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Article: Punctuational evolution is pervasive in distal site metastatic colonization.

Butler, George / Amend, Sarah R / Axelrod, Robert / Venditti, Chris / Pienta, Kenneth J

bioRxiv : the preprint server for biology

2024

Abstract: The evolution of metastasis represents a lethal stage of cancer progression. Yet, the evolutionary kinetics of metastatic disease remain unresolved. Here, using single cell CRISPR-Cas9 lineage tracing data, we show that in metastatic disease, gradual ... ...

Abstract	The evolution of metastasis represents a lethal stage of cancer progression. Yet, the evolutionary kinetics of metastatic disease remain unresolved. Here, using single cell CRISPR-Cas9 lineage tracing data, we show that in metastatic disease, gradual molecular evolution is punctuated by episodes of rapid evolutionary change associated with lineage divergence. By measuring punctuational effects across the metastatic cascade, we show that punctuational effects contribute more to the molecular diversity at distal site metastases compared to the paired primary tumor, suggesting qualitatively different modes of evolution may drive primary and metastatic tumor progression. This is the first empirical evidence for distinct patterns of molecular evolution at early and late stages of metastasis and demonstrates the complex interplay of cell intrinsic and extrinsic factors that shape lethal cancer.
Language	English
Publishing date	2024-04-11
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.08.588529
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Article: Escherichia coli

Butler, George / Bos, Julia / Austin, Robert H / Amend, Sarah R / Pienta, Kenneth J

Royal Society open science

2023 Volume 10, Issue 8, Page(s) 230338

Abstract: The evolution of antibiotic resistance is a fundamental problem in disease management but is rarely quantified on a single-cell level owing to challenges associated with capturing the spatial and temporal variation across a population. To evaluate cell ... ...

Abstract	The evolution of antibiotic resistance is a fundamental problem in disease management but is rarely quantified on a single-cell level owing to challenges associated with capturing the spatial and temporal variation across a population. To evaluate cell biological phenotypic responses, we tracked the single-cell dynamics of filamentous bacteria through time in response to ciprofloxacin antibiotic stress. We measured the degree of phenotypic variation in nucleoid length and the accumulation of protein damage under ciprofloxacin antibiotic and quantified the impact on bacterial survival. Increased survival was correlated with increased nucleoid length and the variation in this response was inversely correlated with antibiotic concentration. Survival time was also increased through clearance of misfolded proteins, an unexpected mechanism of stress relief deployed by the filamentous bacteria. Our results reveal a diverse range of survival tactics employed by bacteria in response to ciprofloxacin and suggest potential evolutionary routes to resistance.
Language	English
Publishing date	2023-08-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2787755-3
ISSN	2054-5703
ISSN	2054-5703
DOI	10.1098/rsos.230338
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Article ; Online: Updating the Definition of Cancer.

Brown, Joel S / Amend, Sarah R / Austin, Robert H / Gatenby, Robert A / Hammarlund, Emma U / Pienta, Kenneth J

Molecular cancer research : MCR

2023 Volume 21, Issue 11, Page(s) 1142–1147

Abstract: Most definitions of cancer broadly conform to the current NCI definition: "Cancer is a disease in which some of the body's cells grow uncontrollably and spread to other parts of the body." These definitions tend to describe what cancer "looks like" or " ... ...

Abstract	Most definitions of cancer broadly conform to the current NCI definition: "Cancer is a disease in which some of the body's cells grow uncontrollably and spread to other parts of the body." These definitions tend to describe what cancer "looks like" or "does" but do not describe what cancer "is" or "has become." While reflecting past insights, current definitions have not kept pace with the understanding that the cancer cell is itself transformed and evolving. We propose a revised definition of cancer: Cancer is a disease of uncontrolled proliferation by transformed cells subject to evolution by natural selection. We believe this definition captures the essence of the majority of previous and current definitions. To the simplest definition of cancer as a disease of uncontrolled proliferation of cells, our definition adds in the adjective "transformed" to capture the many tumorigenic processes that cancer cells adopt to metastasize. To the concept of uncontrolled proliferation of transformed cells, our proposed definition then adds "subject to evolution by natural selection." The subject to evolution by natural selection modernizes the definition to include the genetic and epigenetic changes that accumulate within a population of cancer cells that lead to the lethal phenotype. Cancer is a disease of uncontrolled proliferation by transformed cells subject to evolution by natural selection.
MeSH term(s)	Humans ; Selection, Genetic ; Neoplasms/genetics
Language	English
Publishing date	2023-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-23-0411
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Article ; Online: Cancer as a Social Dysfunction-Why Cancer Research Needs New Thinking.

