Haoqiang Ying
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View article: Supplementary Figure S1 from KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer
Supplementary Figure S1 from KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer Open
Figure S1 shows characterization of premalignant lesions in KRAS G12C and G12D mice.
View article: Supplementary Figure S4 from KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer
Supplementary Figure S4 from KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer Open
Figure S4 shows targeting CD24 sensitizes pancreatic cancer to KRAS inhibitors.
View article: Supplementary Table S3 from KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer
Supplementary Table S3 from KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer Open
Supplementary Table S3 shows the percentage of immune cells in mouse KRAS G12C and G12D tumors tissues.
View article: 1288 TME and molecular characteristics of <i>KRAS</i> <sup>Q61</sup> mutated gastrointestinal malignancies and clinical outcomes
1288 TME and molecular characteristics of <i>KRAS</i> <sup>Q61</sup> mutated gastrointestinal malignancies and clinical outcomes Open
View article: KRAS mutation detection by liquid biopsy for pancreatic ductal adenocarcinoma
KRAS mutation detection by liquid biopsy for pancreatic ductal adenocarcinoma Open
View article: Targeting a chemo-induced adaptive signaling circuit confers therapeutic vulnerabilities in pancreatic cancer
Targeting a chemo-induced adaptive signaling circuit confers therapeutic vulnerabilities in pancreatic cancer Open
Advanced pancreatic ductal adenocarcinomas (PDACs) respond poorly to all therapies, including the first-line treatment, chemotherapy, the latest immunotherapies, and KRAS-targeting therapies. Despite an enormous effort to improve therapeut…
View article: All-trans retinoic acid-mediated ADAR1 degradation synergizes with PD-1 blockade to suppress pancreatic cancer
All-trans retinoic acid-mediated ADAR1 degradation synergizes with PD-1 blockade to suppress pancreatic cancer Open
As a double-stranded RNA–editing enzyme and an interferon-stimulated gene, double-stranded RNA-specific adenosine deaminase (ADAR1) suppresses interferon signaling and contributes to immunotherapy resistance. Suppression of ADAR1 overcomes…
View article: Molecular and Clinical Features of Pancreatic Acinar Cell Carcinoma: A Single-Institution Case Series
Molecular and Clinical Features of Pancreatic Acinar Cell Carcinoma: A Single-Institution Case Series Open
Objectives: Acinar cell carcinoma (ACC) accounts for about 1% of pancreatic cancers. The molecular and clinical features of ACC are less characterized than those of pancreatic ductal adenocarcinoma. Methods: We retrospectively evaluated th…
View article: Molecular and Clinical Features of Pancreatic Acinar Cell Carcinoma: A Single Institution Case Series
Molecular and Clinical Features of Pancreatic Acinar Cell Carcinoma: A Single Institution Case Series Open
Acinar cell carcinoma (ACC) accounts for about 1% of pancreatic cancers. The molecular and clinical features of ACC are less characterized than pancreatic ductal adenocarcinoma. We retrospectively evaluated the clinical and molecular featu…
View article: Therapeutic targeting of Syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers
Therapeutic targeting of Syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers Open
The therapeutic benefit of recently developed mutant KRAS (mKRAS) inhibitors has been limited by the rapid onset of resistance. Here, we aimed to delineate the mechanisms underlying acquired resistance to mKRAS inhibition and identify acti…
View article: Nanoclustering and signaling of KRAS G12C and KRAS G12D respond to lipid acyl chain remodeling in an allele-specific manner
Nanoclustering and signaling of KRAS G12C and KRAS G12D respond to lipid acyl chain remodeling in an allele-specific manner Open
Small GTPase KRAS mutated at hotspots, such as G12, G13 and Q61, are major drivers of cancer and display allele-specific oncogenic properties, which are not well understood. KRAS mutants require precise spatiotemporal distribution to the p…
View article: Clonal dominance defines metastatic dissemination in pancreatic cancer
Clonal dominance defines metastatic dissemination in pancreatic cancer Open
Tumors represent ecosystems where subclones compete during tumor growth. While extensively investigated, a comprehensive picture of the interplay of clonal lineages during dissemination is still lacking. Using patient-derived pancreatic ca…
View article: KRAS Inhibition Activates an Actionable CD24 “Don’t Eat Me” Signal in Pancreatic Cancer
KRAS Inhibition Activates an Actionable CD24 “Don’t Eat Me” Signal in Pancreatic Cancer Open
KRAS G12C inhibitors (G12Ci) have produced encouraging, albeit modest and transient, clinical benefit in pancreatic ductal adenocarcinoma (PDAC). Identifying and targeting resistance mechanisms to G12Ci treatment is therefore crucial. To b…
View article: Modulation of the proteostasis network promotes tumor resistance to oncogenic KRAS inhibitors
Modulation of the proteostasis network promotes tumor resistance to oncogenic KRAS inhibitors Open
Despite substantial advances in targeting mutant KRAS, tumor resistance to KRAS inhibitors (KRASi) remains a major barrier to progress. Here, we report proteostasis reprogramming as a key convergence point of multiple KRASi-resistance mech…
