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  1. AU="Vázquez-García, Ignacio"
  2. AU="Yumoto, Ami"
  3. AU="Holbrook, Beth C"
  4. AU="Ananda, Virly Y"
  5. AU="Wenwu Xie"
  6. AU=Greenwood Jonathan
  7. AU="Mella, Sebastian"
  8. AU="Pogurschi, Elena"
  9. AU="Ali, Athar"
  10. AU="Chen, DeChao"
  11. AU=Markman Maurie
  12. AU="Tembo, Yamanya"
  13. AU="Vogel, Gretchen"
  14. AU="Bernd W Böttiger"
  15. AU="Burk, Robert D"
  16. AU=Hussain Mushtaq AU=Hussain Mushtaq
  17. AU="Reuter, Susanne"
  18. AU="Thomas P. Quinn"
  19. AU="Grant, April"
  20. AU="Naddaf, Elie"
  21. AU="Park, Do-Hyun"
  22. AU="Posti, Jussi P"
  23. AU="Singh, Gargi"
  24. AU="Fuhrman, Dana Y"
  25. AU="Cholak, Spencer"
  26. AU="Tanowitz, Herbert B."
  27. AU="Gao, Jia-Pei"
  28. AU="Alvarez-Lerma, Francisco"
  29. AU="Junno, Juho-Antti"
  30. AU="Livermore, Polly"
  31. AU="Pervin, Irin"
  32. AU=Upadhyay Avnish K AU=Upadhyay Avnish K
  33. AU="Yabu, Hiroshi"
  34. AU="Soares, Mario J."
  35. AU="Haeusler, Gabrielle M"
  36. AU="Wang, Weiqing"
  37. AU="Fehr, Fabio"
  38. AU="Sasirekha, R" AU="Sasirekha, R"
  39. AU="Rajendraprasad, Girish"
  40. AU="Golbek, Thaddeus W"
  41. AU="Pranav Keshan"

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  1. Artikel: CINner: modeling and simulation of chromosomal instability in cancer at single-cell resolution.

    Dinh, Khanh N / Vázquez-García, Ignacio / Chan, Andrew / Malhotra, Rhea / Weiner, Adam / McPherson, Andrew W / Tavaré, Simon

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Cancer development is characterized by chromosomal instability, manifesting in frequent occurrences of different genomic alteration mechanisms ranging in extent and impact. Mathematical modeling can help evaluate the role of each mutational process ... ...

    Abstract Cancer development is characterized by chromosomal instability, manifesting in frequent occurrences of different genomic alteration mechanisms ranging in extent and impact. Mathematical modeling can help evaluate the role of each mutational process during tumor progression, however existing frameworks can only capture certain aspects of chromosomal instability (CIN). We present CINner, a mathematical framework for modeling genomic diversity and selection during tumor evolution. The main advantage of CINner is its flexibility to incorporate many genomic events that directly impact cellular fitness, from driver gene mutations to copy number alterations (CNAs), including focal amplifications and deletions, missegregations and whole-genome duplication (WGD). We apply CINner to find chromosome-arm selection parameters that drive tumorigenesis in the absence of WGD in chromosomally stable cancer types. We found that the selection parameters predict WGD prevalence among different chromosomally unstable tumors, hinting that the selective advantage of WGD cells hinges on their tolerance for aneuploidy and escape from nullisomy. Direct application of CINner to model the WGD proportion and fraction of genome altered (FGA) further uncovers the increase in CNA probabilities associated with WGD in each cancer type. CINner can also be utilized to study chromosomally stable cancer types, by applying a selection model based on driver gene mutations and focal amplifications or deletions. Finally, we used CINner to analyze the impact of CNA probabilities, chromosome selection parameters, tumor growth dynamics and population size on cancer fitness and heterogeneity. We expect that CINner will provide a powerful modeling tool for the oncology community to quantify the impact of newly uncovered genomic alteration mechanisms on shaping tumor progression and adaptation.
    Sprache Englisch
    Erscheinungsdatum 2024-04-03
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.04.03.587939
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Single-cell DNA replication dynamics in genomically unstable cancers.

