We are analyzing https://link.springer.com/article/10.1007/s13402-014-0210-8.

Title:
Anti-tumor activity of the TGF-β receptor kinase inhibitor galunisertib (LY2157299 monohydrate) in patient-derived tumor xenografts | Cellular Oncology
Description:
Purpose The transforming growth factor-beta (TGF-β) signaling pathway is known to play a critical role in promoting tumor growth. Consequently, blocking this pathway has been found to inhibit tumor growth. In order to achieve an optimal anti-tumor effect, however, it remains to be established whether blocking the TGF-β signaling pathway alone is sufficient, or whether the tumor microenvironment plays an additional, possibly synergistic, role. Methods To investigate the relevance of blocking TGF-β signaling in tumor cells within the context of their respective tissue microenvironments, we treated a panel of patient-derived xenografts (PDX) with the selective TGF-β receptor kinase inhibitor LY2157299 monohydrate (galunisertib) and assessed both the in vitro and in vivo effects. Results Galunisertib was found to inhibit the growth in an in vitro clonogenic assay in 6.3 % (5/79) of the examined PDX. Evaluation of the expression profiles of a number of genes, representing both canonical and non-canonical TGF-β signaling pathways, revealed that most PDX exhibited expression changes affecting TGF-β downstream signaling. Next, we subjected 13 of the PDX to an in vivo assessment and, by doing so, observed distinct response patterns. These results suggest that, next to intrinsic, also extrinsic or microenvironmental factors can affect galunisertib response. pSMAD2 protein expression and TGF-βRI mRNA expression levels were found to correlate with the in vivo galunisertib effects. Conclusions From our data we conclude that intrinsic, tumor-dependent TGF-β signaling does not fully explain the anti-tumor effect of galunisertib. Hence, in vivo xenograft models may be more appropriate than in vitro clonogenic assays to assess the anti-tumor activity of TGF-β inhibitors such as galunisertib.
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Keywords {🔍}

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Topics {✒️}

tgf-beta family signalling }}_{\boldsymbol{control}}-\boldsymbol{au}{\boldsymbol{ }}_{\boldsymbol{treatment}}}{\boldsymbol{au}{\boldsymbol{ aacr-nci-eortc international conference transforming growth factor-beta tgf-β-dependent autocrine loop tumor-dependent tgf-β signaling smad-dependent tgf-β signaling tgfβ signalling pathway tgf-β receptor ii tgf-β receptor signaling patient-derived tumor xenografts tgf-β signaling cascade jun n-terminal kinase cell line-derived xenografts =\frac{\boldsymbol{au}{\boldsymbol{ tgf-β signaling pathway transforming growth factor tgf-β-dependent signaling article google scholar tgf-β inhibitor galunisertib cas google scholar patient-derived melanoma xenografts patient-derived xenograft samples secondary hrp-coupled antibody primary patient-derived cells tgf-βri mrna expression tgf-β signaling pathways canonical tgf-β pathway canonical tgf-β pathway blocking tgf-β signaling tgf-beta signaling results cd8-positive t-cells goat anti-rabbit igg optimal anti-tumor effect characterizing anti-tumor activities selectively target tgf-βri elicit anti-tumor effects targeted anticancer agents canonical tgf-β1signaling pathway vivo anti-tumor activity tgf-beta receptor celltiter-glo® viability assay small-molecule alk5 inhibitors article download pdf pharmacologically targeted concentration anti-tumor effect appeared epidermal growth factor tgf-β receptor patient-derived xenograft

Schema {🗺️}

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         description:The transforming growth factor-beta (TGF-β) signaling pathway is known to play a critical role in promoting tumor growth. Consequently, blocking this pathway has been found to inhibit tumor growth. In order to achieve an optimal anti-tumor effect, however, it remains to be established whether blocking the TGF-β signaling pathway alone is sufficient, or whether the tumor microenvironment plays an additional, possibly synergistic, role. To investigate the relevance of blocking TGF-β signaling in tumor cells within the context of their respective tissue microenvironments, we treated a panel of patient-derived xenografts (PDX) with the selective TGF-β receptor kinase inhibitor LY2157299 monohydrate (galunisertib) and assessed both the in vitro and in vivo effects. Galunisertib was found to inhibit the growth in an in vitro clonogenic assay in 6.3 % (5/79) of the examined PDX. Evaluation of the expression profiles of a number of genes, representing both canonical and non-canonical TGF-β signaling pathways, revealed that most PDX exhibited expression changes affecting TGF-β downstream signaling. Next, we subjected 13 of the PDX to an in vivo assessment and, by doing so, observed distinct response patterns. These results suggest that, next to intrinsic, also extrinsic or microenvironmental factors can affect galunisertib response. pSMAD2 protein expression and TGF-βRI mRNA expression levels were found to correlate with the in vivo galunisertib effects. From our data we conclude that intrinsic, tumor-dependent TGF-β signaling does not fully explain the anti-tumor effect of galunisertib. Hence, in vivo xenograft models may be more appropriate than in vitro clonogenic assays to assess the anti-tumor activity of TGF-β inhibitors such as galunisertib.
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      headline:Anti-tumor activity of the TGF-β receptor kinase inhibitor galunisertib (LY2157299 monohydrate) in patient-derived tumor xenografts
      description:The transforming growth factor-beta (TGF-β) signaling pathway is known to play a critical role in promoting tumor growth. Consequently, blocking this pathway has been found to inhibit tumor growth. In order to achieve an optimal anti-tumor effect, however, it remains to be established whether blocking the TGF-β signaling pathway alone is sufficient, or whether the tumor microenvironment plays an additional, possibly synergistic, role. To investigate the relevance of blocking TGF-β signaling in tumor cells within the context of their respective tissue microenvironments, we treated a panel of patient-derived xenografts (PDX) with the selective TGF-β receptor kinase inhibitor LY2157299 monohydrate (galunisertib) and assessed both the in vitro and in vivo effects. Galunisertib was found to inhibit the growth in an in vitro clonogenic assay in 6.3 % (5/79) of the examined PDX. Evaluation of the expression profiles of a number of genes, representing both canonical and non-canonical TGF-β signaling pathways, revealed that most PDX exhibited expression changes affecting TGF-β downstream signaling. Next, we subjected 13 of the PDX to an in vivo assessment and, by doing so, observed distinct response patterns. These results suggest that, next to intrinsic, also extrinsic or microenvironmental factors can affect galunisertib response. pSMAD2 protein expression and TGF-βRI mRNA expression levels were found to correlate with the in vivo galunisertib effects. From our data we conclude that intrinsic, tumor-dependent TGF-β signaling does not fully explain the anti-tumor effect of galunisertib. Hence, in vivo xenograft models may be more appropriate than in vitro clonogenic assays to assess the anti-tumor activity of TGF-β inhibitors such as galunisertib.
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         Gene expression
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            address:
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               type:PostalAddress
            type:Organization
      name:Vincent Vuaroqueaux
      affiliation:
            name:Oncotest GmbH
            address:
               name:Biomaker Development, Oncotest GmbH, Freiburg, Germany
               type:PostalAddress
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      name:Biomaker Development, Oncotest GmbH, Freiburg, Germany
      name:Early Phase Clinical Investigation, Eli Lilly and Company, Indianapolis, USA
      name:Bethesda, USA

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