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  1. Analyzed Page
  2. Matching Content Categories
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  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s10555-008-9173-4.

Title:
Mechanics, malignancy, and metastasis: The force journey of a tumor cell | Cancer and Metastasis Reviews
Description:
A cell undergoes many genetic and epigenetic changes as it transitions to malignancy. Malignant transformation is also accompanied by a progressive loss of tissue homeostasis and perturbations in tissue architecture that ultimately culminates in tumor cell invasion into the parenchyma and metastasis to distant organ sites. Increasingly, cancer biologists have begun to recognize that a critical component of this transformation journey involves marked alterations in the mechanical phenotype of the cell and its surrounding microenvironment. These mechanical differences include modifications in cell and tissue structure, adaptive force-induced changes in the environment, altered processing of micromechanical cues encoded in the extracellular matrix (ECM), and cell-directed remodeling of the extracellular stroma. Here, we review critical steps in this “force journey,” including mechanical contributions to tissue dysplasia, invasion of the ECM, and metastasis. We discuss the biophysical basis of this force journey and present recent advances in the measurement of cellular mechanical properties in vitro and in vivo. We end by describing examples of molecular mechanisms through which tumor cells sense, process and respond to mechanical forces in their environment. While our understanding of the mechanical components of tumor growth, survival and motility remains in its infancy, considerable work has already yielded valuable insight into the molecular basis of force-dependent tumor pathophysiology, which offers new directions in cancer chemotherapeutics.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 8,151,168 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

cell, google, scholar, pubmed, cas, cells, tumor, mechanical, journal, force, adhesion, tissue, cancer, biology, ecm, focal, forces, mechanics, cellular, properties, biophysical, matrix, stress, living, cytoskeletal, invasion, kinase, afm, metastasis, molecular, rho, laser, growth, cultured, actin, fak, research, journey, migration, signaling, including, structures, contractility, endothelial, remodeling, stiffness, methods, nature, extracellular, mammary,

Topics {✒️}

integrin-mediated signal-transduction linked src-dependent pi3k/akt pathway multiple-particle-tracking microrheology characterize physically-defined microenvironments n-wasp-arp2/3 complex pathway simple irrigator-aspirator cannula micron-scale macromolecular complexes drosophila foregut/stomodeal primordium adhesion-dependent cell mechanosensitivity high-throughput rheological measurements cell-derived contractile forces promote anchorage-independent survival polyacrylamide-based substrates produces force-dependent tumor pathophysiology specific receptor-ligand interactions pubmed  google scholar broad-spectrum pharmacological inhibition traditionally-trained cancer biologists human breast cancer—observations c-elegans developing embryos multiple-particle tracking defined cell-cell junctions penetrate cell-cell junctions including tumor de-adhesion rho gtpase-dependent contractility stiffness-dependent cell contractility article download pdf tumor-induced stromal stiffening subcellular laser ablation intra-operative 3d ultrasound altered cell-cell adhesion rock inhibitor fasudil probing single-cell micromechanics adhesion-mediated mechanosensitivity laser-severed stress fibers chemokine receptor cxcr2 nonreceptor tyrosine kinase colon carcinoma cells cell-directed ecm dynamics enable real-time tracking collagen-based ecm substrates focal adhesion kinase atomic force microscopy atomic-force microscopy increased intracranial pressure nuclear deformation—require local epithelial-mesenchymal transition privacy choices/manage cookies stem cell populations collagen gels affixed