Axelrod, Robert / Pienta, Kenneth J

Molecular cancer research : MCR

2018 Volume 16, Issue 9, Page(s) 1346–1347

Abstract: The incidence and mortality for many cancers continue to rise. As such, critical action is needed on many fronts to reshape how a society thinks, discusses, and fights cancer especially as the population grows and ages. Cancer can be described as a ... ...

Abstract	The incidence and mortality for many cancers continue to rise. As such, critical action is needed on many fronts to reshape how a society thinks, discusses, and fights cancer especially as the population grows and ages. Cancer can be described as a broken social contract that requires different conceptual frameworks such as game theory. To this end, it is our hope that this perspective will catalyze a discussion to rethink the way we approach, communicate, and fund cancer research; thinking of cancer as a broken social contract is only one example. Importantly, this endeavor will require infusion of ideas from other fields such as physics, computational medicine, complexity science, agent-based modeling, sociology, and ecology, all of which have the capacity to drive new insights into cancer biology and clinical medicine.
MeSH term(s)	Biomedical Research/methods ; Humans ; Medical Oncology/methods ; Neoplasms/psychology ; Social Environment
Language	English
Publishing date	2018-05-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-18-0013
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Article ; Online: Modeling cancer's ecological and evolutionary dynamics.

Bukkuri, Anuraag / Pienta, Kenneth J / Hockett, Ian / Austin, Robert H / Hammarlund, Emma U / Amend, Sarah R / Brown, Joel S

Medical oncology (Northwood, London, England)

2023 Volume 40, Issue 4, Page(s) 109

Abstract: In this didactic paper, we present a theoretical modeling framework, called the G-function, that integrates both the ecology and evolution of cancer to understand oncogenesis. The G-function has been used in evolutionary ecology, but has not been widely ... ...

Abstract	In this didactic paper, we present a theoretical modeling framework, called the G-function, that integrates both the ecology and evolution of cancer to understand oncogenesis. The G-function has been used in evolutionary ecology, but has not been widely applied to problems in cancer. Here, we build the G-function framework from fundamental Darwinian principles and discuss how cancer can be seen through the lens of ecology, evolution, and game theory. We begin with a simple model of cancer growth and add on components of cancer cell competition and drug resistance. To aid in exploration of eco-evolutionary modeling with this approach, we also present a user-friendly software tool. By the end of this paper, we hope that readers will be able to construct basic G function models and grasp the usefulness of the framework to understand the games cancer plays in a biologically mechanistic fashion.
MeSH term(s)	Humans ; Carcinogenesis ; Cell Transformation, Neoplastic ; Software
Language	English
Publishing date	2023-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1201189-7
ISSN	1559-131X ; 0736-0118 ; 1357-0560
ISSN (online)	1559-131X
ISSN	0736-0118 ; 1357-0560
DOI	10.1007/s12032-023-01968-0
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Article: The contribution of evolvability to the eco-evolutionary dynamics of competing species.

Bukkuri, Anuraag / Pienta, Kenneth J / Amend, Sarah R / Austin, Robert H / Hammarlund, Emma U / Brown, Joel S

Ecology and evolution

2023 Volume 13, Issue 10, Page(s) e10591

Abstract: Evolvability is the capacity of a population to generate heritable variation that can be acted upon by natural selection. This ability influences the adaptations and fitness of individual organisms. By viewing this capacity as a trait, evolvability is ... ...

