David T. Ting
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View article: Figure 1 FS1 from FGFR mRNA Expression in Cholangiocarcinoma and Its Correlation with <i>FGFR2</i> Fusion Status and Immune Signatures
Figure 1 FS1 from FGFR mRNA Expression in Cholangiocarcinoma and Its Correlation with <i>FGFR2</i> Fusion Status and Immune Signatures Open
Supplementary Figure 1
View article: Data from Differential Kinase Activity Across Prostate Tumor Compartments Defines Sensitivity to Target Inhibition
Data from Differential Kinase Activity Across Prostate Tumor Compartments Defines Sensitivity to Target Inhibition Open
Cancer therapy often results in heterogeneous responses in different metastatic lesions in the same patient. Inter- and intratumor heterogeneity in signaling within various tumor compartments and its impact on therapy are not well characte…
View article: Supplementary Data from Differential Kinase Activity Across Prostate Tumor Compartments Defines Sensitivity to Target Inhibition
Supplementary Data from Differential Kinase Activity Across Prostate Tumor Compartments Defines Sensitivity to Target Inhibition Open
Supplementary Data from Differential Kinase Activity Across Prostate Tumor Compartments Defines Sensitivity to Target Inhibition
View article: Neoadjuvant ablative radiation plus immune therapy favorably remodels the hepatocellular carcinoma tumor microenvironment
Neoadjuvant ablative radiation plus immune therapy favorably remodels the hepatocellular carcinoma tumor microenvironment Open
Although immune therapy regimens have significantly improved treatment options for patients with advanced hepatocellular carcinoma (HCC), optimal use of these regimens in earlier disease stages remains poorly defined. We conducted a single…
View article: A TROP2/Claudin program mediates immune exclusion to impede checkpoint blockade in breast cancer 2059
A TROP2/Claudin program mediates immune exclusion to impede checkpoint blockade in breast cancer 2059 Open
Description Immune exclusion inhibits anti-tumor immunity and response to immunotherapy, but its mechanisms remain poorly defined. Here, we demonstrate that Trophoblast Cell-Surface Antigen 2 (TROP2), a key target of emerging anti-cancer A…
View article: 665 TROP2 remodeling of the immune microenvironment in triple negative breast cancer
665 TROP2 remodeling of the immune microenvironment in triple negative breast cancer Open
View article: Supplemental Table 2: Pattern 1 Pathways from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma
Supplemental Table 2: Pattern 1 Pathways from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma Open
Pattern 1 Pathways
View article: Supplementary Methods and Figures from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma
Supplementary Methods and Figures from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma Open
Supplementary methods and figures
View article: Supplemental Table 3: Pattern 7 Ordered Genes from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma
Supplemental Table 3: Pattern 7 Ordered Genes from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma Open
Pattern_7_ordered_genes
View article: Supplemental Table 1: Pancreas Gene Markers from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma
Supplemental Table 1: Pancreas Gene Markers from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma Open
Pancreas Gene Markers
View article: Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancer
Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancer Open
Durotaxis, cell migration along stiffness gradients, is linked to embryonic development, tissue repair and disease. Despite solid in vitro evidence, its role in vivo remains largely speculative. Here we demonstrate that durotaxis actively …
View article: The Pdgfd-Pdgfrb axis orchestrates tumor-nerve crosstalk in pancreatic cancer
The Pdgfd-Pdgfrb axis orchestrates tumor-nerve crosstalk in pancreatic cancer Open
Nerves are an integral component of the tumor microenvironment, contributing to cancer progression, metastasis, morbidity, and mortality. In pancreatic ductal adenocarcinoma (PDAC), worse clinical outcomes are associated with perineural in…
View article: Figure 3 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Figure 3 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Collagen XVII expression is upregulated in PDAC cells upon interaction with CAFs. A, Western blot analysis of collagen XVII expression in immortalized human pancreatic ductal cells [human pancreatic duct epithelial (HPDE)], six PDAC…
View article: Supplemental Figure S2 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Supplemental Figure S2 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Expression of COL17A1 after Trasnwell co-culture of PDAC cells and CAFs
View article: Figure 1 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Figure 1 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Collagen XVII is expressed in the cancer cells of PDAC tumors and is associated with poor survival. A, Analysis of COL17A1 expression in cancer vs. normal tissues adapted from Oncomine. The numbers in the graphic indicate the…
