Malignancy through cooperation: an evolutionary game theory approach

Liu, Q.; Liu, Z.

doi:10.1111/j.1365-2184.2012.00824.x

Cited by 8 publications

(10 citation statements)

References 44 publications

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“…In this study, clonal populations of tumor cells were used as from these studies show that each clonal population from this cell line expresses a set of intrinsic genes that determine its specific functional behavior, both with respect to metastatic ability, organ/tissue tropism, or responsiveness to the specific tissue environment 42 . Findings from our model system provide evidence for an alternate, noncell autonomous mechanism for acquisition of metastatic activity and support the previous proposed hypothesis that clonal subpopulations within a tumor cooperate with one another to promote metastasis 11,13,[43][44][45][46] . Importantly, our studies demonstrate that these cooperative interactions can be transient.…”

Section: Discussionsupporting

confidence: 88%

Transient Commensal Clonal Interactions Can Drive Tumor Metastasis

Amara

Kuiken

Selfors

et al. 2020

Preprint

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To interrogate functional heterogeneity and crosstalk between tumor cells, we generated clonal populations from a patient-derived ovarian clear cell carcinoma model which forms malignant ascites and solid peritoneal tumors upon intraperitoneal transplantation in mice. The clonal populations were engineered with secreted Gaussia luciferase to monitor tumor growth dynamics and tagged with a unique DNA barcode to track their fate in multiclonal mixtures during tumor progression. Only one clone, CL31, grew robustly, generating exclusively malignant ascites. However, multiclonal mixtures formed large solid peritoneal metastases, populated almost entirely by CL31, suggesting that transient cooperative interclonal interactions were sufficient to promote metastasis of CL31. CL31 uniquely harbored ERBB2 amplification, and its acquired metastatic trait was dependent on transient exposure to amphiregulin, which was exclusively secreted by non-tumorigenic clones. Amphiregulin enhanced CL31 mesothelial clearance, a prerequisite for metastasis. These findings demonstrate that transient, ostensibly innocuous tumor subpopulations can promote metastases via "hitand-run" commensal interactions.

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Section: Discussionsupporting

confidence: 88%

Transient Commensal Clonal Interactions Can Drive Tumor Metastasis

Amara

Kuiken

Selfors

et al. 2020

Preprint

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“…The process of apoptosis is highly complex involving two main pathways, the extrinsic or death receptor pathway (i.e., DR4/DR5) and the intrinsic or mitochondrial-derived pathway (Elmore, 2007). Autophagy is a lysosomal-dependent pathway involving degradation and recycling of cellular components; controlled via an autophagy-related gene network (Liu et al, 2012b). Programed necrosis or necroptosis is a result of the initiation of different receptor-sensor complexes via various stimuli, including TNF-α and ROS species (Han et al, 2011).…”

Section: Identifying Molecular Pathways Involved In Crc Etiologymentioning

confidence: 99%

Identifying Molecular Targets of Lifestyle Modifications in Colon Cancer Prevention

Derry¹,

Raina²,

Agarwal³

et al. 2013

Front. Oncol.

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One in four deaths in the United States is cancer-related, and colorectal cancer (CRC) is the second leading cause of cancer-associated deaths. Screening strategies are utilized but have not reduced disease incidence or mortality. In this regard, there is an interest in cancer preventive strategies focusing on lifestyle intervention, where specific etiologic factors involved in cancer initiation, promotion, and progression could be targeted. For example, exposure to dietary carcinogens, such as nitrosamines and polycyclic aromatic hydrocarbons influences colon carcinogenesis. Furthermore, dietary deficiencies could alter sensitivity to genetic damage and influence carcinogen metabolism contributing to CRC. High alcohol consumption increases the risk of mutations including the fact that acetaldehyde, an ethanol metabolite, is classified as a group 1 carcinogen. Tobacco smoke exposure is also a risk factor for cancer development; approximately 20% of CRCs are associated with smoking. Additionally, obese patients have a higher risk of cancer development, which is further supported by the fact that physical activity decreases CRC risk by 55%. Similarly, chronic inflammatory conditions also increase the risk of CRC development. Moreover, the circadian clock alters digestion and regulates other biochemical, physiological, and behavioral processes that could influence CRC. Taken together, colon carcinogenesis involves a number of etiological factors, and therefore, to create effective preventive strategies, molecular targets need to be identified and beleaguered prior to disease progression. With this in mind, the following is a comprehensive review identifying downstream target proteins of the above lifestyle risk factors, which are modulated during colon carcinogenesis and could be targeted for CRC prevention by novel agents including phytochemicals.

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“…The notation and model parameters are summarized in Table 1. Similarly to the models presented in [Basanta et al 2008;Liu and Liu 2012;Bach et al 2001], the situation described by (1)-(4) could be modeled as a matrix game when the interactions between individual cells are assumed to be pairwise and the payoff matrix is given by…”

Section: Modelmentioning

confidence: 99%

“…In recent years this approach has been applied to study various aspects of cancer. For example, [Basanta et al 2012] uses a three cell species model to investigate prostate cancer tumor-stroma interaction; [Bach et al 2001] and [Liu and Liu 2012] develop respectively two and three species models to study the synergistic effects of 542 KE'YONA BARTON, CORBIN SMITH, JAN RYCHTÁŘ AND TSVETANKA SENDOVA interactions between stromal cells and tumor cells, which often result in malignancy. Gatenby and Vincent [2003] conducted a study on tumor cells and used game theory to improve an existing linear model.…”

Section: Introductionmentioning

confidence: 99%

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Modeling of breast cancer through evolutionary game theory

Barton

Smith

Rychtář

et al. 2018

Involve

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We present a simple mathematical model of the development and progression of breast cancer based on evolutionary game theory. Four types of cellular populations are considered: stromal (native) cells, macrophages, benign tumor cells, and motile (malignant) tumor cells. Despite the relative simplicity of the model, it provides a way to explore the interactions between the various cell types and suggests potential approaches to managing and treating cancer.

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Malignancy through cooperation: an evolutionary game theory approach

Abstract: This study explains some current experimental findings from a theoretical viewpoint, and may provide new approaches for future research in oncology.

Cited by 8 publications

References 44 publications

Transient Commensal Clonal Interactions Can Drive Tumor Metastasis

Transient Commensal Clonal Interactions Can Drive Tumor Metastasis

Identifying Molecular Targets of Lifestyle Modifications in Colon Cancer Prevention

Modeling of breast cancer through evolutionary game theory

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