Abstract	Evolvability is the capacity of a population to generate heritable variation that can be acted upon by natural selection. This ability influences the adaptations and fitness of individual organisms. By viewing this capacity as a trait, evolvability is subject to natural selection and thus plays a critical role in eco-evolutionary dynamics. Understanding this role provides insight into how species respond to changes in their environment and how species coexistence can arise and be maintained. Here, we create a G-function model of competing species, each with a different evolvability. We analyze population and strategy (= heritable phenotype) dynamics of the two populations under clade initiation (when species are introduced into a population), evolutionary tracking (constant, small changes in the environment), adaptive radiation (availability of multiple ecological niches), and evolutionary rescue (extreme environmental disturbances). We find that when species are far from an eco-evolutionary equilibrium, faster-evolving species reach higher population sizes, and when species are close to an equilibrium, slower-evolving species are more successful. Frequent, minor environmental changes promote the extinction of species with small population sizes, regardless of their evolvability. When several niches are available for a species to occupy, coexistence is possible, though slower-evolving species perform slightly better than faster-evolving ones due to the well-recognized inherent cost of evolvability. Finally, disrupting the environment at intermediate frequencies can result in coexistence with cyclical population dynamics of species with different rates of evolution.
Language	English
Publishing date	2023-10-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2635675-2
ISSN	2045-7758
ISSN	2045-7758
DOI	10.1002/ece3.10591
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Article ; Online: A mathematical investigation of polyaneuploid cancer cell memory and cross-resistance in state-structured cancer populations.

Bukkuri, Anuraag / Pienta, Kenneth J / Austin, Robert H / Hammarlund, Emma U / Amend, Sarah R / Brown, Joel S

Scientific reports

2023 Volume 13, Issue 1, Page(s) 15027

Abstract: The polyaneuploid cancer cell (PACC) state promotes cancer lethality by contributing to survival in extreme conditions and metastasis. Recent experimental evidence suggests that post-therapy PACC-derived recurrent populations display cross-resistance to ... ...

Abstract	The polyaneuploid cancer cell (PACC) state promotes cancer lethality by contributing to survival in extreme conditions and metastasis. Recent experimental evidence suggests that post-therapy PACC-derived recurrent populations display cross-resistance to classes of therapies with independent mechanisms of action. We hypothesize that this can occur through PACC memory, whereby cancer cells that have undergone a polyaneuploid transition (PAT) reenter the PACC state more quickly or have higher levels of innate resistance. In this paper, we build on our prior mathematical models of the eco-evolutionary dynamics of cells in the 2N+ and PACC states to investigate these two hypotheses. We show that although an increase in innate resistance is more effective at promoting cross-resistance, this trend can also be produced via PACC memory. We also find that resensitization of cells that acquire increased innate resistance through the PAT have a considerable impact on eco-evolutionary dynamics and extinction probabilities. This study, though theoretical in nature, can help inspire future experimentation to tease apart hypotheses surrounding how cross-resistance in structured cancer populations arises.
MeSH term(s)	Humans ; Neoplasms ; Biological Evolution ; Empirical Research ; Probability ; Research Design
Language	English
Publishing date	2023-09-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-42368-8
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Article ; Online: Nuclear morphology predicts cell survival to cisplatin chemotherapy.

Kim, Chi-Ju / Gonye, Anna Lk / Truskowski, Kevin / Lee, Cheng-Fan / Cho, Yoon-Kyoung / Austin, Robert H / Pienta, Kenneth J / Amend, Sarah R

Neoplasia (New York, N.Y.)

2023 Volume 42, Page(s) 100906

Abstract: The emergence of chemotherapy resistance drives cancer lethality in cancer patients, with treatment initially reducing overall tumor burden followed by resistant recurrent disease. While molecular mechanisms underlying resistance phenotypes have been ... ...