    Weiner, Adam C / Williams, Marc J / Shi, Hongyu / Vázquez-García, Ignacio / Salehi, Sohrab / Rusk, Nicole / Aparicio, Samuel / Shah, Sohrab P / McPherson, Andrew

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Dysregulated DNA replication is both a cause and a consequence of aneuploidy, yet the dynamics of DNA replication in aneuploid cell populations remains understudied. We developed a new method, PERT, for inferring cell-specific DNA replication states from ...

    Abstract Dysregulated DNA replication is both a cause and a consequence of aneuploidy, yet the dynamics of DNA replication in aneuploid cell populations remains understudied. We developed a new method, PERT, for inferring cell-specific DNA replication states from single-cell whole genome sequencing, and investigated clone-specific DNA replication dynamics in >50,000 cells obtained from a collection of aneuploid and clonally heterogeneous cell lines, xenografts and primary cancer tissues. Clone replication timing (RT) profiles correlated with future copy number changes in serially passaged cell lines. Cell type was the strongest determinant of RT heterogeneity, while whole genome doubling and mutational process were associated with accumulation of late S-phase cells and weaker RT associations. Copy number changes affecting chromosome X had striking impact on RT, with loss of the inactive X allele shifting replication earlier, and loss of inactive Xq resulting in reactivation of Xp. Finally, analysis of time series xenografts illustrate how cell cycle distributions approximate clone proliferation, recapitulating expected relationships between proliferation and fitness in treatment-naive and chemotherapeutic contexts.
    Sprache Englisch
    Erscheinungsdatum 2023-09-23
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.04.10.536250
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Single-cell mtDNA dynamics in tumors is driven by coregulation of nuclear and mitochondrial genomes.

    Kim, Minsoo / Gorelick, Alexander N / Vàzquez-García, Ignacio / Williams, Marc J / Salehi, Sohrab / Shi, Hongyu / Weiner, Adam C / Ceglia, Nick / Funnell, Tyler / Park, Tricia / Boscenco, Sonia / O'Flanagan, Ciara H / Jiang, Hui / Grewal, Diljot / Tang, Cerise / Rusk, Nicole / Gammage, Payam A / McPherson, Andrew / Aparicio, Sam /
    Shah, Sohrab P / Reznik, Ed

    Nature genetics

    2024  

    Abstract: The extent of cell-to-cell variation in tumor mitochondrial DNA (mtDNA) copy number and genotype, and the phenotypic and evolutionary consequences of such variation, are poorly characterized. Here we use amplification-free single-cell whole-genome ... ...

    Abstract The extent of cell-to-cell variation in tumor mitochondrial DNA (mtDNA) copy number and genotype, and the phenotypic and evolutionary consequences of such variation, are poorly characterized. Here we use amplification-free single-cell whole-genome sequencing (Direct Library Prep (DLP+)) to simultaneously assay mtDNA copy number and nuclear DNA (nuDNA) in 72,275 single cells derived from immortalized cell lines, patient-derived xenografts and primary human tumors. Cells typically contained thousands of mtDNA copies, but variation in mtDNA copy number was extensive and strongly associated with cell size. Pervasive whole-genome doubling events in nuDNA associated with stoichiometrically balanced adaptations in mtDNA copy number, implying that mtDNA-to-nuDNA ratio, rather than mtDNA copy number itself, mediated downstream phenotypes. Finally, multimodal analysis of DLP+ and single-cell RNA sequencing identified both somatic loss-of-function and germline noncoding variants in mtDNA linked to heteroplasmy-dependent changes in mtDNA copy number and mitochondrial transcription, revealing phenotypic adaptations to disrupted nuclear/mitochondrial balance.
    Sprache Englisch
    Erscheinungsdatum 2024-05-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-024-01724-8
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: The value of monitoring to control evolving populations.

    Fischer, Andrej / Vázquez-García, Ignacio / Mustonen, Ville

    Proceedings of the National Academy of Sciences of the United States of America

    2015  Band 112, Heft 4, Seite(n) 1007–1012

    Abstract: Populations can evolve to adapt to external changes. The capacity to evolve and adapt makes successful treatment of infectious diseases and cancer difficult. Indeed, therapy resistance has become a key challenge for global health. Therefore, ideas of how ...

