{"publist_id":"6301","ec_funded":1,"file_date_updated":"2018-12-12T10:15:15Z","article_number":"14114","volume":8,"date_created":"2018-12-11T11:50:02Z","date_updated":"2023-09-20T11:55:31Z","author":[{"first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","full_name":"Reiter, Johannes"},{"first_name":"Alvin","last_name":"Makohon Moore","full_name":"Makohon Moore, Alvin"},{"last_name":"Gerold","first_name":"Jeffrey","full_name":"Gerold, Jeffrey"},{"first_name":"Ivana","last_name":"Božić","full_name":"Božić, Ivana"},{"id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","first_name":"Krishnendu","last_name":"Chatterjee","full_name":"Chatterjee, Krishnendu"},{"full_name":"Iacobuzio Donahue, Christine","first_name":"Christine","last_name":"Iacobuzio Donahue"},{"full_name":"Vogelstein, Bert","last_name":"Vogelstein","first_name":"Bert"},{"first_name":"Martin","last_name":"Nowak","full_name":"Nowak, Martin"}],"department":[{"_id":"KrCh"}],"publisher":"Nature Publishing Group","publication_status":"published","year":"2017","publication_identifier":{"issn":["20411723"]},"month":"01","language":[{"iso":"eng"}],"doi":"10.1038/ncomms14114","project":[{"call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307"},{"grant_number":"P 23499-N23","_id":"2584A770-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Modern Graph Algorithmic Techniques in Formal Verification"},{"_id":"25863FF4-B435-11E9-9278-68D0E5697425","grant_number":"S11407","call_identifier":"FWF","name":"Game Theory"}],"isi":1,"quality_controlled":"1","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"external_id":{"isi":["000393096600001"]},"abstract":[{"text":"Reconstructing the evolutionary history of metastases is critical for understanding their basic biological principles and has profound clinical implications. Genome-wide sequencing data has enabled modern phylogenomic methods to accurately dissect subclones and their phylogenies from noisy and impure bulk tumour samples at unprecedented depth. However, existing methods are not designed to infer metastatic seeding patterns. Here we develop a tool, called Treeomics, to reconstruct the phylogeny of metastases and map subclones to their anatomic locations. Treeomics infers comprehensive seeding patterns for pancreatic, ovarian, and prostate cancers. Moreover, Treeomics correctly disambiguates true seeding patterns from sequencing artifacts; 7% of variants were misclassified by conventional statistical methods. These artifacts can skew phylogenies by creating illusory tumour heterogeneity among distinct samples. In silico benchmarking on simulated tumour phylogenies across a wide range of sample purities (15–95%) and sequencing depths (25-800 × ) demonstrates the accuracy of Treeomics compared with existing methods.","lang":"eng"}],"type":"journal_article","file":[{"creator":"system","content_type":"application/pdf","file_size":897050,"access_level":"open_access","file_name":"IST-2017-786-v1+1_ncomms14114.pdf","date_updated":"2018-12-12T10:15:15Z","date_created":"2018-12-12T10:15:15Z","file_id":"5133","relation":"main_file"}],"oa_version":"Published Version","pubrep_id":"786","intvolume":" 8","ddc":["004","006"],"status":"public","title":"Reconstructing metastatic seeding patterns of human cancers","_id":"1080","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","has_accepted_license":"1","article_processing_charge":"No","day":"31","scopus_import":"1","date_published":"2017-01-31T00:00:00Z","citation":{"chicago":"Reiter, Johannes, Alvin Makohon Moore, Jeffrey Gerold, Ivana Božić, Krishnendu Chatterjee, Christine Iacobuzio Donahue, Bert Vogelstein, and Martin Nowak. “Reconstructing Metastatic Seeding Patterns of Human Cancers.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14114.","short":"J. Reiter, A. Makohon Moore, J. Gerold, I. Božić, K. Chatterjee, C. Iacobuzio Donahue, B. Vogelstein, M. Nowak, Nature Communications 8 (2017).","mla":"Reiter, Johannes, et al. “Reconstructing Metastatic Seeding Patterns of Human Cancers.” Nature Communications, vol. 8, 14114, Nature Publishing Group, 2017, doi:10.1038/ncomms14114.","apa":"Reiter, J., Makohon Moore, A., Gerold, J., Božić, I., Chatterjee, K., Iacobuzio Donahue, C., … Nowak, M. (2017). Reconstructing metastatic seeding patterns of human cancers. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14114","ieee":"J. Reiter et al., “Reconstructing metastatic seeding patterns of human cancers,” Nature Communications, vol. 8. Nature Publishing Group, 2017.","ista":"Reiter J, Makohon Moore A, Gerold J, Božić I, Chatterjee K, Iacobuzio Donahue C, Vogelstein B, Nowak M. 2017. Reconstructing metastatic seeding patterns of human cancers. Nature Communications. 8, 14114.","ama":"Reiter J, Makohon Moore A, Gerold J, et al. Reconstructing metastatic seeding patterns of human cancers. Nature Communications. 2017;8. doi:10.1038/ncomms14114"},"publication":"Nature Communications"},{"month":"10","external_id":{"pmid":["26466571"]},"oa":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4815041/"}],"quality_controlled":"1","project":[{"call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425"},{"_id":"2584A770-B435-11E9-9278-68D0E5697425","grant_number":"P 23499-N23","call_identifier":"FWF","name":"Modern Graph Algorithmic Techniques in Formal Verification"},{"_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23","call_identifier":"FWF","name":"Rigorous Systems Engineering"}],"doi":"10.1038/nature15395","language":[{"iso":"eng"}],"publist_id":"5484","ec_funded":1,"year":"2015","pmid":1,"publication_status":"published","department":[{"_id":"KrCh"}],"publisher":"Nature Publishing Group","author":[{"full_name":"Landau, Dan","first_name":"Dan","last_name":"Landau"},{"last_name":"Tausch","first_name":"Eugen","full_name":"Tausch, Eugen"},{"full_name":"Taylor Weiner, Amaro","first_name":"Amaro","last_name":"Taylor Weiner"},{"full_name":"Stewart, Chip","last_name":"Stewart","first_name":"Chip"},{"full_name":"Reiter, Johannes","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","first_name":"Johannes","last_name":"Reiter"},{"full_name":"Bahlo, Jasmin","first_name":"Jasmin","last_name":"Bahlo"},{"full_name":"Kluth, Sandra","first_name":"Sandra","last_name":"Kluth"},{"full_name":"Božić, Ivana","last_name":"Božić","first_name":"Ivana"},{"full_name":"Lawrence, Michael","last_name":"Lawrence","first_name":"Michael"},{"full_name":"Böttcher, Sebastian","last_name":"Böttcher","first_name":"Sebastian"},{"full_name":"Carter, Scott","first_name":"Scott","last_name":"Carter"},{"last_name":"Cibulskis","first_name":"Kristian","full_name":"Cibulskis, Kristian"},{"last_name":"Mertens","first_name":"Daniel","full_name":"Mertens, Daniel"},{"first_name":"Carrie","last_name":"Sougnez","full_name":"Sougnez, Carrie"},{"full_name":"Rosenberg, Mara","last_name":"Rosenberg","first_name":"Mara"},{"first_name":"Julian","last_name":"Hess","full_name":"Hess, Julian"},{"first_name":"Jennifer","last_name":"Edelmann","full_name":"Edelmann, Jennifer"},{"full_name":"Kless, Sabrina","last_name":"Kless","first_name":"Sabrina"},{"first_name":"Michael","last_name":"Kneba","full_name":"Kneba, Michael"},{"full_name":"Ritgen, Matthias","last_name":"Ritgen","first_name":"Matthias"},{"last_name":"Fink","first_name":"Anna","full_name":"Fink, Anna"},{"first_name":"Kirsten","last_name":"Fischer","full_name":"Fischer, Kirsten"},{"first_name":"Stacey","last_name":"Gabriel","full_name":"Gabriel, Stacey"},{"full_name":"Lander, Eric","last_name":"Lander","first_name":"Eric"},{"last_name":"Nowak","first_name":"Martin","full_name":"Nowak, Martin"},{"first_name":"Hartmut","last_name":"Döhner","full_name":"Döhner, Hartmut"},{"full_name":"Hallek, Michael","last_name":"Hallek","first_name":"Michael"},{"full_name":"Neuberg, Donna","last_name":"Neuberg","first_name":"Donna"},{"first_name":"Gad","last_name":"Getz","full_name":"Getz, Gad"},{"last_name":"Stilgenbauer","first_name":"Stephan","full_name":"Stilgenbauer, Stephan"},{"first_name":"Catherine","last_name":"Wu","full_name":"Wu, Catherine"}],"date_created":"2018-12-11T11:53:21Z","date_updated":"2021-01-12T06:52:23Z","volume":526,"scopus_import":1,"day":"22","article_processing_charge":"No","publication":"Nature","citation":{"ista":"Landau D, Tausch E, Taylor Weiner A, Stewart C, Reiter J, Bahlo J, Kluth S, Božić I, Lawrence M, Böttcher S, Carter S, Cibulskis K, Mertens D, Sougnez C, Rosenberg M, Hess J, Edelmann J, Kless S, Kneba M, Ritgen M, Fink A, Fischer K, Gabriel S, Lander E, Nowak M, Döhner H, Hallek M, Neuberg D, Getz G, Stilgenbauer S, Wu C. 2015. Mutations driving CLL and their evolution in progression and relapse. Nature. 