Cell migration in tumors

Yamaguchi, Hideki; Wyckoff, Jeffrey; Condeelis, John S.

doi:10.1016/j.ceb.2005.08.002

Cited by 706 publications

(589 citation statements)

References 44 publications

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“…This approach is expected to improve current cancer modeling efforts because a multiscale approach model connects previous work focused on specific scales and specific processes (e.g., single cell motion) by performing 3-dimensional simulations of in vivo tumors. This methodology further allows the possibility to see beyond the current reductionist picture of invasion and migration [78,111,187,198,204,117,206,64,179,75,77,53,172], with the goal to enable prediction of disease progression and treatment response based on patient-specific tumor characteristics. …”

Section: Resultsmentioning

confidence: 99%

Nonlinear Modeling and Simulation of Tumor Growth

Cristini

Frieboes

et al. 2008

Selected Topics in Cancer Modeling

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Section: Resultsmentioning

confidence: 99%

Nonlinear Modeling and Simulation of Tumor Growth

Cristini

Frieboes

et al. 2008

Selected Topics in Cancer Modeling

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“…However, the local activation of a photosensitive caged cofilin shows that the local activation of cofilin in mammary tumour cells generates free actin filament barbed ends, initiates actin polymerization, induces localized protrusion of the cell membrane and determines the direction of cell migration 39 . Cofilin activation is essential for the formation of stable invadopods, which are used during the migration of invasive tumour cells, linking cofilin to tumour cell invasion 49 . Therefore, the local activation of cofilin by any of the mechanisms described above -dephosphorylation, PIP2 hydrolysis and increasing pH -could in principle initiate directional tumour cell motility and invasion.…”

Section: Biochemistry Of the Cofilin Pathwaymentioning

confidence: 99%

The cofilin pathway in breast cancer invasion and metastasis

Wang¹,

2007

Self Cite

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Recent evidence indicates that metastatic capacity is an inherent feature of breast tumours and not a rare, late acquired event. This has led to new models of metastasis. The interpretation of expression-profiling data in the context of these new models has identified the cofilin pathway as a major determinant of metastasis. Recent studies indicate that the overall activity of the cofilin pathway, and not that of any single gene within the pathway, determines the invasive and metastatic phenotype of tumour cells. These results predict that inhibitors directed at the output of the cofilin pathway will have therapeutic benefit in combating metastasis.Tumour cell motility is the hallmark of invasion and an essential step in metastasis 1,2 . The identification of molecular pathways that contribute to tumour cell motility and invasion is essential for understanding how motility is initiated in tumour cells and how the tumour microenvironment contributes to cell migration. The identification of the molecular pathways of tumour cell invasion will provide new diagnostic approaches and targets for the treatment of metastatic cancer. Recent studies using new technologies, including highdensity microarray-based expression profiling, intravital imaging and the collection of invasive tumour cells from live tumours, have started to extend the traditional model of metastasis and supply new diagnostic and therapeutic markers of metastatic disease.According to the traditional model of metastasis, metastases result from a process similar to Darwinian evolution whereby natural selection works on individual tumour cells to select © 2007 Nature Publishing Group Correspondence to: J.C. Condeeli@aecom.yu.edu. Competing interests statementThe authors declare no competing financial interests. for stable genetic changes. The cells so selected are very rare, and the metastatic cells that arise from this progressive selection of stable genetic mutations within the primary tumour cause metastasis late in tumour progression 3 . However, studies of mammary tumours in mice [4][5][6][7] , expression profiling of both whole human breast tumours 8,9 and the invasive subpopulation of tumour cells isolated from rat and mouse mammary tumours [10][11][12] suggest that the metastatic ability of breast tumours is encoded throughout the bulk of the primary tumour, involves transient changes in gene expression and is acquired at much earlier stages of tumour progression than postulated by the traditional model. These results suggest that a Darwinian-like evolution is accompanied by, and may contribute to, microenvironmentinduced transient changes in gene expression that support the invasive and metastatic phenotype. These results have led to new models where the microenvironment initiates the expression of genes that induce cell motility, invasion and metastasis 11,13 . In the 'tumour microenvironment invasion model' it is proposed that oncogenic mutations in tumour cells lead to microenvironments that are potentially encoded throughout the b...

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“…Not surprisingly, perturbations of migration can lead to severe disorders with direct relevance to human survival and health. Cancer, the second leading cause of death in the developed countries worldwide, is characterized by impaired attachment of cells to the matrix and perturbation of the cell migratory mechanisms (see (Yamaguchi et al, 2005 for an overview).…”

Section: Cell Migration and Human Diseasementioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

113

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Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

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Cell migration in tumors

Cited by 706 publications

References 44 publications

Nonlinear Modeling and Simulation of Tumor Growth

Nonlinear Modeling and Simulation of Tumor Growth

The cofilin pathway in breast cancer invasion and metastasis

Cell biology of embryonic migration

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