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Mechanics, malignancy, and metastasis: The force journey of a tumor cell
         description:A cell undergoes many genetic and epigenetic changes as it transitions to malignancy. Malignant transformation is also accompanied by a progressive loss of tissue homeostasis and perturbations in tissue architecture that ultimately culminates in tumor cell invasion into the parenchyma and metastasis to distant organ sites. Increasingly, cancer biologists have begun to recognize that a critical component of this transformation journey involves marked alterations in the mechanical phenotype of the cell and its surrounding microenvironment. These mechanical differences include modifications in cell and tissue structure, adaptive force-induced changes in the environment, altered processing of micromechanical cues encoded in the extracellular matrix (ECM), and cell-directed remodeling of the extracellular stroma. Here, we review critical steps in this “force journey,” including mechanical contributions to tissue dysplasia, invasion of the ECM, and metastasis. We discuss the biophysical basis of this force journey and present recent advances in the measurement of cellular mechanical properties in vitro and in vivo. We end by describing examples of molecular mechanisms through which tumor cells sense, process and respond to mechanical forces in their environment. While our understanding of the mechanical components of tumor growth, survival and motility remains in its infancy, considerable work has already yielded valuable insight into the molecular basis of force-dependent tumor pathophysiology, which offers new directions in cancer chemotherapeutics.
         datePublished:2009-01-21T00:00:00Z
         dateModified:2009-01-21T00:00:00Z
         pageStart:113
         pageEnd:127
         license:https://creativecommons.org/licenses/by-nc/2.0
         sameAs:https://doi.org/10.1007/s10555-008-9173-4
         keywords:
            Cancer
            Extracellular matrix
            Cell mechanics
            Atomic force microscopy
            Subcellular laser ablation
            Rho kinase
            Focal adhesion kinase
            Cancer Research
            Oncology
            Biomedicine
            general
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      headline:Mechanics, malignancy, and metastasis: The force journey of a tumor cell
      description:A cell undergoes many genetic and epigenetic changes as it transitions to malignancy. Malignant transformation is also accompanied by a progressive loss of tissue homeostasis and perturbations in tissue architecture that ultimately culminates in tumor cell invasion into the parenchyma and metastasis to distant organ sites. Increasingly, cancer biologists have begun to recognize that a critical component of this transformation journey involves marked alterations in the mechanical phenotype of the cell and its surrounding microenvironment. These mechanical differences include modifications in cell and tissue structure, adaptive force-induced changes in the environment, altered processing of micromechanical cues encoded in the extracellular matrix (ECM), and cell-directed remodeling of the extracellular stroma. Here, we review critical steps in this “force journey,” including mechanical contributions to tissue dysplasia, invasion of the ECM, and metastasis. We discuss the biophysical basis of this force journey and present recent advances in the measurement of cellular mechanical properties in vitro and in vivo. We end by describing examples of molecular mechanisms through which tumor cells sense, process and respond to mechanical forces in their environment. While our understanding of the mechanical components of tumor growth, survival and motility remains in its infancy, considerable work has already yielded valuable insight into the molecular basis of force-dependent tumor pathophysiology, which offers new directions in cancer chemotherapeutics.
      datePublished:2009-01-21T00:00:00Z
      dateModified:2009-01-21T00:00:00Z
      pageStart:113
      pageEnd:127
      license:https://creativecommons.org/licenses/by-nc/2.0
      sameAs:https://doi.org/10.1007/s10555-008-9173-4
      keywords:
         Cancer
         Extracellular matrix
         Cell mechanics
         Atomic force microscopy
         Subcellular laser ablation
         Rho kinase
         Focal adhesion kinase
         Cancer Research
         Oncology
         Biomedicine
         general
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         name:Springer US
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            name:Sanjay Kumar
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                  name:University of California
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                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Valerie M. Weaver
            affiliation:
                  name:University of California
                  address:
                     name:Department of Surgery and Center for Bioengineering and Tissue Regeneration, Department of Anatomy, Department of Bioengineering and Therapeutics, Institute for Regeneration Medicine, University of California, San Francisco, USA
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      name:University of California
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         name:Department of Bioengineering, University of California, Berkeley, USA
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               name:Department of Bioengineering, University of California, Berkeley, USA
               type:PostalAddress
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      email:[email protected]
      name:Valerie M. Weaver
      affiliation:
            name:University of California
            address:
               name:Department of Surgery and Center for Bioengineering and Tissue Regeneration, Department of Anatomy, Department of Bioengineering and Therapeutics, Institute for Regeneration Medicine, University of California, San Francisco, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Bioengineering, University of California, Berkeley, USA
      name:Department of Surgery and Center for Bioengineering and Tissue Regeneration, Department of Anatomy, Department of Bioengineering and Therapeutics, Institute for Regeneration Medicine, University of California, San Francisco, USA

External Links {🔗}(313)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
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