526(7574), 525–530.","ieee":"D. Landau et al., “Mutations driving CLL and their evolution in progression and relapse,” Nature, vol. 526, no. 7574. Nature Publishing Group, pp. 525–530, 2015.","apa":"Landau, D., Tausch, E., Taylor Weiner, A., Stewart, C., Reiter, J., Bahlo, J., … Wu, C. (2015). Mutations driving CLL and their evolution in progression and relapse. Nature. Nature Publishing Group. https://doi.org/10.1038/nature15395","ama":"Landau D, Tausch E, Taylor Weiner A, et al. Mutations driving CLL and their evolution in progression and relapse. Nature. 2015;526(7574):525-530. doi:10.1038/nature15395","chicago":"Landau, Dan, Eugen Tausch, Amaro Taylor Weiner, Chip Stewart, Johannes Reiter, Jasmin Bahlo, Sandra Kluth, et al. “Mutations Driving CLL and Their Evolution in Progression and Relapse.” Nature. Nature Publishing Group, 2015. https://doi.org/10.1038/nature15395.","mla":"Landau, Dan, et al. “Mutations Driving CLL and Their Evolution in Progression and Relapse.” Nature, vol. 526, no. 7574, Nature Publishing Group, 2015, pp. 525–30, doi:10.1038/nature15395.","short":"D. Landau, E. Tausch, A. Taylor Weiner, C. Stewart, J. Reiter, J. Bahlo, S. Kluth, I. Božić, M. Lawrence, S. Böttcher, S. Carter, K. Cibulskis, D. Mertens, C. Sougnez, M. Rosenberg, J. Hess, J. Edelmann, S. Kless, M. Kneba, M. Ritgen, A. Fink, K. Fischer, S. Gabriel, E. Lander, M. Nowak, H. Döhner, M. Hallek, D. Neuberg, G. Getz, S. Stilgenbauer, C. Wu, Nature 526 (2015) 525–530."},"article_type":"original","page":"525 - 530","date_published":"2015-10-22T00:00:00Z","type":"journal_article","abstract":[{"lang":"eng","text":"Which genetic alterations drive tumorigenesis and how they evolve over the course of disease and therapy are central questions in cancer biology. Here we identify 44 recurrently mutated genes and 11 recurrent somatic copy number variations through whole-exome sequencing of 538 chronic lymphocytic leukaemia (CLL) and matched germline DNA samples, 278 of which were collected in a prospective clinical trial. These include previously unrecognized putative cancer drivers (RPS15, IKZF3), and collectively identify RNA processing and export, MYC activity, and MAPK signalling as central pathways involved in CLL. Clonality analysis of this large data set further enabled reconstruction of temporal relationships between driver events. Direct comparison between matched pre-treatment and relapse samples from 59 patients demonstrated highly frequent clonal evolution. Thus, large sequencing data sets of clinically informative samples enable the discovery of novel genes associated with cancer, the network of relationships between the driver events, and their impact on disease relapse and clinical outcome."}],"issue":"7574","_id":"1665","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Mutations driving CLL and their evolution in progression and relapse","status":"public","intvolume":" 526","oa_version":"Submitted Version"},{"alternative_title":["IST Austria Technical Report"],"type":"technical_report","abstract":[{"lang":"eng","text":"A comprehensive understanding of the clonal evolution of cancer is critical for understanding neoplasia. Genome-wide sequencing data enables evolutionary studies at unprecedented depth. However, classical phylogenetic methods often struggle with noisy sequencing data of impure DNA samples and fail to detect subclones that have different evolutionary trajectories. We have developed a tool, called Treeomics, that allows us to reconstruct the phylogeny of a cancer with commonly available sequencing technologies. Using Bayesian inference and Integer Linear Programming, robust phylogenies consistent with the biological processes underlying cancer evolution were obtained for pancreatic, ovarian, and prostate cancers. Furthermore, Treeomics correctly identified sequencing artifacts such as those resulting from low statistical power; nearly 7% of variants were misclassified by conventional statistical methods. These artifacts can skew phylogenies by creating illusory tumor heterogeneity among distinct samples. Importantly, we show that the evolutionary trees generated with Treeomics are mathematically optimal."}],"file_date_updated":"2020-07-14T12:46:58Z","department":[{"_id":"KrCh"}],"publisher":"IST Austria","publication_status":"published","title":"Reconstructing robust phylogenies of metastatic cancers","ddc":["000","576"],"status":"public","_id":"5444","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2015","oa_version":"Published Version","file":[{"file_name":"IST-2015-399-v1+1_treeomics.pdf","access_level":"open_access","creator":"system","content_type":"application/pdf","file_size":3533200,"file_id":"5485","relation":"main_file","date_created":"2018-12-12T11:53:24Z","date_updated":"2020-07-14T12:46:58Z","checksum":"c47d33bdda06181753c0af36f16e7b5d"}],"date_updated":"2020-07-14T23:05:07Z","date_created":"2018-12-12T11:39:22Z","pubrep_id":"399","author":[{"last_name":"Reiter","first_name":"Johannes","orcid":"0000-0002-0170-7353","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","full_name":"Reiter, Johannes"},{"last_name":"Makohon-Moore","first_name":"Alvin","full_name":"Makohon-Moore, Alvin"},{"first_name":"Jeffrey","last_name":"Gerold","full_name":"Gerold, Jeffrey"},{"full_name":"Bozic, Ivana","first_name":"Ivana","last_name":"Bozic"},{"last_name":"Chatterjee","first_name":"Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","full_name":"Chatterjee, Krishnendu"},{"first_name":"Christine","last_name":"Iacobuzio-Donahue","full_name":"Iacobuzio-Donahue, Christine"},{"last_name":"Vogelstein","first_name":"Bert","full_name":"Vogelstein, Bert"},{"last_name":"Nowak","first_name":"Martin","full_name":"Nowak, Martin"}],"publication_identifier":{"issn":["2664-1690"]},"has_accepted_license":"1","month":"12","day":"30","page":"25","oa":1,"citation":{"ista":"Reiter J, Makohon-Moore A, Gerold J, Bozic I, Chatterjee K, Iacobuzio-Donahue C, Vogelstein B, Nowak M. 2015. Reconstructing robust phylogenies of metastatic cancers, IST Austria, 25p.","apa":"Reiter, J., Makohon-Moore, A., Gerold, J., Bozic, I., Chatterjee, K., Iacobuzio-Donahue, C., … Nowak, M. (2015). Reconstructing robust phylogenies of metastatic cancers. IST Austria. https://doi.org/10.15479/AT:IST-2015-399-v1-1","ieee":"J. Reiter et al., Reconstructing robust phylogenies of metastatic cancers. IST Austria, 2015.","ama":"Reiter J, Makohon-Moore A, Gerold J, et al. Reconstructing Robust Phylogenies of Metastatic Cancers. IST Austria; 2015. doi:10.15479/AT:IST-2015-399-v1-1","chicago":"Reiter, Johannes, Alvin Makohon-Moore, Jeffrey Gerold, Ivana Bozic, Krishnendu Chatterjee, Christine Iacobuzio-Donahue, Bert Vogelstein, and Martin Nowak. Reconstructing Robust Phylogenies of Metastatic Cancers. IST Austria, 2015. https://doi.org/10.15479/AT:IST-2015-399-v1-1.","mla":"Reiter, Johannes, et al. Reconstructing Robust Phylogenies of Metastatic Cancers. IST Austria, 2015, doi:10.15479/AT:IST-2015-399-v1-1.","short":"J. Reiter, A. Makohon-Moore, J. Gerold, I. Bozic, K. Chatterjee, C. Iacobuzio-Donahue, B. Vogelstein, M. Nowak, Reconstructing Robust Phylogenies of Metastatic Cancers, IST Austria, 2015."},"language":[{"iso":"eng"}],"date_published":"2015-12-30T00:00:00Z","doi":"10.15479/AT:IST-2015-399-v1-1"},{"scopus_import":1,"day":"15","article_processing_charge":"No","article_type":"original","publication":"Proceedings of the Royal Society of London Series B Biological Sciences","citation":{"mla":"Reiter, Johannes, et al. “Biological Auctions with Multiple Rewards.” Proceedings of the Royal Society of London Series B Biological Sciences, vol. 282, no. 1812, Royal Society, 2015, doi:10.1098/rspb.2015.1041.","short":"J. Reiter, A. Kanodia, R. Gupta, M. Nowak, K. Chatterjee, Proceedings of the Royal Society of London Series B Biological Sciences 282 (2015).","chicago":"Reiter, Johannes, Ayush Kanodia, Raghav Gupta, Martin Nowak, and Krishnendu Chatterjee. “Biological Auctions with Multiple Rewards.” Proceedings of the Royal Society of London Series B Biological Sciences. Royal Society, 2015. https://doi.org/10.1098/rspb.2015.1041.","ama":"Reiter J, Kanodia A, Gupta R, Nowak M, Chatterjee K. Biological auctions with multiple rewards. Proceedings of the Royal Society of London Series B Biological Sciences. 