--- _id: '454' 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. 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." article_number: '555' article_processing_charge: No author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Christian full_name: Hilbe, Christian id: 2FDF8F3C-F248-11E8-B48F-1D18A9856A87 last_name: Hilbe orcid: 0000-0001-5116-955X - first_name: David full_name: Rand, David last_name: Rand - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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 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 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. 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. 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. 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). date_created: 2018-12-11T11:46:34Z date_published: 2018-02-07T00:00:00Z date_updated: 2023-09-11T12:51:03Z day: '07' ddc: - '004' department: - _id: KrCh doi: 10.1038/s41467-017-02721-8 ec_funded: 1 external_id: isi: - '000424318200001' file: - access_level: open_access checksum: b6b90367545b4c615891c960ab0567f1 content_type: application/pdf creator: system date_created: 2018-12-12T10:09:18Z date_updated: 2020-07-14T12:46:31Z file_id: '4741' file_name: IST-2018-964-v1+1_2018_Hilbe_Crosstalk_in.pdf file_size: 843646 relation: main_file file_date_updated: 2020-07-14T12:46:31Z has_accepted_license: '1' intvolume: ' 9' isi: 1 issue: '1' language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ month: '02' oa: 1 oa_version: Published Version project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '7368' pubrep_id: '964' quality_controlled: '1' scopus_import: '1' status: public title: Crosstalk in concurrent repeated games impedes direct reciprocity and requires stronger levels of forgiveness tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 9 year: '2018' ... --- _id: '653' abstract: - lang: eng 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. 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.).' article_processing_charge: No article_type: original author: - first_name: Alvin full_name: Makohon Moore, Alvin last_name: Makohon Moore - first_name: Ming full_name: Zhang, Ming last_name: Zhang - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Benjamin full_name: Allen, Benjamin last_name: Allen - first_name: Deepanjan full_name: Kundu, Deepanjan id: 1d4c0f4f-e8a3-11ec-a351-e36772758c45 last_name: Kundu - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Fay full_name: Wong, Fay last_name: Wong - first_name: Yuchen full_name: Jiao, Yuchen last_name: Jiao - first_name: Zachary full_name: Kohutek, Zachary last_name: Kohutek - first_name: Jungeui full_name: Hong, Jungeui last_name: Hong - first_name: Marc full_name: Attiyeh, Marc last_name: Attiyeh - first_name: Breanna full_name: Javier, Breanna last_name: Javier - first_name: Laura full_name: Wood, Laura last_name: Wood - first_name: Ralph full_name: Hruban, Ralph last_name: Hruban - first_name: Martin full_name: Nowak, Martin last_name: Nowak - first_name: Nickolas full_name: Papadopoulos, Nickolas last_name: Papadopoulos - first_name: Kenneth full_name: Kinzler, Kenneth last_name: Kinzler - first_name: Bert full_name: Vogelstein, Bert last_name: Vogelstein - first_name: Christine full_name: Iacobuzio Donahue, Christine last_name: Iacobuzio Donahue citation: 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 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. 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. 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. 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. date_created: 2018-12-11T11:47:43Z date_published: 2017-03-01T00:00:00Z date_updated: 2022-06-10T09:55:08Z day: '01' ddc: - '000' department: - _id: KrCh doi: 10.1038/ng.3764 ec_funded: 1 external_id: pmid: - '28092682' file: - access_level: open_access checksum: e442dc3b7420a36ec805e9bb45cc1a2e content_type: application/pdf creator: dernst date_created: 2019-11-19T08:13:50Z date_updated: 2020-07-14T12:47:33Z file_id: '7050' file_name: 2017_NatureGenetics_Makohon.pdf file_size: 908099 relation: main_file file_date_updated: 2020-07-14T12:47:33Z has_accepted_license: '1' intvolume: ' 49' issue: '3' language: - iso: eng month: '03' oa: 1 oa_version: Submitted Version page: 358 - 366 pmid: 1 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory publication: Nature Genetics publication_identifier: issn: - '10614036' publication_status: published publisher: Nature Publishing Group publist_id: '7092' quality_controlled: '1' scopus_import: '1' status: public title: Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 49 year: '2017' ... --- _id: '1080' abstract: - lang: eng 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. article_number: '14114' article_processing_charge: No author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Alvin full_name: Makohon Moore, Alvin last_name: Makohon Moore - first_name: Jeffrey full_name: Gerold, Jeffrey last_name: Gerold - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Christine full_name: Iacobuzio Donahue, Christine last_name: Iacobuzio Donahue - first_name: Bert full_name: Vogelstein, Bert last_name: Vogelstein - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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 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 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. 