---
_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
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: '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: '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: '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: '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: '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: '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: '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
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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: '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
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checksum: e2955b3889f8a823c3d5a72cb16f8957
content_type: application/pdf
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file_size: 1172037
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oa: 1
oa_version: Published Version
page: 34 - 45
project:
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call_identifier: FP7
grant_number: '279307'
name: 'Quantitative Graph Games: Theory and Applications'
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call_identifier: FWF
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publication_status: published
publisher: Wiley-Blackwell
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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: '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
arxiv: 1
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:
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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'
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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: '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:
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department:
- _id: KrCh
doi: 10.1371/journal.pone.0080814
ec_funded: 1
file:
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project:
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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: '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:
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checksum: 2cc8c6e157eca1271128db80bb3dec80
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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:
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relation: later_version
status: public
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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: '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'
...