2015;282(1812). doi:10.1098/rspb.2015.1041","ista":"Reiter J, Kanodia A, Gupta R, Nowak M, Chatterjee K. 2015. Biological auctions with multiple rewards. Proceedings of the Royal Society of London Series B Biological Sciences. 282(1812).","ieee":"J. Reiter, A. Kanodia, R. Gupta, M. Nowak, and K. Chatterjee, “Biological auctions with multiple rewards,” Proceedings of the Royal Society of London Series B Biological Sciences, vol. 282, no. 1812. Royal Society, 2015.","apa":"Reiter, J., Kanodia, A., Gupta, R., Nowak, M., & Chatterjee, K. (2015). Biological auctions with multiple rewards. Proceedings of the Royal Society of London Series B Biological Sciences. Royal Society. https://doi.org/10.1098/rspb.2015.1041"},"date_published":"2015-07-15T00:00:00Z","type":"journal_article","abstract":[{"lang":"eng","text":"The competition for resources among cells, individuals or species is a fundamental characteristic of evolution. Biological all-pay auctions have been used to model situations where multiple individuals compete for a single resource. However, in many situations multiple resources with various values exist and single reward auctions are not applicable. We generalize the model to multiple rewards and study the evolution of strategies. In biological all-pay auctions the bid of an individual corresponds to its strategy and is equivalent to its payment in the auction. The decreasingly ordered rewards are distributed according to the decreasingly ordered bids of the participating individuals. The reproductive success of an individual is proportional to its fitness given by the sum of the rewards won minus its payments. Hence, successful bidding strategies spread in the population. We find that the results for the multiple reward case are very different from the single reward case. While the mixed strategy equilibrium in the single reward case with more than two players consists of mostly low-bidding individuals, we show that the equilibrium can convert to many high-bidding individuals and a few low-bidding individuals in the multiple reward case. Some reward values lead to a specialization among the individuals where one subpopulation competes for the rewards and the other subpopulation largely avoids costly competitions. Whether the mixed strategy equilibrium is an evolutionarily stable strategy (ESS) depends on the specific values of the rewards."}],"issue":"1812","title":"Biological auctions with multiple rewards","status":"public","intvolume":" 282","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1709","oa_version":"Submitted Version","month":"07","quality_controlled":"1","project":[{"grant_number":"S 11407_N23","_id":"25832EC2-B435-11E9-9278-68D0E5697425","name":"Rigorous Systems Engineering","call_identifier":"FWF"},{"grant_number":"P 23499-N23","_id":"2584A770-B435-11E9-9278-68D0E5697425","name":"Modern Graph Algorithmic Techniques in Formal Verification","call_identifier":"FWF"},{"name":"Microsoft Research Faculty Fellowship","_id":"2587B514-B435-11E9-9278-68D0E5697425"}],"external_id":{"pmid":["26180069"]},"oa":1,"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528522/"}],"language":[{"iso":"eng"}],"doi":"10.1098/rspb.2015.1041","publist_id":"5425","publication_status":"published","publisher":"Royal Society","department":[{"_id":"KrCh"}],"year":"2015","acknowledgement":"This work was supported by grants from the John Templeton Foundation, ERC Start Grant (279307: Graph Games), FWF NFN Grant (No S11407N23 RiSE/SHiNE), FWF Grant (No P23499N23) and a Microsoft faculty fellows award.","pmid":1,"date_created":"2018-12-11T11:53:35Z","date_updated":"2023-09-07T11:40:43Z","volume":282,"author":[{"full_name":"Reiter, Johannes","first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353"},{"full_name":"Kanodia, Ayush","last_name":"Kanodia","first_name":"Ayush"},{"full_name":"Gupta, Raghav","first_name":"Raghav","last_name":"Gupta"},{"last_name":"Nowak","first_name":"Martin","full_name":"Nowak, Martin"},{"last_name":"Chatterjee","first_name":"Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","full_name":"Chatterjee, Krishnendu"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"1400"}]}},{"supervisor":[{"full_name":"Chatterjee, Krishnendu","first_name":"Krishnendu","last_name":"Chatterjee","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X"}],"degree_awarded":"PhD","language":[{"iso":"eng"}],"date_published":"2015-04-01T00:00:00Z","page":"183","citation":{"ista":"Reiter J. 2015. The subclonal evolution of cancer. Institute of Science and Technology Austria.","apa":"Reiter, J. (2015). The subclonal evolution of cancer. Institute of Science and Technology Austria.","ieee":"J. Reiter, “The subclonal evolution of cancer,” Institute of Science and Technology Austria, 2015.","ama":"Reiter J. The subclonal evolution of cancer. 2015.","chicago":"Reiter, Johannes. “The Subclonal Evolution of Cancer.” Institute of Science and Technology Austria, 2015.","mla":"Reiter, Johannes. The Subclonal Evolution of Cancer. Institute of Science and Technology Austria, 2015.","short":"J. Reiter, The Subclonal Evolution of Cancer, Institute of Science and Technology Austria, 2015."},"day":"01","month":"04","article_processing_charge":"No","publication_identifier":{"issn":["2663-337X"]},"date_created":"2018-12-11T11:51:48Z","date_updated":"2023-09-07T11:40:44Z","oa_version":"None","author":[{"full_name":"Reiter, Johannes","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","first_name":"Johannes","last_name":"Reiter"}],"related_material":{"record":[{"id":"1709","relation":"part_of_dissertation","status":"public"},{"id":"2000","relation":"part_of_dissertation","status":"public"},{"id":"2247","relation":"part_of_dissertation","status":"public"},{"id":"2816","relation":"part_of_dissertation","status":"public"},{"relation":"part_of_dissertation","status":"public","id":"2858"},{"id":"3157","status":"public","relation":"part_of_dissertation"},{"relation":"part_of_dissertation","status":"public","id":"3260"}]},"title":"The subclonal evolution of cancer","status":"public","publication_status":"published","publisher":"Institute of Science and Technology Austria","department":[{"_id":"KrCh"}],"year":"2015","_id":"1400","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","abstract":[{"lang":"eng","text":"Cancer results from an uncontrolled growth of abnormal cells. Sequentially accumulated genetic and epigenetic alterations decrease cell death and increase cell replication. We used mathematical models to quantify the effect of driver gene mutations. The recently developed targeted therapies can lead to dramatic regressions. However, in solid cancers, clinical responses are often short-lived because resistant cancer cells evolve. We estimated that approximately 50 different mutations can confer resistance to a typical targeted therapeutic agent. We find that resistant cells are likely to be present in expanded subclones before the start of the treatment. The dominant strategy to prevent the evolution of resistance is combination therapy. Our analytical results suggest that in most patients, dual therapy, but not monotherapy, can result in long-term disease control. However, long-term control can only occur if there are no possible mutations in the genome that can cause cross-resistance to both drugs. Furthermore, we showed that simultaneous therapy with two drugs is much more likely to result in long-term disease control than sequential therapy with the same drugs. To improve our understanding of the underlying subclonal evolution we reconstruct the evolutionary history of a patient's cancer from next-generation sequencing data of spatially-distinct DNA samples. Using a quantitative measure of genetic relatedness, we found that pancreatic cancers and their metastases demonstrated a higher level of relatedness than that expected for any two cells randomly taken from a normal tissue. This minimal amount of genetic divergence among advanced lesions indicates that genetic heterogeneity, when quantitatively defined, is not a fundamental feature of the natural history of untreated pancreatic cancers. Our newly developed, phylogenomic tool Treeomics finds evidence for seeding patterns of metastases and can directly be used to discover rules governing the evolution of solid malignancies to transform cancer into a more predictable disease."