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. 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. short: J. Reiter, A. Makohon Moore, J. Gerold, I. Božić, K. Chatterjee, C. Iacobuzio Donahue, B. Vogelstein, M. Nowak, Nature Communications 8 (2017). date_created: 2018-12-11T11:50:02Z date_published: 2017-01-31T00:00:00Z date_updated: 2023-09-20T11:55:31Z day: '31' ddc: - '004' - '006' department: - _id: KrCh doi: 10.1038/ncomms14114 ec_funded: 1 external_id: isi: - '000393096600001' file: - access_level: open_access content_type: application/pdf creator: system date_created: 2018-12-12T10:15:15Z date_updated: 2018-12-12T10:15:15Z file_id: '5133' file_name: IST-2017-786-v1+1_ncomms14114.pdf file_size: 897050 relation: main_file file_date_updated: 2018-12-12T10:15:15Z has_accepted_license: '1' intvolume: ' 8' isi: 1 language: - iso: eng month: '01' oa: 1 oa_version: Published Version project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '6301' pubrep_id: '786' quality_controlled: '1' scopus_import: '1' status: public title: Reconstructing metastatic seeding patterns of human cancers tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 8 year: '2017' ... --- _id: '1665' 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. article_processing_charge: No article_type: original author: - first_name: Dan full_name: Landau, Dan last_name: Landau - first_name: Eugen full_name: Tausch, Eugen last_name: Tausch - first_name: Amaro full_name: Taylor Weiner, Amaro last_name: Taylor Weiner - first_name: Chip full_name: Stewart, Chip last_name: Stewart - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Jasmin full_name: Bahlo, Jasmin last_name: Bahlo - first_name: Sandra full_name: Kluth, Sandra last_name: Kluth - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Michael full_name: Lawrence, Michael last_name: Lawrence - first_name: Sebastian full_name: Böttcher, Sebastian last_name: Böttcher - first_name: Scott full_name: Carter, Scott last_name: Carter - first_name: Kristian full_name: Cibulskis, Kristian last_name: Cibulskis - first_name: Daniel full_name: Mertens, Daniel last_name: Mertens - first_name: Carrie full_name: Sougnez, Carrie last_name: Sougnez - first_name: Mara full_name: Rosenberg, Mara last_name: Rosenberg - first_name: Julian full_name: Hess, Julian last_name: Hess - first_name: Jennifer full_name: Edelmann, Jennifer last_name: Edelmann - first_name: Sabrina full_name: Kless, Sabrina last_name: Kless - first_name: Michael full_name: Kneba, Michael last_name: Kneba - first_name: Matthias full_name: Ritgen, Matthias last_name: Ritgen - first_name: Anna full_name: Fink, Anna last_name: Fink - first_name: Kirsten full_name: Fischer, Kirsten last_name: Fischer - first_name: Stacey full_name: Gabriel, Stacey last_name: Gabriel - first_name: Eric full_name: Lander, Eric last_name: Lander - first_name: Martin full_name: Nowak, Martin last_name: Nowak - first_name: Hartmut full_name: Döhner, Hartmut last_name: Döhner - first_name: Michael full_name: Hallek, Michael last_name: Hallek - first_name: Donna full_name: Neuberg, Donna last_name: Neuberg - first_name: Gad full_name: Getz, Gad last_name: Getz - first_name: Stephan full_name: Stilgenbauer, Stephan last_name: Stilgenbauer - first_name: Catherine full_name: Wu, Catherine last_name: Wu citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:53:21Z date_published: 2015-10-22T00:00:00Z date_updated: 2021-01-12T06:52:23Z day: '22' department: - _id: KrCh doi: 10.1038/nature15395 ec_funded: 1 external_id: pmid: - '26466571' intvolume: ' 526' issue: '7574' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4815041/ month: '10' oa: 1 oa_version: Submitted Version page: 525 - 530 pmid: 1 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25832EC2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S 11407_N23 name: Rigorous Systems Engineering publication: Nature publication_status: published publisher: Nature Publishing Group publist_id: '5484' quality_controlled: '1' scopus_import: 1 status: public title: Mutations driving CLL and their evolution in progression and relapse type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 526 year: '2015' ... --- _id: '5444' 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. alternative_title: - IST Austria Technical Report author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Alvin full_name: Makohon-Moore, Alvin last_name: Makohon-Moore - first_name: Jeffrey full_name: Gerold, Jeffrey last_name: Gerold - first_name: Ivana full_name: Bozic, Ivana last_name: Bozic - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Christine full_name: Iacobuzio-Donahue, Christine last_name: Iacobuzio-Donahue - first_name: Bert full_name: Vogelstein, Bert last_name: Vogelstein - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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 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 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. ieee: J. Reiter et al., Reconstructing robust phylogenies of metastatic cancers. IST Austria, 2015. 