    Abstract Populations can evolve to adapt to external changes. The capacity to evolve and adapt makes successful treatment of infectious diseases and cancer difficult. Indeed, therapy resistance has become a key challenge for global health. Therefore, ideas of how to control evolving populations to overcome this threat are valuable. Here we use the mathematical concepts of stochastic optimal control to study what is needed to control evolving populations. Following established routes to calculate control strategies, we first study how a polymorphism can be maintained in a finite population by adaptively tuning selection. We then introduce a minimal model of drug resistance in a stochastically evolving cancer cell population and compute adaptive therapies. When decisions are in this manner based on monitoring the response of the tumor, this can outperform established therapy paradigms. For both case studies, we demonstrate the importance of high-resolution monitoring of the target population to achieve a given control objective, thus quantifying the intuition that to control, one must monitor.
    Mesh-Begriff(e) Drug Resistance, Neoplasm ; Humans ; Models, Biological ; Neoplasms/genetics ; Neoplasms/metabolism
    Sprache Englisch
    Erscheinungsdatum 2015-01-13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1409403112
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  5. Artikel ; Online: Contrasting the impact of cytotoxic and cytostatic drug therapies on tumour progression.

    Anttila, Jani V / Shubin, Mikhail / Cairns, Johannes / Borse, Florian / Guo, Qingli / Mononen, Tommi / Vázquez-García, Ignacio / Pulkkinen, Otto / Mustonen, Ville

    PLoS computational biology

    2019  Band 15, Heft 11, Seite(n) e1007493

    Abstract: A tumour grows when the total division (birth) rate of its cells exceeds their total mortality (death) rate. The capability for uncontrolled growth within the host tissue is acquired via the accumulation of driver mutations which enable the tumour to ... ...

    Abstract A tumour grows when the total division (birth) rate of its cells exceeds their total mortality (death) rate. The capability for uncontrolled growth within the host tissue is acquired via the accumulation of driver mutations which enable the tumour to progress through various hallmarks of cancer. We present a mathematical model of the penultimate stage in such a progression. We assume the tumour has reached the limit of its present growth potential due to cell competition that either results in total birth rate reduction or death rate increase. The tumour can then progress to the final stage by either seeding a metastasis or acquiring a driver mutation. We influence the ensuing evolutionary dynamics by cytotoxic (increasing death rate) or cytostatic (decreasing birth rate) therapy while keeping the effect of the therapy on net growth reduction constant. Comparing the treatments head to head we derive conditions for choosing optimal therapy. We quantify how the choice and the related gain of optimal therapy depends on driver mutation, metastasis, intrinsic cell birth and death rates, and the details of cell competition. We show that detailed understanding of the cell population dynamics could be exploited in choosing the right mode of treatment with substantial therapy gains.
    Mesh-Begriff(e) Antineoplastic Agents/pharmacology ; Biological Evolution ; Cytostatic Agents/pharmacology ; Cytotoxins/pharmacology ; Disease Progression ; Humans ; Models, Biological ; Models, Theoretical ; Mutation ; Neoplasms/drug therapy ; Neoplastic Processes
    Chemische Substanzen Antineoplastic Agents ; Cytostatic Agents ; Cytotoxins
    Sprache Englisch
    Erscheinungsdatum 2019-11-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2193340-6
    ISSN 1553-7358 ; 1553-734X
    ISSN (online) 1553-7358
    ISSN 1553-734X
    DOI 10.1371/journal.pcbi.1007493
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: High-definition reconstruction of clonal composition in cancer.

    Fischer, Andrej / Vázquez-García, Ignacio / Illingworth, Christopher J R / Mustonen, Ville

    Cell reports

    2014  Band 7, Heft 5, Seite(n) 1740–1752

    Abstract: The extensive genetic heterogeneity of cancers can greatly affect therapy success due to the existence of subclonal mutations conferring resistance. However, the characterization of subclones in mixed-cell populations is computationally challenging due ... ...