}],"publist_id":"5807","alternative_title":["ISTA Thesis"],"type":"dissertation"},{"date_published":"2014-12-04T00:00:00Z","language":[{"iso":"eng"}],"publication":"Blood","main_file_link":[{"url":"http://www.bloodjournal.org/content/124/21/1952?sso-checked=true"}],"citation":{"chicago":"Landau, Dan, Chip Stewart, Johannes Reiter, Michael Lawrence, Carrie Sougnez, Jennifer Brown, Armando Lopez Guillermo, et al. “Novel Putative Driver Gene Mutations in Chronic Lymphocytic Leukemia (CLL): Results from a Combined Analysis of Whole Exome Sequencing of 262 Primary CLL Aamples.” Blood. American Society of Hematology, 2014.","short":"D. Landau, C. Stewart, J. Reiter, M. Lawrence, C. Sougnez, J. Brown, A. Lopez Guillermo, S. Gabriel, E. Lander, D. Neuberg, C. López Otín, E. Campo, G. Getz, C. Wu, Blood 124 (2014) 1952–1952.","mla":"Landau, Dan, et al. “Novel Putative Driver Gene Mutations in Chronic Lymphocytic Leukemia (CLL): Results from a Combined Analysis of Whole Exome Sequencing of 262 Primary CLL Aamples.” Blood, vol. 124, no. 21, American Society of Hematology, 2014, pp. 1952–1952.","ieee":"D. Landau et al., “Novel putative driver gene mutations in chronic lymphocytic leukemia (CLL): results from a combined analysis of whole exome sequencing of 262 primary CLL aamples,” Blood, vol. 124, no. 21. American Society of Hematology, pp. 1952–1952, 2014.","apa":"Landau, D., Stewart, C., Reiter, J., Lawrence, M., Sougnez, C., Brown, J., … Wu, C. (2014). Novel putative driver gene mutations in chronic lymphocytic leukemia (CLL): results from a combined analysis of whole exome sequencing of 262 primary CLL aamples. Blood. American Society of Hematology.","ista":"Landau D, Stewart C, Reiter J, Lawrence M, Sougnez C, Brown J, Lopez Guillermo A, Gabriel S, Lander E, Neuberg D, López Otín C, Campo E, Getz G, Wu C. 2014. Novel putative driver gene mutations in chronic lymphocytic leukemia (CLL): results from a combined analysis of whole exome sequencing of 262 primary CLL aamples. Blood. 124(21), 1952–1952.","ama":"Landau D, Stewart C, Reiter J, et al. Novel putative driver gene mutations in chronic lymphocytic leukemia (CLL): results from a combined analysis of whole exome sequencing of 262 primary CLL aamples. Blood. 2014;124(21):1952-1952."},"page":"1952 - 1952","month":"12","day":"04","author":[{"first_name":"Dan","last_name":"Landau","full_name":"Landau, Dan"},{"full_name":"Stewart, Chip","last_name":"Stewart","first_name":"Chip"},{"full_name":"Reiter, Johannes","first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353"},{"full_name":"Lawrence, Michael","last_name":"Lawrence","first_name":"Michael"},{"full_name":"Sougnez, Carrie","last_name":"Sougnez","first_name":"Carrie"},{"last_name":"Brown","first_name":"Jennifer","full_name":"Brown, Jennifer"},{"first_name":"Armando","last_name":"Lopez Guillermo","full_name":"Lopez Guillermo, Armando"},{"full_name":"Gabriel, Stacey","first_name":"Stacey","last_name":"Gabriel"},{"last_name":"Lander","first_name":"Eric","full_name":"Lander, Eric"},{"full_name":"Neuberg, Donna","last_name":"Neuberg","first_name":"Donna"},{"first_name":"Carlos","last_name":"López Otín","full_name":"López Otín, Carlos"},{"last_name":"Campo","first_name":"Elias","full_name":"Campo, Elias"},{"full_name":"Getz, Gad","last_name":"Getz","first_name":"Gad"},{"full_name":"Wu, Catherine","first_name":"Catherine","last_name":"Wu"}],"date_updated":"2021-01-12T06:53:50Z","date_created":"2018-12-11T11:54:32Z","volume":124,"oa_version":"None","year":"2014","_id":"1884","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","title":"Novel putative driver gene mutations in chronic lymphocytic leukemia (CLL): results from a combined analysis of whole exome sequencing of 262 primary CLL aamples","publication_status":"published","status":"public","intvolume":" 124","department":[{"_id":"KrCh"}],"publisher":"American Society of Hematology","abstract":[{"lang":"eng","text":"Unbiased high-throughput massively parallel sequencing methods have transformed the process of discovery of novel putative driver gene mutations in cancer. In chronic lymphocytic leukemia (CLL), these methods have yielded several unexpected findings, including the driver genes SF3B1, NOTCH1 and POT1. Recent analysis, utilizing down-sampling of existing datasets, has shown that the discovery process of putative drivers is far from complete across cancer. In CLL, while driver gene mutations affecting >10% of patients were efficiently discovered with previously published CLL cohorts of up to 160 samples subjected to whole exome sequencing (WES), this sample size has only 0.78 power to detect drivers affecting 5% of patients, and only 0.12 power for drivers affecting 2% of patients. These calculations emphasize the need to apply unbiased WES to larger patient cohorts."}],"publist_id":"5211","issue":"21","type":"journal_article"},{"doi":"10.15479/AT:IST-2013-104-v1-1","date_published":"2013-01-11T00:00:00Z","language":[{"iso":"eng"}],"citation":{"ista":"Reiter J, Bozic I, Chatterjee K, Nowak M. 2013. TTP: Tool for Tumor Progression, IST Austria, 17p.","apa":"Reiter, J., Bozic, I., Chatterjee, K., & Nowak, M. (2013). TTP: Tool for Tumor Progression. IST Austria. https://doi.org/10.15479/AT:IST-2013-104-v1-1","ieee":"J. Reiter, I. Bozic, K. Chatterjee, and M. Nowak, TTP: Tool for Tumor Progression. IST Austria, 2013.","ama":"Reiter J, Bozic I, Chatterjee K, Nowak M. TTP: Tool for Tumor Progression. IST Austria; 2013. doi:10.15479/AT:IST-2013-104-v1-1","chicago":"Reiter, Johannes, Ivana Bozic, Krishnendu Chatterjee, and Martin Nowak. TTP: Tool for Tumor Progression. IST Austria, 2013. https://doi.org/10.15479/AT:IST-2013-104-v1-1.","mla":"Reiter, Johannes, et al. TTP: Tool for Tumor Progression. IST Austria, 2013, doi:10.15479/AT:IST-2013-104-v1-1.","short":"J. Reiter, I. Bozic, K. Chatterjee, M. Nowak, TTP: Tool for Tumor Progression, IST Austria, 2013."},"oa":1,"page":"17","day":"11","month":"01","publication_identifier":{"issn":["2664-1690"]},"has_accepted_license":"1","author":[{"full_name":"Reiter, Johannes","first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353"},{"last_name":"Bozic","first_name":"Ivana","full_name":"Bozic, Ivana"},{"id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","first_name":"Krishnendu","last_name":"Chatterjee","full_name":"Chatterjee, Krishnendu"},{"full_name":"Nowak, Martin","first_name":"Martin","last_name":"Nowak"}],"related_material":{"record":[{"relation":"later_version","status":"public","id":"2000"}]},"pubrep_id":"104","date_updated":"2023-02-23T10:23:57Z","date_created":"2018-12-12T11:39:07Z","oa_version":"Published Version","file":[{"checksum":"2cc8c6e157eca1271128db80bb3dec80","date_updated":"2020-07-14T12:46:44Z","date_created":"2018-12-12T11:54:20Z","relation":"main_file","file_id":"5542","file_size":1471954,"content_type":"application/pdf","creator":"system","access_level":"open_access","file_name":"IST-2013-104-v1+1_tumortool.pdf"}],"_id":"5399","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2013","publication_status":"published","status":"public","ddc":["000"],"title":"TTP: Tool for Tumor Progression","publisher":"IST Austria","department":[{"_id":"KrCh"}],"abstract":[{"lang":"eng","text":"In this work we present a flexible tool for tumor progression, which simulates the evolutionary dynamics of cancer. Tumor progression implements a multi-type branching process where the key parameters are the fitness landscape, the mutation rate, and the average time of cell division. The fitness of a cancer cell depends on the mutations it has accumulated. The input to our tool could be any fitness landscape, mutation rate, and cell division time, and the tool produces the growth dynamics and all relevant statistics."