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. 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. date_created: 2018-12-12T11:39:22Z date_published: 2015-12-30T00:00:00Z date_updated: 2020-07-14T23:05:07Z day: '30' ddc: - '000' - '576' department: - _id: KrCh doi: 10.15479/AT:IST-2015-399-v1-1 file: - access_level: open_access checksum: c47d33bdda06181753c0af36f16e7b5d content_type: application/pdf creator: system date_created: 2018-12-12T11:53:24Z date_updated: 2020-07-14T12:46:58Z file_id: '5485' file_name: IST-2015-399-v1+1_treeomics.pdf file_size: 3533200 relation: main_file file_date_updated: 2020-07-14T12:46:58Z has_accepted_license: '1' language: - iso: eng month: '12' oa: 1 oa_version: Published Version page: '25' publication_identifier: issn: - 2664-1690 publication_status: published publisher: IST Austria pubrep_id: '399' status: public title: Reconstructing robust phylogenies of metastatic cancers type: technical_report user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2015' ... --- _id: '1709' 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. 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.' article_processing_charge: No article_type: original author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Ayush full_name: Kanodia, Ayush last_name: Kanodia - first_name: Raghav full_name: Gupta, Raghav last_name: Gupta - first_name: Martin full_name: Nowak, Martin last_name: Nowak - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X citation: 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 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 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. 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. 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). 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). date_created: 2018-12-11T11:53:35Z date_published: 2015-07-15T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '15' department: - _id: KrCh doi: 10.1098/rspb.2015.1041 external_id: pmid: - '26180069' intvolume: ' 282' issue: '1812' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528522/ month: '07' oa: 1 oa_version: Submitted Version pmid: 1 project: - _id: 25832EC2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S 11407_N23 name: Rigorous Systems Engineering - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 2587B514-B435-11E9-9278-68D0E5697425 name: Microsoft Research Faculty Fellowship publication: Proceedings of the Royal Society of London Series B Biological Sciences publication_status: published publisher: Royal Society publist_id: '5425' quality_controlled: '1' related_material: record: - id: '1400' relation: dissertation_contains status: public scopus_import: 1 status: public title: Biological auctions with multiple rewards type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 282 year: '2015' ... --- _id: '1400' 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. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 citation: ama: Reiter J. The subclonal evolution of cancer. 2015. apa: Reiter, J. (2015). The subclonal evolution of cancer. Institute of Science and Technology Austria. chicago: Reiter, Johannes. “The Subclonal Evolution of Cancer.” Institute of Science and Technology Austria, 2015. ieee: J. Reiter, “The subclonal evolution of cancer,” Institute of Science and Technology Austria, 2015. ista: Reiter J. 2015. The subclonal evolution of cancer. Institute of Science and Technology Austria. 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. date_created: 2018-12-11T11:51:48Z date_published: 2015-04-01T00:00:00Z date_updated: 2023-09-07T11:40:44Z day: '01' degree_awarded: PhD department: - _id: KrCh language: - iso: eng month: '04' oa_version: None page: '183' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '5807' 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 - id: '2858' relation: part_of_dissertation status: public - id: '3157' relation: part_of_dissertation status: public - id: '3260' relation: part_of_dissertation status: public status: public supervisor: - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X title: The subclonal evolution of cancer type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2015' ... --- _id: '1884' 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. author: - first_name: Dan full_name: Landau, Dan last_name: Landau - first_name: Chip full_name: Stewart, Chip last_name: Stewart - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Michael full_name: Lawrence, Michael last_name: Lawrence - first_name: Carrie full_name: Sougnez, Carrie last_name: Sougnez - first_name: Jennifer full_name: Brown, Jennifer last_name: Brown - first_name: Armando full_name: Lopez Guillermo, Armando last_name: Lopez Guillermo - first_name: Stacey full_name: Gabriel, Stacey last_name: Gabriel - first_name: Eric full_name: Lander, Eric last_name: Lander - first_name: Donna full_name: Neuberg, Donna last_name: Neuberg - first_name: Carlos full_name: López Otín, Carlos last_name: López Otín - first_name: Elias full_name: Campo, Elias last_name: Campo - first_name: Gad full_name: Getz, Gad last_name: Getz - first_name: Catherine full_name: Wu, Catherine last_name: Wu citation: 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.' 