View article: Supplementary Table S2 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Supplementary Table S2 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Patient characteristics of tumors used for RNA-seq analysis of hemidesmosome components
View article: Supplemental Figure S4 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Supplemental Figure S4 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Changes in gene expression and active AKT levels in collagen XVII-deficient cells
View article: Supplemental Figure S1 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Supplemental Figure S1 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Plots correlating expression of COLXVII with other hemidesmosome components
View article: Figure 2 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Figure 2 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Hemidesmosome components integrin β4, integrin α6, and laminin-5 are not correlated with survival in patients with PDAC. A, Representative images of IHC staining of integrin β4, integrin α6, and laminin-5 in normal pancreas and PDAC…
View article: Figure 6 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Figure 6 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
The expression of PIK3R5 and activation of AKT is dependent on collagen XVII. A, Bubble plots illustrating two upregulated gene ontology programs in collagen XVII–deficient MGH1275 cells. B, Volcano plot showing DEGs in tumor…
View article: Figure 5 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Figure 5 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Reduced tumor forming potential of COL17A1-deficient PDAC cells. A, Schematic of orthotopic implantations of PDAC cells into the pancreata of NSG mice and photographs of orthotopic tumors formed by MGH1319 and MGH1275 cells e…
View article: Supplementary Table S1 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Supplementary Table S1 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Patient characteristics of tumors used immunohistochemical analysis of hemidesmosome components
View article: Supplemental Figure S3 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Supplemental Figure S3 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Immunohistochemical and histologic analysis of collagen and fibroblast content of tumors formed by COLXVII-deficient PDAC cells
View article: Data from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Data from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Pancreatic ductal adenocarcinoma (PDAC) is a highly chemoresistant malignancy with a dismal 11% 5-year survival rate. PDAC tumors are composed of a dense desmoplastic stroma, and the interaction of this collagen-rich tumor microenvironment…
View article: Figure 4 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Figure 4 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Viability and metastatic potential of PDAC cells is dependent on collagen XVII. A, Western blot analysis of collagen XVII in MGH1319, MGH1275, and MGH1108 cells expressing an NTC shRNA and COL17A1-specific shRNAs. The express…
View article: Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5
Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5 Open
Pancreatic ductal adenocarcinoma (PDAC) is a highly chemoresistant malignancy with a dismal 11% 5-year survival rate. PDAC tumors are composed of a dense desmoplastic stroma, and the interaction of this collagen-rich tumor microenvironment…
View article: CDKN1B (p27/kip1) enhances drug-tolerant persister CTCs by restricting polyploidy following mitotic inhibitors
CDKN1B (p27/kip1) enhances drug-tolerant persister CTCs by restricting polyploidy following mitotic inhibitors Open
The mitotic inhibitor docetaxel (DTX) is often used to treat endocrine-refractory metastatic breast cancer, but initial responses are mitigated as patients develop disease progression. Using a cohort of ex vivo cultured circulating tumor c…
View article: Supplementary Figure 1 from Dynamic Evolution of Fibroblasts Revealed by Single-Cell RNA Sequencing of Human Pancreatic Cancer
Supplementary Figure 1 from Dynamic Evolution of Fibroblasts Revealed by Single-Cell RNA Sequencing of Human Pancreatic Cancer Open
Supplementary Figure 1
View article: Supplementary Figure 5 from Dynamic Evolution of Fibroblasts Revealed by Single-Cell RNA Sequencing of Human Pancreatic Cancer
Supplementary Figure 5 from Dynamic Evolution of Fibroblasts Revealed by Single-Cell RNA Sequencing of Human Pancreatic Cancer Open
Supplementary Figure 5
View article: Supplementary Figure 2 from Dynamic Evolution of Fibroblasts Revealed by Single-Cell RNA Sequencing of Human Pancreatic Cancer
Supplementary Figure 2 from Dynamic Evolution of Fibroblasts Revealed by Single-Cell RNA Sequencing of Human Pancreatic Cancer Open
Supplementary Figure 2