    Abstract The extensive genetic heterogeneity of cancers can greatly affect therapy success due to the existence of subclonal mutations conferring resistance. However, the characterization of subclones in mixed-cell populations is computationally challenging due to the short length of sequence reads that are generated by current sequencing technologies. Here, we report cloneHD, a probabilistic algorithm for the performance of subclone reconstruction from data generated by high-throughput DNA sequencing: read depth, B-allele counts at germline heterozygous loci, and somatic mutation counts. The algorithm can exploit the added information present in correlated longitudinal or multiregion samples and takes into account correlations along genomes caused by events such as copy-number changes. We apply cloneHD to two case studies: a breast cancer sample and time-resolved samples of chronic lymphocytic leukemia, where we demonstrate that monitoring the response of a patient to therapy regimens is feasible. Our work provides new opportunities for tracking cancer development.
    Mesh-Begriff(e) Algorithms ; Breast Neoplasms/genetics ; Clonal Evolution ; Humans ; Leukemia, Lymphoid/genetics ; Models, Genetic ; Mutation
    Sprache Englisch
    Erscheinungsdatum 2014-05-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2014.04.055
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Buch ; Online: The value of monitoring to control evolving populations

    Fischer, Andrej / Vazquez-Garcia, Ignacio / Mustonen, Ville

    2014  

    Abstract: Populations can evolve in order to adapt to external changes. The capacity to evolve and adapt makes successful treatment of infectious diseases and cancer difficult. Indeed, therapy resistance has quickly become a key challenge for global health. ... ...

    Abstract Populations can evolve in order to adapt to external changes. The capacity to evolve and adapt makes successful treatment of infectious diseases and cancer difficult. Indeed, therapy resistance has quickly become a key challenge for global health. Therefore, ideas of how to control evolving populations in order to overcome this threat are valuable. Here we use the mathematical concepts of stochastic optimal control to study what is needed to control evolving populations. Following established routes to calculate control strategies, we first study how a polymorphism can be maintained in a finite population by adaptively tuning selection. We then introduce a minimal model of drug resistance in a stochastically evolving cancer cell population and compute adaptive therapies, where decisions are based on monitoring the response of the tumor, which can outperform established therapy paradigms. For both case studies, we demonstrate the importance of high-resolution monitoring of the target population in order to achieve a given control objective: to control one must monitor.

    Comment: 27 pages
    Schlagwörter Quantitative Biology - Populations and Evolution
    Thema/Rubrik (Code) 629
    Erscheinungsdatum 2014-06-26
    Erscheinungsland us
    Dokumenttyp Buch ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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  8. Artikel ; Online: Imaging and Molecular Annotation of Xenographs and Tumours (IMAXT): High throughput data and analysis infrastructure.

    González-Solares, Eduardo A / Dariush, Ali / González-Fernández, Carlos / Küpcü Yoldaş, Aybüke / Molaeinezhad, Alireza / Al Sa'd, Mohammad / Smith, Leigh / Whitmarsh, Tristan / Millar, Neil / Chornay, Nicholas / Falciatori, Ilaria / Fatemi, Atefeh / Goodwin, Daniel / Kuett, Laura / Mulvey, Claire M / Páez Ribes, Marta / Qosaj, Fatime / Roth, Andrew / Vázquez-García, Ignacio /
    Watson, Spencer S / Windhager, Jonas / Aparicio, Samuel / Bodenmiller, Bernd / Boyden, Ed / Caldas, Carlos / Harris, Owen / Shah, Sohrab P / Tavaré, Simon / Bressan, Dario / Hannon, Gregory J / Walton, Nicholas A

    Biological imaging

    2023  Band 3, Seite(n) e11

    Abstract: With the aim of producing a 3D representation of tumors, imaging and molecular annotation of xenografts and tumors (IMAXT) uses a large variety of modalities in order to acquire tumor samples and produce a map of every cell in the tumor and its host ... ...