}],"file_date_updated":"2020-07-14T12:46:44Z","type":"technical_report","alternative_title":["IST Austria Technical Report"]},{"type":"research_data_reference","abstract":[{"lang":"eng","text":"Cooperative behavior, where one individual incurs a cost to help another, is a wide spread phenomenon. Here we study direct reciprocity in the context of the alternating Prisoner's Dilemma. We consider all strategies that can be implemented by one and two-state automata. We calculate the payoff matrix of all pairwise encounters in the presence of noise. We explore deterministic selection dynamics with and without mutation. Using different error rates and payoff values, we observe convergence to a small number of distinct equilibria. Two of them are uncooperative strict Nash equilibria representing always-defect (ALLD) and Grim. The third equilibrium is mixed and represents a cooperative alliance of several strategies, dominated by a strategy which we call Forgiver. Forgiver cooperates whenever the opponent has cooperated; it defects once when the opponent has defected, but subsequently Forgiver attempts to re-establish cooperation even if the opponent has defected again. Forgiver is not an evolutionarily stable strategy, but the alliance, which it rules, is asymptotically stable. For a wide range of parameter values the most commonly observed outcome is convergence to the mixed equilibrium, dominated by Forgiver. Our results show that although forgiving might incur a short-term loss it can lead to a long-term gain. Forgiveness facilitates stable cooperation in the presence of exploitation and noise."}],"year":"2013","_id":"9749","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","publisher":"Public Library of Science","department":[{"_id":"KrCh"}],"title":"Forgiver triumphs in alternating prisoner's dilemma ","status":"public","related_material":{"record":[{"status":"public","relation":"used_in_publication","id":"2247"}]},"author":[{"full_name":"Zagorsky, Benjamin","last_name":"Zagorsky","first_name":"Benjamin"},{"id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","first_name":"Johannes","last_name":"Reiter","full_name":"Reiter, Johannes"},{"last_name":"Chatterjee","first_name":"Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","full_name":"Chatterjee, Krishnendu"},{"full_name":"Nowak, Martin","last_name":"Nowak","first_name":"Martin"}],"oa_version":"Published Version","date_updated":"2023-02-23T10:34:39Z","date_created":"2021-07-28T15:45:07Z","article_processing_charge":"No","day":"12","month":"12","citation":{"ama":"Zagorsky B, Reiter J, Chatterjee K, Nowak M. Forgiver triumphs in alternating prisoner’s dilemma . 2013. doi:10.1371/journal.pone.0080814.s001","ista":"Zagorsky B, Reiter J, Chatterjee K, Nowak M. 2013. Forgiver triumphs in alternating prisoner’s dilemma , Public Library of Science, 10.1371/journal.pone.0080814.s001.","ieee":"B. Zagorsky, J. Reiter, K. Chatterjee, and M. Nowak, “Forgiver triumphs in alternating prisoner’s dilemma .” Public Library of Science, 2013.","apa":"Zagorsky, B., Reiter, J., Chatterjee, K., & Nowak, M. (2013). Forgiver triumphs in alternating prisoner’s dilemma . Public Library of Science. https://doi.org/10.1371/journal.pone.0080814.s001","mla":"Zagorsky, Benjamin, et al. Forgiver Triumphs in Alternating Prisoner’s Dilemma . Public Library of Science, 2013, doi:10.1371/journal.pone.0080814.s001.","short":"B. Zagorsky, J. Reiter, K. Chatterjee, M. Nowak, (2013).","chicago":"Zagorsky, Benjamin, Johannes Reiter, Krishnendu Chatterjee, and Martin Nowak. “Forgiver Triumphs in Alternating Prisoner’s Dilemma .” Public Library of Science, 2013. https://doi.org/10.1371/journal.pone.0080814.s001."},"date_published":"2013-12-12T00:00:00Z","doi":"10.1371/journal.pone.0080814.s001"},{"abstract":[{"lang":"eng","text":"Cooperative behavior, where one individual incurs a cost to help another, is a wide spread phenomenon. Here we study direct reciprocity in the context of the alternating Prisoner's Dilemma. We consider all strategies that can be implemented by one and two-state automata. We calculate the payoff matrix of all pairwise encounters in the presence of noise. We explore deterministic selection dynamics with and without mutation. Using different error rates and payoff values, we observe convergence to a small number of distinct equilibria. Two of them are uncooperative strict Nash equilibria representing always-defect (ALLD) and Grim. The third equilibrium is mixed and represents a cooperative alliance of several strategies, dominated by a strategy which we call Forgiver. Forgiver cooperates whenever the opponent has cooperated; it defects once when the opponent has defected, but subsequently Forgiver attempts to re-establish cooperation even if the opponent has defected again. Forgiver is not an evolutionarily stable strategy, but the alliance, which it rules, is asymptotically stable. For a wide range of parameter values the most commonly observed outcome is convergence to the mixed equilibrium, dominated by Forgiver. Our results show that although forgiving might incur a short-term loss it can lead to a long-term gain. Forgiveness facilitates stable cooperation in the presence of exploitation and noise."}],"issue":"12","type":"journal_article","oa_version":"Published Version","file":[{"content_type":"application/pdf","file_size":1050042,"creator":"system","file_name":"IST-2016-409-v1+1_journal.pone.0080814.pdf","access_level":"open_access","date_updated":"2020-07-14T12:45:34Z","date_created":"2018-12-12T10:11:15Z","checksum":"808e8b9e6e89658bee4ffbbfac1bd19d","relation":"main_file","file_id":"4868"}],"pubrep_id":"409","title":"Forgiver triumphs in alternating prisoner's dilemma ","ddc":["000"],"status":"public","intvolume":" 8","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"2247","day":"12","has_accepted_license":"1","scopus_import":1,"date_published":"2013-12-12T00:00:00Z","publication":"PLoS One","citation":{"ama":"Zagorsky B, Reiter J, Chatterjee K, Nowak M. Forgiver triumphs in alternating prisoner’s dilemma . PLoS One. 2013;8(12). doi:10.1371/journal.pone.0080814","apa":"Zagorsky, B., Reiter, J., Chatterjee, K., & Nowak, M. (2013). Forgiver triumphs in alternating prisoner’s dilemma . PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0080814","ieee":"B. Zagorsky, J. Reiter, K. Chatterjee, and M. Nowak, “Forgiver triumphs in alternating prisoner’s dilemma ,” PLoS One, vol. 8, no. 12. Public Library of Science, 2013.","ista":"Zagorsky B, Reiter J, Chatterjee K, Nowak M. 2013. Forgiver triumphs in alternating prisoner’s dilemma . PLoS One. 8(12), e80814.","short":"B. Zagorsky, J. Reiter, K. Chatterjee, M. Nowak, PLoS One 8 (2013).","mla":"Zagorsky, Benjamin, et al. “Forgiver Triumphs in Alternating Prisoner’s Dilemma .” PLoS One, vol. 8, no. 12, e80814, Public Library of Science, 2013, doi:10.1371/journal.pone.0080814.","chicago":"Zagorsky, Benjamin, Johannes Reiter, Krishnendu Chatterjee, and Martin Nowak. “Forgiver Triumphs in Alternating Prisoner’s Dilemma .” PLoS One. Public Library of Science, 2013. https://doi.org/10.1371/journal.pone.0080814."