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.' 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.' 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.' 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.' 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.' 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. date_created: 2018-12-11T11:54:32Z date_published: 2014-12-04T00:00:00Z date_updated: 2021-01-12T06:53:50Z day: '04' department: - _id: KrCh intvolume: ' 124' issue: '21' language: - iso: eng main_file_link: - url: http://www.bloodjournal.org/content/124/21/1952?sso-checked=true month: '12' oa_version: None page: 1952 - 1952 publication: Blood publication_status: published publisher: American Society of Hematology publist_id: '5211' status: public 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' type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 124 year: '2014' ... --- _id: '5399' 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: - IST Austria Technical Report author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Ivana full_name: Bozic, Ivana last_name: Bozic - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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' 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' 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.' ieee: 'J. Reiter, I. Bozic, K. Chatterjee, and M. Nowak, TTP: Tool for Tumor Progression. IST Austria, 2013.' ista: 'Reiter J, Bozic I, Chatterjee K, Nowak M. 2013. TTP: Tool for Tumor Progression, IST Austria, 17p.' 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.' date_created: 2018-12-12T11:39:07Z date_published: 2013-01-11T00:00:00Z date_updated: 2023-02-23T10:23:57Z day: '11' ddc: - '000' department: - _id: KrCh doi: 10.15479/AT:IST-2013-104-v1-1 file: - access_level: open_access checksum: 2cc8c6e157eca1271128db80bb3dec80 content_type: application/pdf creator: system date_created: 2018-12-12T11:54:20Z date_updated: 2020-07-14T12:46:44Z file_id: '5542' file_name: IST-2013-104-v1+1_tumortool.pdf file_size: 1471954 relation: main_file file_date_updated: 2020-07-14T12:46:44Z has_accepted_license: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: '17' publication_identifier: issn: - 2664-1690 publication_status: published publisher: IST Austria pubrep_id: '104' related_material: record: - id: '2000' relation: later_version status: public status: public title: 'TTP: Tool for Tumor Progression' type: technical_report user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2013' ... --- _id: '9749' 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. article_processing_charge: No author: - first_name: Benjamin full_name: Zagorsky, Benjamin last_name: Zagorsky - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak 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 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 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. ieee: B. Zagorsky, J. Reiter, K. Chatterjee, and M. Nowak, “Forgiver triumphs in alternating prisoner’s dilemma .” Public Library of Science, 2013. 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. 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). date_created: 2021-07-28T15:45:07Z date_published: 2013-12-12T00:00:00Z date_updated: 2023-02-23T10:34:39Z day: '12' department: - _id: KrCh doi: 10.1371/journal.pone.0080814.s001 month: '12' oa_version: Published Version publisher: Public Library of Science related_material: record: - id: '2247' relation: used_in_publication status: public status: public title: 'Forgiver triumphs in alternating prisoner''s dilemma ' type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2013' ... --- _id: '2247' 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. article_number: e80814 author: - first_name: Benjamin full_name: Zagorsky, Benjamin last_name: Zagorsky - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak 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 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. 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. 