Metastasis and the evolution of dispersal

Tissot, Tazzio; Massol, François; Újvári, Beáta; Alix‐Panabières, Catherine; Loeuille, Nicolas; Thomas, Fréderic

doi:10.1098/rspb.2019.2186

Cited by 14 publications

(18 citation statements)

References 127 publications

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“…Polyclonal seeding occurs when CTC clusters collectively invade instead of single cells and are associated with improved survival in the bloodstream, higher colonization success in distant tissues and promotion of stem-like behaviour [ 75 , 88 , 114 , 115 ]. Clusters may have up to a 50-fold higher rate of metastasis compared with single cells [ 63 , 116 ]. While cell-intrinsic properties and specific driver mutations lead to the epithelial to mesenchymal transitions that precede metastasis, cells with these mutations alone may not survive migrating in the circulatory system to establish new lesions at distant organs [ 106 , 115 , 117 ].…”

Section: Resultsmentioning

confidence: 99%

Genetic diversity through social heterosis can increase virulence in RNA viral infections and cancer progression

Ebrahimi¹,

Nonacs²

2021

R. Soc. open sci.

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In viral infections and cancer tumours, negative health outcomes often correlate with increasing genetic diversity. Possible evolutionary processes for such relationships include mutant lineages escaping host control or diversity, per se , creating too many immune system targets. Another possibility is social heterosis where mutations and replicative errors create clonal lineages varying in intrinsic capability for successful dispersal; improved environmental buffering; resource extraction or effective defence against immune systems. Rather than these capabilities existing in one genome, social heterosis proposes complementary synergies occur across lineages in close proximity. Diverse groups overcome host defences as interacting ‘social genomes’ with group genetic tool kits exceeding limited individual plasticity. To assess the possibility of social heterosis in viral infections and cancer progression, we conducted extensive literature searches for examples consistent with general and specific predictions from the social heterosis hypothesis. Numerous studies found supportive patterns in cancers across multiple tissues and in several families of RNA viruses. In viruses, social heterosis mechanisms probably result from long coevolutionary histories of competition between pathogen and host. Conversely, in cancers, social heterosis is a by-product of recent mutations. Investigating how social genomes arise and function in viral quasi-species swarms and cancer tumours may lead to new therapeutic approaches.

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Section: Resultsmentioning

confidence: 99%

Genetic diversity through social heterosis can increase virulence in RNA viral infections and cancer progression

Ebrahimi¹,

Nonacs²

2021

R. Soc. open sci.

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“…However, the proximate and ultimate causes of this phenomenon are not completely understood [ 70 ]. As proposed by many evolutionary ecologists and cancer biologists, metastasis could be considered through the lens of biological dispersal [ 71 ]. In the light of the previous literature on the colonist/nomad game (see Box 2 ), it is useful to explore the metastatic process within the framework of Parrondo’s paradox.…”

Section: Parrondo’s Paradox In Cancer?mentioning

confidence: 99%

Does Cancer Biology Rely on Parrondo’s Principles?

Capp¹,

Nedelcu

Dujon

et al. 2021

Cancers

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Many aspects of cancer biology remain puzzling, including the proliferative and survival success of malignant cells in spite of their high genetic and epigenetic instability as well as their ability to express migrating phenotypes and/or enter dormancy despite possible fitness loss. Understanding the potential adaptive value of these phenotypic traits is confounded by the fact that, when considered separately, they seem to be rather detrimental at the cell level, at least in the short term. Here, we argue that cancer’s biology and success could frequently be governed by processes underlying Parrondo’s paradox, whereby combinations of intrinsically losing strategies may result in winning outcomes. Oncogenic selection would favor Parrondo’s dynamics because, given the environmental adversity in which malignant cells emerge and evolve, alternating between various less optimal strategies would represent the sole viable option to counteract the changing and deleterious environments cells are exposed to during tumorigenesis. We suggest that malignant processes could be viewed through this lens, and we discuss how Parrondo’s principles are also important when designing therapies against cancer.

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“…On the other hand, CTC clusters are less likely to escape these filters but are more efficient in metastasis formation. Different cancer types might use one or both ways to disseminate, in function of their stage or location ( 58 ).…”

Section: Embolization and Tumor Cell Survivalmentioning

confidence: 99%

The Metastatic Cascade as the Basis for Liquid Biopsy Development

Eslami-S¹,

Cortés‐Hernández²,

Alix‐Panabières³

2020

Front. Oncol.

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The metastatic cascade describes the process whereby aggressive cancer cells leave the primary tumor, travel through the bloodstream, and eventually reach distant organs to develop one or several metastases. During the last decade, innovative technologies have exploited the recent biological knowledge to identify new circulating biomarkers for the screening and early detection of cancer, real-time monitoring of treatment response, assessment of tumor relapse risk (prognosis), identification of new therapeutic targets and resistance mechanisms, patient stratification, and therapeutic decision-making. These techniques are broadly described using the term of Liquid Biopsy . This field is in constant progression and is based on the detection of circulating tumor cells, circulating free nucleic acids (e.g., circulating tumor DNA), circulating tumor-derived extracellular vesicles, and tumor-educated platelets. The aim of this review is to describe the biological principles underlying the liquid biopsy concept and to discuss how functional studies can expand the clinical applications of these circulating biomarkers.

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Metastasis and the evolution of dispersal

Cited by 14 publications

References 127 publications

Genetic diversity through social heterosis can increase virulence in RNA viral infections and cancer progression

Genetic diversity through social heterosis can increase virulence in RNA viral infections and cancer progression

Does Cancer Biology Rely on Parrondo’s Principles?

The Metastatic Cascade as the Basis for Liquid Biopsy Development

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