Luke Cassereau
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View article: 1047 Protein design and inducible expression allow context-dependent, localized IL-12 activity to enhance solid tumor T cell therapies
1047 Protein design and inducible expression allow context-dependent, localized IL-12 activity to enhance solid tumor T cell therapies Open
Background IL-12 is a pleiotropic immune-stimulatory cytokine that can modulate the tumor microenvironment to promote innate and adaptive immune responses and support cytotoxic activity of T and NK cells. However, systemic delivery of IL-1…
View article: Supplemental Figure 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
ECM cues, malignant transformation, and integrin signaling, promote cell spreading and invasion.
View article: Supplemental Table 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Table 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
List of Adhesome, Oncogene and Control Genes used in Bioinformatics Analysis.
View article: Supplemental Figure 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
ECM cues, malignant transformation, and integrin signaling, promote cell spreading and invasion.
View article: Supplemental Table 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Table 1 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
List of Adhesome, Oncogene and Control Genes used in Bioinformatics Analysis.
View article: Data from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Data from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Extracellular matrix (ECM) stiffness induces focal adhesion assembly to drive malignant transformation and tumor metastasis. Nevertheless, how force alters focal adhesions to promote tumor progression remains unclear. Here, we explored the…
View article: Supplemental Figure 3 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 3 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Vinculin nanoscale localization reflects altered molecular activity.
View article: Supplemental Figure 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
MECs remodel 3D collagen gels for cell invasion. Individual collagen fibers are stiff and >500nm in diameter.
View article: Supplemental Figure 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
MECs remodel 3D collagen gels for cell invasion. Individual collagen fibers are stiff and >500nm in diameter.
View article: Supplemental Table 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Table 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
List of Cancer Tissue with Unbiased Matched Normal Tissue used in Bioinformatics Analysis.
View article: Supplemental Table 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Table 2 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
List of Cancer Tissue with Unbiased Matched Normal Tissue used in Bioinformatics Analysis.
View article: Supplemental Figure 5 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 5 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Vinculin is localized to cell-ECM borders in invasive breast cancer and adhesome proteins are upregulated across human cancers.
View article: Supplemental Figure 4 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 4 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Scanning angle interference microscopy - validation experiments.
View article: Supplemental Figure 4 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 4 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Scanning angle interference microscopy - validation experiments.
View article: Data from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Data from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Extracellular matrix (ECM) stiffness induces focal adhesion assembly to drive malignant transformation and tumor metastasis. Nevertheless, how force alters focal adhesions to promote tumor progression remains unclear. Here, we explored the…
View article: Supplemental Methods, References and Figure Legends from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Methods, References and Figure Legends from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Supplemental Methods, References, and Figure Legends
View article: Supplemental Figure 5 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 5 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Vinculin is localized to cell-ECM borders in invasive breast cancer and adhesome proteins are upregulated across human cancers.
View article: Supplemental Methods, References and Figure Legends from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Methods, References and Figure Legends from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Supplemental Methods, References, and Figure Legends
View article: Supplemental Figure 3 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate
Supplemental Figure 3 from Force Engages Vinculin and Promotes Tumor Progression by Enhancing PI3K Activation of Phosphatidylinositol (3,4,5)-Triphosphate Open
Vinculin nanoscale localization reflects altered molecular activity.
View article: A comparative study elucidating the substantial functional defects of electroporated T cells relative to a mechanical SQZ-based approach
A comparative study elucidating the substantial functional defects of electroporated T cells relative to a mechanical SQZ-based approach Open
Background: Ex vivo manipulation of primary cells is critical to the success of cell-based therapies, however, limitations of existing ex vivo delivery approaches may dramatically restrict the use of cell engineering to treat disease. Meth…
View article: Cell engineering with microfluidic squeezing preserves functionality of primary immune cells in vivo
Cell engineering with microfluidic squeezing preserves functionality of primary immune cells in vivo Open
Significance Ex vivo manipulation of primary cells is critical to the success of this emerging generation of cell-based therapies, such as chimeric antigen receptor T cells for the treatment of cancer and CRISPR for the correction of devel…
View article: Integrin-mediated traction force enhances paxillin molecular associations and adhesion dynamics that increase the invasiveness of tumor cells into a three-dimensional extracellular matrix
Integrin-mediated traction force enhances paxillin molecular associations and adhesion dynamics that increase the invasiveness of tumor cells into a three-dimensional extracellular matrix Open
Metastasis requires tumor cells to navigate through a stiff stroma and squeeze through confined microenvironments. Whether tumors exploit unique biophysical properties to metastasize remains unclear. Data show that invading mammary tumor c…
View article: Human breast cancer invasion and aggression correlates with ECM stiffening and immune cell infiltration
Human breast cancer invasion and aggression correlates with ECM stiffening and immune cell infiltration Open
Tumors are stiff and data suggest that the extracellular matrix stiffening that correlates with experimental mammary malignancy drives tumor invasion and metastasis. Nevertheless, the relationship between tissue and extracellular matrix st…
View article: Tissue Stiffness Drives Breast Cancer Malignant Progression
Tissue Stiffness Drives Breast Cancer Malignant Progression Open
Breast cancer is the most common cancer of women worldwide and the second leading cause of cancer death in women in the United States. Despite new therapies that show efficacy in treating the primary tumor there is a significant lack of th…