},"file_date_updated":"2020-07-14T12:45:34Z","ec_funded":1,"publist_id":"4702","article_number":"e80814","date_created":"2018-12-11T11:56:33Z","date_updated":"2023-09-07T11:40:43Z","volume":8,"author":[{"last_name":"Zagorsky","first_name":"Benjamin","full_name":"Zagorsky, Benjamin"},{"first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","full_name":"Reiter, Johannes"},{"orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","last_name":"Chatterjee","first_name":"Krishnendu","full_name":"Chatterjee, Krishnendu"},{"full_name":"Nowak, Martin","last_name":"Nowak","first_name":"Martin"}],"related_material":{"record":[{"status":"public","relation":"research_data","id":"9749"},{"relation":"dissertation_contains","status":"public","id":"1400"}]},"publication_status":"published","department":[{"_id":"KrCh"}],"publisher":"Public Library of Science","year":"2013","month":"12","language":[{"iso":"eng"}],"doi":"10.1371/journal.pone.0080814","quality_controlled":"1","project":[{"_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307","call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications"},{"_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23","name":"Rigorous Systems Engineering","call_identifier":"FWF"},{"name":"Modern Graph Algorithmic Techniques in Formal Verification","call_identifier":"FWF","grant_number":"P 23499-N23","_id":"2584A770-B435-11E9-9278-68D0E5697425"},{"_id":"2587B514-B435-11E9-9278-68D0E5697425","name":"Microsoft Research Faculty Fellowship"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1},{"pubrep_id":"415","file":[{"file_id":"5173","relation":"main_file","checksum":"e2955b3889f8a823c3d5a72cb16f8957","date_updated":"2020-07-14T12:45:51Z","date_created":"2018-12-12T10:15:50Z","access_level":"open_access","file_name":"IST-2016-415-v1+1_Reiter_et_al-2013-Evolutionary_Applications.pdf","creator":"system","content_type":"application/pdf","file_size":1172037}],"oa_version":"Published Version","_id":"2858","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","title":"The effect of one additional driver mutation on tumor progression","ddc":["570"],"intvolume":" 6","abstract":[{"lang":"eng","text":"Tumor growth is caused by the acquisition of driver mutations, which enhance the net reproductive rate of cells. Driver mutations may increase cell division, reduce cell death, or allow cells to overcome density-limiting effects. We study the dynamics of tumor growth as one additional driver mutation is acquired. Our models are based on two-type branching processes that terminate in either tumor disappearance or tumor detection. In our first model, both cell types grow exponentially, with a faster rate for cells carrying the additional driver. We find that the additional driver mutation does not affect the survival probability of the lesion, but can substantially reduce the time to reach the detectable size if the lesion is slow growing. In our second model, cells lacking the additional driver cannot exceed a fixed carrying capacity, due to density limitations. In this case, the time to detection depends strongly on this carrying capacity. Our model provides a quantitative framework for studying tumor dynamics during different stages of progression. We observe that early, small lesions need additional drivers, while late stage metastases are only marginally affected by them. These results help to explain why additional driver mutations are typically not detected in fast-growing metastases."}],"issue":"1","type":"journal_article","date_published":"2013-01-01T00:00:00Z","publication":"Evolutionary Applications","citation":{"short":"J. Reiter, I. Božić, B. Allen, K. Chatterjee, M. Nowak, Evolutionary Applications 6 (2013) 34–45.","mla":"Reiter, Johannes, et al. “The Effect of One Additional Driver Mutation on Tumor Progression.” Evolutionary Applications, vol. 6, no. 1, Wiley-Blackwell, 2013, pp. 34–45, doi:10.1111/eva.12020.","chicago":"Reiter, Johannes, Ivana Božić, Benjamin Allen, Krishnendu Chatterjee, and Martin Nowak. “The Effect of One Additional Driver Mutation on Tumor Progression.” Evolutionary Applications. Wiley-Blackwell, 2013. https://doi.org/10.1111/eva.12020.","ama":"Reiter J, Božić I, Allen B, Chatterjee K, Nowak M. The effect of one additional driver mutation on tumor progression. Evolutionary Applications. 2013;6(1):34-45. doi:10.1111/eva.12020","apa":"Reiter, J., Božić, I., Allen, B., Chatterjee, K., & Nowak, M. (2013). The effect of one additional driver mutation on tumor progression. Evolutionary Applications. Wiley-Blackwell. https://doi.org/10.1111/eva.12020","ieee":"J. Reiter, I. Božić, B. Allen, K. Chatterjee, and M. Nowak, “The effect of one additional driver mutation on tumor progression,” Evolutionary Applications, vol. 6, no. 1. Wiley-Blackwell, pp. 34–45, 2013.","ista":"Reiter J, Božić I, Allen B, Chatterjee K, Nowak M. 2013. The effect of one additional driver mutation on tumor progression. Evolutionary Applications. 6(1), 34–45."},"page":"34 - 45","day":"01","has_accepted_license":"1","scopus_import":1,"author":[{"full_name":"Reiter, Johannes","last_name":"Reiter","first_name":"Johannes","orcid":"0000-0002-0170-7353","id":"4A918E98-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Ivana","last_name":"Božić","full_name":"Božić, Ivana"},{"full_name":"Allen, Benjamin","first_name":"Benjamin","last_name":"Allen","id":"135B5B70-E9D2-11E9-BD74-BB415DA2B523"},{"full_name":"Chatterjee, Krishnendu","last_name":"Chatterjee","first_name":"Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Nowak, Martin","last_name":"Nowak","first_name":"Martin"}],"related_material":{"record":[{"id":"1400","status":"public","relation":"dissertation_contains"}]},"date_created":"2018-12-11T11:59:58Z","date_updated":"2023-09-07T11:40:43Z","volume":6,"year":"2013","publication_status":"published","publisher":"Wiley-Blackwell","department":[{"_id":"KrCh"}],"file_date_updated":"2020-07-14T12:45:51Z","publist_id":"3931","ec_funded":1,"doi":"10.1111/eva.12020","language":[{"iso":"eng"}],"oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"quality_controlled":"1","project":[{"name":"Quantitative Graph Games: Theory and Applications","call_identifier":"FP7","_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307"},{"grant_number":"S11407","_id":"25863FF4-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Game Theory"}],"month":"01"},{"type":"journal_article","abstract":[{"lang":"eng","text":"In solid tumors, targeted treatments can lead to dramatic regressions, but responses are often short-lived because resistant cancer cells arise. The major strategy proposed for overcoming resistance is combination therapy. We present a mathematical model describing the evolutionary dynamics of lesions in response to treatment. We first studied 20 melanoma patients receiving vemurafenib. We then applied our model to an independent set of pancreatic, colorectal, and melanoma cancer patients with metastatic disease. We find that dual therapy results in long-term disease control for most patients, if there are no single mutations that cause cross-resistance to both drugs; in patients with large disease burden, triple therapy is needed. We also find that simultaneous therapy with two drugs is much more effective than sequential therapy. Our results provide realistic expectations for the efficacy of new drug combinations and inform the design of trials for new cancer therapeutics."}],"status":"public","title":"Evolutionary dynamics of cancer in response to targeted combination therapy","ddc":["570","610"],"intvolume":" 2","_id":"2816","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"file_name":"IST-2013-134-v1+1_e00747.full.pdf","access_level":"open_access","creator":"system","content_type":"application/pdf","file_size":3358321,"file_id":"4967","relation":"main_file","date_updated":"2020-07-14T12:45:49Z","date_created":"2018-12-12T10:12:48Z","checksum":"2c38c47815eacd8fa66cb8b404cf7c61"}],"oa_version":"Published Version","pubrep_id":"134","scopus_import":1,"day":"25","has_accepted_license":"1","publication":"eLife","citation":{"ista":"Božić I, Reiter J, Allen B, Antal T, Chatterjee K, Shah P, Moon Y, Yaqubie A, Kelly N, Le D, Lipson E, Chapman P, Diaz L, Vogelstein B, Nowak M. 2013. Evolutionary dynamics of cancer in response to targeted combination therapy. eLife. 2, e00747.","apa":"Božić, I., Reiter, J., Allen, B., Antal, T., Chatterjee, K., Shah, P., … Nowak, M. (2013). Evolutionary dynamics of cancer in response to targeted combination therapy. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.00747","ieee":"I. Božić et al., “Evolutionary dynamics of cancer in response to targeted combination therapy,” eLife, vol. 2. eLife Sciences Publications, 2013.","ama":"Božić I, Reiter J, Allen B, et al. Evolutionary dynamics of cancer in response to targeted combination therapy. eLife. 