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. short: B. Zagorsky, J. Reiter, K. Chatterjee, M. Nowak, PLoS One 8 (2013). date_created: 2018-12-11T11:56:33Z date_published: 2013-12-12T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '12' ddc: - '000' department: - _id: KrCh doi: 10.1371/journal.pone.0080814 ec_funded: 1 file: - access_level: open_access checksum: 808e8b9e6e89658bee4ffbbfac1bd19d content_type: application/pdf creator: system date_created: 2018-12-12T10:11:15Z date_updated: 2020-07-14T12:45:34Z file_id: '4868' file_name: IST-2016-409-v1+1_journal.pone.0080814.pdf file_size: 1050042 relation: main_file file_date_updated: 2020-07-14T12:45:34Z has_accepted_license: '1' intvolume: ' 8' issue: '12' language: - iso: eng month: '12' oa: 1 oa_version: Published Version project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 25832EC2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S 11407_N23 name: Rigorous Systems Engineering - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 2587B514-B435-11E9-9278-68D0E5697425 name: Microsoft Research Faculty Fellowship publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '4702' pubrep_id: '409' quality_controlled: '1' related_material: record: - id: '9749' relation: research_data status: public - id: '1400' relation: dissertation_contains status: public scopus_import: 1 status: public title: 'Forgiver triumphs in alternating prisoner''s dilemma ' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2013' ... --- _id: '2858' 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. author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Benjamin full_name: Allen, Benjamin id: 135B5B70-E9D2-11E9-BD74-BB415DA2B523 last_name: Allen - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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 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. 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. 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. short: J. Reiter, I. Božić, B. Allen, K. Chatterjee, M. Nowak, Evolutionary Applications 6 (2013) 34–45. date_created: 2018-12-11T11:59:58Z date_published: 2013-01-01T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '01' ddc: - '570' department: - _id: KrCh doi: 10.1111/eva.12020 ec_funded: 1 file: - access_level: open_access checksum: e2955b3889f8a823c3d5a72cb16f8957 content_type: application/pdf creator: system date_created: 2018-12-12T10:15:50Z date_updated: 2020-07-14T12:45:51Z file_id: '5173' file_name: IST-2016-415-v1+1_Reiter_et_al-2013-Evolutionary_Applications.pdf file_size: 1172037 relation: main_file file_date_updated: 2020-07-14T12:45:51Z has_accepted_license: '1' intvolume: ' 6' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 34 - 45 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory publication: Evolutionary Applications publication_status: published publisher: Wiley-Blackwell publist_id: '3931' pubrep_id: '415' quality_controlled: '1' related_material: record: - id: '1400' relation: dissertation_contains status: public scopus_import: 1 status: public title: The effect of one additional driver mutation on tumor progression tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2013' ... --- _id: '2816' 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. article_number: e00747 author: - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Benjamin full_name: Allen, Benjamin last_name: Allen - first_name: Tibor full_name: Antal, Tibor last_name: Antal - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Preya full_name: Shah, Preya last_name: Shah - first_name: Yo full_name: Moon, Yo last_name: Moon - first_name: Amin full_name: Yaqubie, Amin last_name: Yaqubie - first_name: Nicole full_name: Kelly, Nicole last_name: Kelly - first_name: Dung full_name: Le, Dung last_name: Le - first_name: Evan full_name: Lipson, Evan last_name: Lipson - first_name: Paul full_name: Chapman, Paul last_name: Chapman - first_name: Luis full_name: Diaz, Luis last_name: Diaz - first_name: Bert full_name: Vogelstein, Bert last_name: Vogelstein - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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 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 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. ieee: I. Božić et al., “Evolutionary dynamics of cancer in response to targeted combination therapy,” eLife, vol. 2. eLife Sciences Publications, 2013. 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. 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_created: 2018-12-11T11:59:45Z date_published: 2013-06-25T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '25' ddc: - '570' - '610' department: - _id: KrCh doi: 10.7554/eLife.00747 file: - access_level: open_access checksum: 2c38c47815eacd8fa66cb8b404cf7c61 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:48Z date_updated: 2020-07-14T12:45:49Z file_id: '4967' file_name: IST-2013-134-v1+1_e00747.full.pdf file_size: 3358321 relation: main_file file_date_updated: 2020-07-14T12:45:49Z has_accepted_license: '1' intvolume: ' 2' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: eLife publication_status: published publisher: eLife Sciences Publications publist_id: '3985' pubrep_id: '134' quality_controlled: '1' related_material: record: - id: '1400' relation: dissertation_contains status: public scopus_import: 1 status: public title: Evolutionary dynamics of cancer in response to targeted combination therapy tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 2 year: '2013' ... --- _id: '2000' 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 author: - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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' 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' 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.' 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.' 