Abstract	The emergence of chemotherapy resistance drives cancer lethality in cancer patients, with treatment initially reducing overall tumor burden followed by resistant recurrent disease. While molecular mechanisms underlying resistance phenotypes have been explored, less is known about the cell biological characteristics of cancer cells that survive to eventually seed the recurrence. To identify the unique phenotypic characteristics associated with survival upon chemotherapy exposure, we characterized nuclear morphology and function as prostate cancer cells recovered following cisplatin treatment. Cells that survived in the days and weeks after treatment and resisted therapy-induced cell death showed increasing cell size and nuclear size, enabled by continuous endocycling resulting in repeated whole genome doubling. We further found that cells that survive after therapy release were predominantly mononucleated and likely employ more efficient DNA damage repair. Finally, we show that surviving cancer cells exhibit a distinct nucleolar phenotype and increased rRNA levels. These data support a paradigm where soon after therapy release, the treated population mostly contains cells with a high level of widespread and catastrophic DNA damage that leads to apoptosis, while the minority of cells that have successful DDR are more likely to access a pro-survival state. These findings are consistent with accession of the polyaneuploid cancer cell (PACC) state, a recently described mechanism of therapy resistance and tumor recurrence. Our findings demonstrate the fate of cancer cells following cisplatin treatment and define key cell phenotypic characteristics of the PACC state. This work is essential for understanding and, ultimately, targeting cancer resistance and recurrence.
MeSH term(s)	Humans ; Male ; Cisplatin/pharmacology ; Cell Survival/genetics ; Neoplasm Recurrence, Local ; DNA Repair ; DNA Damage ; Apoptosis/genetics ; Drug Resistance, Neoplasm/genetics ; Cell Line, Tumor
Chemical Substances	Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2023-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2023.100906
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Article ; Online: Withdrawal: The role of CXCR7/RDC1 as a chemokine receptor for CXCL12/SDF-1 in prostate cancer.

Wang, Jianhua / Shiozawa, Yusuke / Wang, Jincheng / Wang, Yu / Jung, Younghun / Pienta, Kenneth J / Mehra, Rohit / Loberg, Robert / Taichman, Russell S

The Journal of biological chemistry

2022 Volume 298, Issue 7, Page(s) 102126

Language	English
Publishing date	2022-06-20
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.102126
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Article ; Online: Exploration of drug resistance mechanisms in triple negative breast cancer cells using a microfluidic device and patient tissues.

Lim, Wanyoung / Hwang, Inwoo / Zhang, Jiande / Chen, Zhenzhong / Han, Jeonghun / Jeon, Jaehyung / Koo, Bon-Kyoung / Kim, Sangmin / Lee, Jeong Eon / Kim, Youngkwan / Pienta, Kenneth J / Amend, Sarah R / Austin, Robert H / Ahn, Jee-Yin / Park, Sungsu

eLife

2024 Volume 12

Abstract: Chemoresistance is a major cause of treatment failure in many cancers. However, the life cycle of cancer cells as they respond to and survive environmental and therapeutic stress is understudied. In this study, we utilized a microfluidic device to induce ...

Abstract	Chemoresistance is a major cause of treatment failure in many cancers. However, the life cycle of cancer cells as they respond to and survive environmental and therapeutic stress is understudied. In this study, we utilized a microfluidic device to induce the development of doxorubicin-resistant (DOXR) cells from triple negative breast cancer (TNBC) cells within 11 days by generating gradients of DOX and medium. In vivo chemoresistant xenograft models, an unbiased genome-wide transcriptome analysis, and a patient data/tissue analysis all showed that chemoresistance arose from failed epigenetic control of the nuclear protein-1 (NUPR1)/histone deacetylase 11 (HDAC11) axis, and high
MeSH term(s)	Humans ; Triple Negative Breast Neoplasms/genetics ; Drug Resistance, Neoplasm ; Doxorubicin/pharmacology ; Nuclear Proteins/metabolism ; Lab-On-A-Chip Devices ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic
Chemical Substances	Doxorubicin (80168379AG) ; Nuclear Proteins
Language	English
Publishing date	2024-03-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.88830
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