2013;2. doi:10.7554/eLife.00747","chicago":"Božić, Ivana, Johannes Reiter, Benjamin Allen, Tibor Antal, Krishnendu Chatterjee, Preya Shah, Yo Moon, et al. “Evolutionary Dynamics of Cancer in Response to Targeted Combination Therapy.” ELife. eLife Sciences Publications, 2013. https://doi.org/10.7554/eLife.00747.","mla":"Božić, Ivana, et al. “Evolutionary Dynamics of Cancer in Response to Targeted Combination Therapy.” ELife, vol. 2, e00747, eLife Sciences Publications, 2013, doi:10.7554/eLife.00747.","short":"I. Božić, J. Reiter, B. Allen, T. Antal, K. Chatterjee, P. Shah, Y. Moon, A. Yaqubie, N. Kelly, D. Le, E. Lipson, P. Chapman, L. Diaz, B. Vogelstein, M. Nowak, ELife 2 (2013)."},"date_published":"2013-06-25T00:00:00Z","article_number":"e00747","file_date_updated":"2020-07-14T12:45:49Z","publist_id":"3985","publication_status":"published","publisher":"eLife Sciences Publications","department":[{"_id":"KrCh"}],"year":"2013","date_updated":"2023-09-07T11:40:43Z","date_created":"2018-12-11T11:59:45Z","volume":2,"author":[{"first_name":"Ivana","last_name":"Božić","full_name":"Božić, Ivana"},{"first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","full_name":"Reiter, Johannes"},{"full_name":"Allen, Benjamin","first_name":"Benjamin","last_name":"Allen"},{"last_name":"Antal","first_name":"Tibor","full_name":"Antal, Tibor"},{"full_name":"Chatterjee, Krishnendu","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","first_name":"Krishnendu","last_name":"Chatterjee"},{"last_name":"Shah","first_name":"Preya","full_name":"Shah, Preya"},{"last_name":"Moon","first_name":"Yo","full_name":"Moon, Yo"},{"full_name":"Yaqubie, Amin","first_name":"Amin","last_name":"Yaqubie"},{"full_name":"Kelly, Nicole","first_name":"Nicole","last_name":"Kelly"},{"first_name":"Dung","last_name":"Le","full_name":"Le, Dung"},{"full_name":"Lipson, Evan","first_name":"Evan","last_name":"Lipson"},{"full_name":"Chapman, Paul","first_name":"Paul","last_name":"Chapman"},{"first_name":"Luis","last_name":"Diaz","full_name":"Diaz, Luis"},{"last_name":"Vogelstein","first_name":"Bert","full_name":"Vogelstein, Bert"},{"full_name":"Nowak, Martin","first_name":"Martin","last_name":"Nowak"}],"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"1400"}]},"month":"06","quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"language":[{"iso":"eng"}],"doi":"10.7554/eLife.00747"},{"language":[{"iso":"eng"}],"conference":{"end_date":"2013-07-19","start_date":"2013-07-13","location":"St. Petersburg, Russia","name":"CAV: Computer Aided Verification"},"doi":"10.1007/978-3-642-39799-8_6","quality_controlled":"1","project":[{"call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307"},{"call_identifier":"FWF","name":"Rigorous Systems Engineering","_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23"},{"grant_number":"P 23499-N23","_id":"2584A770-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Modern Graph Algorithmic Techniques in Formal Verification"},{"_id":"2587B514-B435-11E9-9278-68D0E5697425","name":"Microsoft Research Faculty Fellowship"}],"oa":1,"external_id":{"arxiv":["1303.5251"]},"main_file_link":[{"url":"https://arxiv.org/abs/1303.5251","open_access":"1"}],"month":"01","date_created":"2018-12-11T11:55:08Z","date_updated":"2023-09-07T11:40:43Z","volume":8044,"author":[{"full_name":"Reiter, Johannes","last_name":"Reiter","first_name":"Johannes","orcid":"0000-0002-0170-7353","id":"4A918E98-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Božić","first_name":"Ivana","full_name":"Božić, Ivana"},{"id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","first_name":"Krishnendu","last_name":"Chatterjee","full_name":"Chatterjee, Krishnendu"},{"last_name":"Nowak","first_name":"Martin","full_name":"Nowak, Martin"}],"related_material":{"record":[{"status":"public","relation":"earlier_version","id":"5399"},{"relation":"dissertation_contains","status":"public","id":"1400"}]},"publication_status":"published","publisher":"Springer","department":[{"_id":"KrCh"}],"year":"2013","ec_funded":1,"publist_id":"5077","date_published":"2013-01-01T00:00:00Z","page":"101 - 106","publication":"Proceedings of 25th Int. Conf. on Computer Aided Verification","citation":{"mla":"Reiter, Johannes, et al. “TTP: Tool for Tumor Progression.” Proceedings of 25th Int. Conf. on Computer Aided Verification, vol. 8044, Springer, 2013, pp. 101–06, doi:10.1007/978-3-642-39799-8_6.","short":"J. Reiter, I. Božić, K. Chatterjee, M. Nowak, in:, Proceedings of 25th Int. Conf. on Computer Aided Verification, Springer, 2013, pp. 101–106.","chicago":"Reiter, Johannes, Ivana Božić, Krishnendu Chatterjee, and Martin Nowak. “TTP: Tool for Tumor Progression.” In Proceedings of 25th Int. Conf. on Computer Aided Verification, 8044:101–6. Lecture Notes in Computer Science. Springer, 2013. https://doi.org/10.1007/978-3-642-39799-8_6.","ama":"Reiter J, Božić I, Chatterjee K, Nowak M. TTP: Tool for tumor progression. In: Proceedings of 25th Int. Conf. on Computer Aided Verification. Vol 8044. Lecture Notes in Computer Science. Springer; 2013:101-106. doi:10.1007/978-3-642-39799-8_6","ista":"Reiter J, Božić I, Chatterjee K, Nowak M. 2013. TTP: Tool for tumor progression. Proceedings of 25th Int. Conf. on Computer Aided Verification. CAV: Computer Aided VerificationLecture Notes in Computer Science, LNCS, vol. 8044, 101–106.","ieee":"J. Reiter, I. Božić, K. Chatterjee, and M. Nowak, “TTP: Tool for tumor progression,” in Proceedings of 25th Int. Conf. on Computer Aided Verification, St. Petersburg, Russia, 2013, vol. 8044, pp. 101–106.","apa":"Reiter, J., Božić, I., Chatterjee, K., & Nowak, M. (2013). TTP: Tool for tumor progression. In Proceedings of 25th Int. Conf. on Computer Aided Verification (Vol. 8044, pp. 101–106). St. Petersburg, Russia: Springer. https://doi.org/10.1007/978-3-642-39799-8_6"},"day":"01","series_title":"Lecture Notes in Computer Science","scopus_import":1,"oa_version":"Preprint","status":"public","title":"TTP: Tool for tumor progression","intvolume":" 8044","_id":"2000","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","abstract":[{"lang":"eng","text":"In this work we present a flexible tool for tumor progression, which simulates the evolutionary dynamics of cancer. Tumor progression implements a multi-type branching process where the key parameters are the fitness landscape, the mutation rate, and the average time of cell division. The fitness of a cancer cell depends on the mutations it has accumulated. The input to our tool could be any fitness landscape, mutation rate, and cell division time, and the tool produces the growth dynamics and all relevant statistics."}],"alternative_title":["LNCS"],"type":"conference"},{"month":"06","project":[{"call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307"},{"call_identifier":"FWF","name":"Rigorous Systems Engineering","_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23"}],"quality_controlled":"1","external_id":{"pmid":["22722843"]},"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436069/"}],"oa":1,"language":[{"iso":"eng"}],"doi":"10.1038/nature11219","ec_funded":1,"publist_id":"3537","publisher":"Nature Publishing Group","department":[{"_id":"KrCh"}],"publication_status":"published","pmid":1,"year":"2012","volume":486,"date_updated":"2023-09-07T11:40:43Z","date_created":"2018-12-11T12:01:43Z","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"1400"}]},"author":[{"first_name":"Luis","last_name":"Diaz Jr","full_name":"Diaz Jr, Luis"},{"full_name":"Williams, Richard","first_name":"Richard","last_name":"Williams"},{"last_name":"Wu","first_name":"Jian","full_name":"Wu, Jian"},{"first_name":"Isaac","last_name":"Kinde","full_name":"Kinde, Isaac"},{"first_name":"Joel","last_name":"Hecht","full_name":"Hecht, Joel"},{"full_name":"Berlin, Jordan","last_name":"Berlin","first_name":"Jordan"},{"first_name":"Benjamin","last_name":"Allen","full_name":"Allen, Benjamin"},{"last_name":"Božić","first_name":"Ivana","full_name":"Božić, Ivana"},{"full_name":"Reiter, Johannes","orcid":"0000-0002-0170-7353","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","last_name":"Reiter","first_name":"Johannes"},{"first_name":"Martin","last_name":"Nowak","full_name":"Nowak, Martin"},{"full_name":"Kinzler, Kenneth","first_name":"Kenneth","last_name":"Kinzler"},{"full_name":"Oliner, Kelly","first_name":"Kelly","last_name":"Oliner"},{"last_name":"Vogelstein","first_name":"Bert","full_name":"Vogelstein, Bert"}],"scopus_import":1,"day":"28","page":"537 - 540","citation":{"ama":"Diaz Jr L, Williams R, Wu J, et al. The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers. Nature. 