    Abstract With the aim of producing a 3D representation of tumors, imaging and molecular annotation of xenografts and tumors (IMAXT) uses a large variety of modalities in order to acquire tumor samples and produce a map of every cell in the tumor and its host environment. With the large volume and variety of data produced in the project, we developed automatic data workflows and analysis pipelines. We introduce a research methodology where scientists connect to a cloud environment to perform analysis close to where data are located, instead of bringing data to their local computers. Here, we present the data and analysis infrastructure, discuss the unique computational challenges and describe the analysis chains developed and deployed to generate molecularly annotated tumor models. Registration is achieved by use of a novel technique involving spherical fiducial marks that are visible in all imaging modalities used within IMAXT. The automatic pipelines are highly optimized and allow to obtain processed datasets several times quicker than current solutions narrowing the gap between data acquisition and scientific exploitation.
    Sprache Englisch
    Erscheinungsdatum 2023-04-14
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 2633-903X
    ISSN (online) 2633-903X
    DOI 10.1017/S2633903X23000090
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Shared Molecular Targets Confer Resistance over Short and Long Evolutionary Timescales.

    Li, Jing / Vázquez-García, Ignacio / Persson, Karl / González, Asier / Yue, Jia-Xing / Barré, Benjamin / Hall, Michael N / Long, Anthony / Warringer, Jonas / Mustonen, Ville / Liti, Gianni

    Molecular biology and evolution

    2019  Band 36, Heft 4, Seite(n) 691–708

    Abstract: Pre-existing and de novo genetic variants can both drive adaptation to environmental changes, but their relative contributions and interplay remain poorly understood. Here we investigated the evolutionary dynamics in drug-treated yeast populations with ... ...

    Abstract Pre-existing and de novo genetic variants can both drive adaptation to environmental changes, but their relative contributions and interplay remain poorly understood. Here we investigated the evolutionary dynamics in drug-treated yeast populations with different levels of pre-existing variation by experimental evolution coupled with time-resolved sequencing and phenotyping. We found a doubling of pre-existing variation alone boosts the adaptation by 64.1% and 51.5% in hydroxyurea and rapamycin, respectively. The causative pre-existing and de novo variants were selected on shared targets: RNR4 in hydroxyurea and TOR1, TOR2 in rapamycin. Interestingly, the pre-existing and de novo TOR variants map to different functional domains and act via distinct mechanisms. The pre-existing TOR variants from two domesticated strains exhibited opposite rapamycin resistance effects, reflecting lineage-specific functional divergence. This study provides a dynamic view on how pre-existing and de novo variants interactively drive adaptation and deepens our understanding of clonally evolving populations.
    Mesh-Begriff(e) Biological Evolution ; Cell Cycle Proteins/genetics ; Drug Resistance, Fungal/genetics ; Hydroxyurea ; Mutation ; Phosphatidylinositol 3-Kinases/genetics ; Quantitative Trait Loci ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics ; Selection, Genetic ; Sirolimus
    Chemische Substanzen Cell Cycle Proteins ; Saccharomyces cerevisiae Proteins ; TOR1 protein, S cerevisiae (EC 2.7.1.137) ; TOR2 protein, S cerevisiae (EC 2.7.1.137) ; Sirolimus (W36ZG6FT64) ; Hydroxyurea (X6Q56QN5QC)
    Sprache Englisch
    Erscheinungsdatum 2019-01-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 998579-7
    ISSN 1537-1719 ; 0737-4038
    ISSN (online) 1537-1719
    ISSN 0737-4038
    DOI 10.1093/molbev/msz006
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Author Correction: Fundamental immune-oncogenicity trade-offs define driver mutation fitness.

    Hoyos, David / Zappasodi, Roberta / Schulze, Isabell / Sethna, Zachary / de Andrade, Kelvin César / Bajorin, Dean F / Bandlamudi, Chaitanya / Callahan, Margaret K / Funt, Samuel A / Hadrup, Sine R / Holm, Jeppe S / Rosenberg, Jonathan E / Shah, Sohrab P / Vázquez-García, Ignacio / Weigelt, Britta / Wu, Michelle / Zamarin, Dmitriy / Campitelli, Laura F / Osborne, Edward J /
    Klinger, Mark / Robins, Harlan S / Khincha, Payal P / Savage, Sharon A / Balachandran, Vinod P / Wolchok, Jedd D / Hellmann, Matthew D / Merghoub, Taha / Levine, Arnold J / Łuksza, Marta / Greenbaum, Benjamin D

    Nature

    2022  Band 606, Heft 7914, Seite(n) E5

    Sprache Englisch
    Erscheinungsdatum 2022-05-31
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-022-04879-8
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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