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.' 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. conference: end_date: 2013-07-19 location: St. Petersburg, Russia name: 'CAV: Computer Aided Verification' start_date: 2013-07-13 date_created: 2018-12-11T11:55:08Z date_published: 2013-01-01T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '01' department: - _id: KrCh doi: 10.1007/978-3-642-39799-8_6 ec_funded: 1 external_id: arxiv: - '1303.5251' intvolume: ' 8044' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1303.5251 month: '01' oa: 1 oa_version: Preprint page: 101 - 106 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 25832EC2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S 11407_N23 name: Rigorous Systems Engineering - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 2587B514-B435-11E9-9278-68D0E5697425 name: Microsoft Research Faculty Fellowship publication: Proceedings of 25th Int. Conf. on Computer Aided Verification publication_status: published publisher: Springer publist_id: '5077' quality_controlled: '1' related_material: record: - id: '5399' relation: earlier_version status: public - id: '1400' relation: dissertation_contains status: public scopus_import: 1 series_title: Lecture Notes in Computer Science status: public title: 'TTP: Tool for tumor progression' type: conference user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8044 year: '2013' ... --- _id: '3157' abstract: - lang: eng 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. author: - first_name: Luis full_name: Diaz Jr, Luis last_name: Diaz Jr - first_name: Richard full_name: Williams, Richard last_name: Williams - first_name: Jian full_name: Wu, Jian last_name: Wu - first_name: Isaac full_name: Kinde, Isaac last_name: Kinde - first_name: Joel full_name: Hecht, Joel last_name: Hecht - first_name: Jordan full_name: Berlin, Jordan last_name: Berlin - first_name: Benjamin full_name: Allen, Benjamin last_name: Allen - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Martin full_name: Nowak, Martin last_name: Nowak - first_name: Kenneth full_name: Kinzler, Kenneth last_name: Kinzler - first_name: Kelly full_name: Oliner, Kelly last_name: Oliner - first_name: Bert full_name: Vogelstein, Bert last_name: Vogelstein 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 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. 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. 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. 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. date_created: 2018-12-11T12:01:43Z date_published: 2012-06-28T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '28' department: - _id: KrCh doi: 10.1038/nature11219 ec_funded: 1 external_id: pmid: - '22722843' intvolume: ' 486' issue: '7404' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436069/ month: '06' oa: 1 oa_version: Submitted Version page: 537 - 540 pmid: 1 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 25832EC2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S 11407_N23 name: Rigorous Systems Engineering publication: Nature publication_status: published publisher: Nature Publishing Group publist_id: '3537' quality_controlled: '1' related_material: record: - id: '1400' relation: dissertation_contains status: public scopus_import: 1 status: public title: The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 486 year: '2012' ... --- _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" author: - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: 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 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 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. 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. ista: Chatterjee K, Reiter J, Nowak M. 2012. Evolutionary dynamics of biological auctions. Theoretical Population Biology. 81(1), 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. short: K. Chatterjee, J. Reiter, M. Nowak, Theoretical Population Biology 81 (2012) 69–80. date_created: 2018-12-11T12:02:19Z date_published: 2012-02-01T00:00:00Z date_updated: 2023-09-07T11:40:43Z day: '01' department: - _id: KrCh doi: 10.1016/j.tpb.2011.11.003 ec_funded: 1 external_id: pmid: - '22120126' intvolume: ' 81' issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: 'http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279759/ ' month: '02' oa: 1 oa_version: Submitted Version page: 69 - 80 pmid: 1 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 25832EC2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S 11407_N23 name: Rigorous Systems Engineering - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 2587B514-B435-11E9-9278-68D0E5697425 name: Microsoft Research Faculty Fellowship publication: Theoretical Population Biology publication_status: published publisher: Academic Press publist_id: '3388' quality_controlled: '1' related_material: record: - id: '1400' relation: dissertation_contains status: public scopus_import: 1 status: public title: Evolutionary dynamics of biological auctions type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 81 year: '2012' ...