2012;486(7404):537-540. doi:10.1038/nature11219","apa":"Diaz Jr, L., Williams, R., Wu, J., Kinde, I., Hecht, J., Berlin, J., … Vogelstein, B. (2012). The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers. Nature. Nature Publishing Group. https://doi.org/10.1038/nature11219","ieee":"L. Diaz Jr et al., “The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers,” Nature, vol. 486, no. 7404. Nature Publishing Group, pp. 537–540, 2012.","ista":"Diaz Jr L, Williams R, Wu J, Kinde I, Hecht J, Berlin J, Allen B, Božić I, Reiter J, Nowak M, Kinzler K, Oliner K, Vogelstein B. 2012. The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers. Nature. 486(7404), 537–540.","short":"L. Diaz Jr, R. Williams, J. Wu, I. Kinde, J. Hecht, J. Berlin, B. Allen, I. Božić, J. Reiter, M. Nowak, K. Kinzler, K. Oliner, B. Vogelstein, Nature 486 (2012) 537–540.","mla":"Diaz Jr, Luis, et al. “The Molecular Evolution of Acquired Resistance to Targeted EGFR Blockade in Colorectal Cancers.” Nature, vol. 486, no. 7404, Nature Publishing Group, 2012, pp. 537–40, doi:10.1038/nature11219.","chicago":"Diaz Jr, Luis, Richard Williams, Jian Wu, Isaac Kinde, Joel Hecht, Jordan Berlin, Benjamin Allen, et al. “The Molecular Evolution of Acquired Resistance to Targeted EGFR Blockade in Colorectal Cancers.” Nature. Nature Publishing Group, 2012. https://doi.org/10.1038/nature11219."},"publication":"Nature","date_published":"2012-06-28T00:00:00Z","type":"journal_article","issue":"7404","abstract":[{"text":"Colorectal tumours that are wild type for KRAS are often sensitive to EGFR blockade, but almost always develop resistance within several months of initiating therapy. The mechanisms underlying this acquired resistance to anti-EGFR antibodies are largely unknown. This situation is in marked contrast to that of small-molecule targeted agents, such as inhibitors of ABL, EGFR, BRAF and MEK, in which mutations in the genes encoding the protein targets render the tumours resistant to the effects of the drugs. The simplest hypothesis to account for the development of resistance to EGFR blockade is that rare cells with KRAS mutations pre-exist at low levels in tumours with ostensibly wild-type KRAS genes. Although this hypothesis would seem readily testable, there is no evidence in pre-clinical models to support it, nor is there data from patients. To test this hypothesis, we determined whether mutant KRAS DNA could be detected in the circulation of 28 patients receiving monotherapy with panitumumab, a therapeutic anti-EGFR antibody. We found that 9 out of 24 (38%) patients whose tumours were initially KRAS wild type developed detectable mutations in KRAS in their sera, three of which developed multiple different KRAS mutations. The appearance of these mutations was very consistent, generally occurring between 5 and 6months following treatment. Mathematical modelling indicated that the mutations were present in expanded subclones before the initiation of panitumumab treatment. These results suggest that the emergence of KRAS mutations is a mediator of acquired resistance to EGFR blockade and that these mutations can be detected in a non-invasive manner. They explain why solid tumours develop resistance to targeted therapies in a highly reproducible fashion.","lang":"eng"}],"intvolume":" 486","status":"public","title":"The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"3157","oa_version":"Submitted Version"},{"oa_version":"Submitted Version","status":"public","title":"Evolutionary dynamics of biological auctions","intvolume":" 81","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"3260","abstract":[{"lang":"eng","text":"Many scenarios in the living world, where individual organisms compete for winning positions (or resources), have properties of auctions. Here we study the evolution of bids in biological auctions. For each auction, n individuals are drawn at random from a population of size N. Each individual makes a bid which entails a cost. The winner obtains a benefit of a certain value. Costs and benefits are translated into reproductive success (fitness). Therefore, successful bidding strategies spread in the population. We compare two types of auctions. In “biological all-pay auctions”, the costs are the bid for every participating individual. In “biological second price all-pay auctions”, the cost for everyone other than the winner is the bid, but the cost for the winner is the second highest bid. Second price all-pay auctions are generalizations of the “war of attrition” introduced by Maynard Smith. We study evolutionary dynamics in both types of auctions. We calculate pairwise invasion plots and evolutionarily stable distributions over the continuous strategy space. We find that the average bid in second price all-pay auctions is higher than in all-pay auctions, but the average cost for the winner is similar in both auctions. In both cases, the average bid is a declining function of the number of participants, n. The more individuals participate in an auction the smaller is the chance of winning, and thus expensive bids must be avoided.\r\n"}],"issue":"1","type":"journal_article","date_published":"2012-02-01T00:00:00Z","page":"69 - 80","publication":"Theoretical Population Biology","citation":{"ieee":"K. Chatterjee, J. Reiter, and M. Nowak, “Evolutionary dynamics of biological auctions,” Theoretical Population Biology, vol. 81, no. 1. Academic Press, pp. 69–80, 2012.","apa":"Chatterjee, K., Reiter, J., & Nowak, M. (2012). Evolutionary dynamics of biological auctions. Theoretical Population Biology. Academic Press. https://doi.org/10.1016/j.tpb.2011.11.003","ista":"Chatterjee K, Reiter J, Nowak M. 2012. Evolutionary dynamics of biological auctions. Theoretical Population Biology. 81(1), 69–80.","ama":"Chatterjee K, Reiter J, Nowak M. Evolutionary dynamics of biological auctions. Theoretical Population Biology. 2012;81(1):69-80. doi:10.1016/j.tpb.2011.11.003","chicago":"Chatterjee, Krishnendu, Johannes Reiter, and Martin Nowak. “Evolutionary Dynamics of Biological Auctions.” Theoretical Population Biology. Academic Press, 2012. https://doi.org/10.1016/j.tpb.2011.11.003.","short":"K. Chatterjee, J. Reiter, M. Nowak, Theoretical Population Biology 81 (2012) 69–80.","mla":"Chatterjee, Krishnendu, et al. “Evolutionary Dynamics of Biological Auctions.” Theoretical Population Biology, vol. 81, no. 1, Academic Press, 2012, pp. 69–80, doi:10.1016/j.tpb.2011.11.003."},"day":"01","scopus_import":1,"date_updated":"2023-09-07T11:40:43Z","date_created":"2018-12-11T12:02:19Z","volume":81,"author":[{"last_name":"Chatterjee","first_name":"Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","full_name":"Chatterjee, Krishnendu"},{"first_name":"Johannes","last_name":"Reiter","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0170-7353","full_name":"Reiter, Johannes"},{"full_name":"Nowak, Martin","last_name":"Nowak","first_name":"Martin"}],"related_material":{"record":[{"id":"1400","relation":"dissertation_contains","status":"public"}]},"publication_status":"published","department":[{"_id":"KrCh"}],"publisher":"Academic Press","year":"2012","pmid":1,"ec_funded":1,"publist_id":"3388","language":[{"iso":"eng"}],"doi":"10.1016/j.tpb.2011.11.003","quality_controlled":"1","project":[{"grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425","name":"Quantitative Graph Games: Theory and Applications","call_identifier":"FP7"},{"name":"Rigorous Systems Engineering","call_identifier":"FWF","grant_number":"S 11407_N23","_id":"25832EC2-B435-11E9-9278-68D0E5697425"},{"name":"Modern Graph Algorithmic Techniques in Formal Verification","call_identifier":"FWF","_id":"2584A770-B435-11E9-9278-68D0E5697425","grant_number":"P 23499-N23"},{"_id":"2587B514-B435-11E9-9278-68D0E5697425","name":"Microsoft Research Faculty Fellowship"}],"main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279759/ ","open_access":"1"}],"oa":1,"external_id":{"pmid":["22120126"]},"month":"02"}]