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How Scatter Factor Receptor c-MET Contributes to Tumor Radioresistance: Ready, Set, Scatter!

CancerSpectrum Knowledge Environment (Impact Factor: 15.16). 04/2011; 103(8):617-9. DOI: 10.1093/jnci/djr103
Source: PubMed
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    • "D'un point de vue clinique, ce modèle non linéaire (chaotique ?) de « cancer » reproduit qualitativement certains résultats thérapeutiques. Les immunothérapies n'ont en effet pas encore rencontrées les succès espérés alors que le ciblage des tissus non tumoraux apporte des résultats cliniques significatifs (traitements anti-angiogéniques) ou prometteurs (anti-périostine, anti c-Met, anti IL6, etc.) [27] [28] [29] [30] [31]. Cela ne peut être le fruit du « hasard » (le modèle ne résulte pas d'une construction par tirage au sort) et la « lecture » de la dynamique de ce modèle par la théorie du chaos révèle bien un lien réel avec la dynamique clinico-biologique observée. "
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    ABSTRACT: Although the same simple laws govern cancer outcome (cell division repeated again and again), each tumour has a different outcome before as well as after irradiation therapy. The linear-quadratic radiosensitivity model allows an assessment of tumor sensitivity to radiotherapy. This model presents some limitations in clinical practice because it does not take into account the interactions between tumour cells and non-tumoral bystander cells (such as endothelial cells, fibroblasts, immune cells…) that modulate radiosensitivity and tumor growth dynamics. These interactions can lead to non-linear and complex tumor growth which appears to be random but that is not since there is not so many tumors spontaneously regressing. In this paper we propose to develop a deterministic approach for tumour growth dynamics using chaos theory. Various characteristics of cancer dynamics and tumor radiosensitivity can be explained using mathematical models of competing cell species.
    Cancer/Radiothérapie 09/2012; 16(s 5–6):404–409. DOI:10.1016/j.canrad.2012.05.004 · 1.11 Impact Factor
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    • "D'un point de vue clinique, ce modèle non linéaire (chaotique ?) de « cancer » reproduit qualitativement certains résultats thérapeutiques. Les immunothérapies n'ont en effet pas encore rencontrées les succès espérés alors que le ciblage des tissus non tumoraux apporte des résultats cliniques significatifs (traitements anti-angiogéniques) ou prometteurs (anti-périostine, anti c-Met, anti IL6, etc.) [27] [28] [29] [30] [31]. Cela ne peut être le fruit du « hasard » (le modèle ne résulte pas d'une construction par tirage au sort) et la « lecture » de la dynamique de ce modèle par la théorie du chaos révèle bien un lien réel avec la dynamique clinico-biologique observée. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Although the same simple laws govern cancer outcome (cell division repeated again and again), each tumour has a different outcome before as well as after irradiation therapy. The linear-quadratic radiosensitivity model allows an assessment of tumor sensitivity to radiotherapy. This model presents some limitations in clinical practice because it does not take into account the interactions between tumour cells and non-tumoral bystander cells (such as endothelial cells, fibroblasts, immune cells…) that modulate radiosensitivity and tumor growth dynamics. These interactions can lead to non-linear and complex tumor growth which appears to be random but that is not since there is not so many tumors spontaneously regressing. In this paper we propose to develop a deterministic approach for tumour growth dynamics using chaos theory. Various characteristics of cancer dynamics and tumor radiosensitivity can be explained using mathematical models of competing cell species.
    Cancer/Radiothérapie 07/2012; 16(5-6):404-9. · 1.11 Impact Factor
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    ABSTRACT: MET is a versatile receptor tyrosine kinase within the human kinome which is activated by its specific natural ligand hepatocyte growth factor (HGF). MET signaling plays an important physiologic role in embryogenesis and early development, whereas its deregulation from an otherwise quiescent signaling state in mature adult tissues can lead to upregulated cell proliferation, survival, scattering, motility and migration, angiogenesis, invasion, and metastasis in tumorigenesis and tumor progression. Studies have shown that MET pathway is activated in many solid and hematological malignancies, including lung cancer, and can be altered through ligand or receptor overexpression, genomic amplification, MET mutations, and alternative splicing. The MET signaling pathway is known to be an important novel target for therapeutic intervention in human cancer. A number of novel therapeutic agents that target the MET/HGF pathway have been tested in early-phase clinical studies with promising results. Phase 3 studies of MET targeting agents have just been initiated. We will review the MET signaling pathway and biology in lung cancer and the recent clinical development and advances of MET/HGF targeting agents with emphasis on discussion of issues and strategies needed to optimize the personalized therapy and further clinical development.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 02/2012; 7(2):459-67. DOI:10.1097/JTO.0b013e3182417e44 · 5.80 Impact Factor
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