View article: KRASG12D inhibition reprograms the microenvironment of early and advanced pancreatic cancer to promote FAS-mediated killing by CD8+ T cells
KRASG12D inhibition reprograms the microenvironment of early and advanced pancreatic cancer to promote FAS-mediated killing by CD8+ T cells Open
View article: Elimination of oncogenic KRAS in genetic mouse models eradicates pancreatic cancer by inducing FAS-dependent apoptosis by CD8+ T cells
Elimination of oncogenic KRAS in genetic mouse models eradicates pancreatic cancer by inducing FAS-dependent apoptosis by CD8+ T cells Open
View article: Ether phospholipids are required for mitochondrial reactive oxygen species homeostasis
Ether phospholipids are required for mitochondrial reactive oxygen species homeostasis Open
Mitochondria are hubs where bioenergetics, redox homeostasis, and anabolic metabolism pathways integrate through a tightly coordinated flux of metabolites. The contributions of mitochondrial metabolism to tumor growth and therapy resistanc…
View article: Supplementary Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1
Supplementary Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1 Open
Supplementary Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1
View article: Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1
Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1 Open
Despite the popular use of dietary supplements during conventional cancer treatments, their impacts on the efficacies of prevalent immunotherapies, including immune-checkpoint therapy (ICT), are unknown. Surprisingly, our analyses of elect…
View article: Supplementary Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1
Supplementary Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1 Open
Supplementary Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1
View article: Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1
Data from Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1 Open
Despite the popular use of dietary supplements during conventional cancer treatments, their impacts on the efficacies of prevalent immunotherapies, including immune-checkpoint therapy (ICT), are unknown. Surprisingly, our analyses of elect…
View article: Supplementary Tables 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma
Supplementary Tables 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma Open
PDF file - 1.1MB, Supplementary Table 1: list of 290 TCGA samples used in the study. Supplementary Table 2: list of miR-mRNA edges identified by CLR. Supplementary Table 3: list of putative direct miR-mRNA edges in the network. Supplementa…
View article: Data from Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment
Data from Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment Open
A hallmark of pancreatic ductal adenocarcinoma (PDAC) is an exuberant stroma comprised of diverse cell types that enable or suppress tumor progression. Here, we explored the role of oncogenic KRAS in protumorigenic signaling interactions b…
View article: Supplementary Tables 1-2, Figures 1-8 from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network
Supplementary Tables 1-2, Figures 1-8 from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network Open
Supplementary Tables 1-2, Figures 1-8 from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network
View article: Supplementary Methods, Figure Legends 1-13, Table Legends 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma
Supplementary Methods, Figure Legends 1-13, Table Legends 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma Open
PDF file - 198K
View article: Supplementary Tables 1-2, Figures 1-8 from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network
Supplementary Tables 1-2, Figures 1-8 from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network Open
Supplementary Tables 1-2, Figures 1-8 from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network
View article: Data from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network
Data from PTEN Is a Major Tumor Suppressor in Pancreatic Ductal Adenocarcinoma and Regulates an NF-κB–Cytokine Network Open
Initiation of pancreatic ductal adenocarcinoma (PDAC) is driven by oncogenic KRAS mutation, and disease progression is associated with frequent loss of tumor suppressors. In this study, human PDAC genome analyses revealed frequent d…
View article: Supplementary Figures 1-13 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma
Supplementary Figures 1-13 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma Open
PDF file - 854K, Supplementary Figure 1: miR-mRNA relationship (miR-34a; PDGFRA) detected by CLR in all GBM samples. Supplementary Figure 2: loss of p53 and Pten in murine neural stem cells and progenitor cells promotes the formation of pr…
View article: Supplementary Tables 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma
Supplementary Tables 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma Open
PDF file - 1.1MB, Supplementary Table 1: list of 290 TCGA samples used in the study. Supplementary Table 2: list of miR-mRNA edges identified by CLR. Supplementary Table 3: list of putative direct miR-mRNA edges in the network. Supplementa…
View article: Supplementary Methods, Figure Legends 1-13, Table Legends 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma
Supplementary Methods, Figure Legends 1-13, Table Legends 1-10 from microRNA Regulatory Network Inference Identifies miR-34a as a Novel Regulator of TGF-β Signaling in Glioblastoma Open
PDF file - 198K