Shiyong Neo
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View article: Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment
Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment Open
Viral etiologies of cancers have been widely studied for tumorigenesis and in recent years, widely recognized for their potential influence on immune regulation and response to immune checkpoint blockade (ICB). Here, we review the current …
View article: VHL restoration in clear cell renal cell carcinoma improves NK cell infiltration and function
VHL restoration in clear cell renal cell carcinoma improves NK cell infiltration and function Open
Background The von Hippel–Lindau (VHL) gene is frequently mutated in clear cell renal cell carcinoma (ccRCC) which results in stabilization of hypoxia-inducible factor (HIF). Despite the well-known immunosuppressive effect of HIF, ccRCC is…
View article: Figure S5 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S5 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S5
View article: Figure S3 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S3 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S3
View article: Supplementary Table 2 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Supplementary Table 2 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
DEGs for all NK subclusters
View article: Figure S6 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S6 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S6
View article: Figure S2 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S2 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S2
View article: Figure S4 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S4 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S4
View article: Supplementary Table 1 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Supplementary Table 1 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Key Resources Table
View article: Figure S7 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S7 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S7
View article: Data from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Data from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Adaptive NK (aNK) cells have emerged as a subset of NK cells with memory-like properties and specific cytotoxicity, offering promising therapeutic potential in cancer immunotherapy. In this study, we explored the role of aNK cells in high-…
View article: Supplementary Table 3 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Supplementary Table 3 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
DEGs for all myeloid cell clusters
View article: Figure S1 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Figure S1 from Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Supplementary Figure S1
View article: Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer
Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer Open
Adaptive NK (aNK) cells have emerged as a subset of NK cells with memory-like properties and specific cytotoxicity, offering promising therapeutic potential in cancer immunotherapy. In this study, we explored the role of aNK cells in high-…
View article: Cellular and secretome profiling uncover immunological biomarkers in the prognosis of renal cell carcinoma patients
Cellular and secretome profiling uncover immunological biomarkers in the prognosis of renal cell carcinoma patients Open
Renal cell carcinoma (RCC) is recognized as an immunogenic tumor, yet tumor-infiltrating lymphocytes often exhibit diminished effector function. However, the mechanisms underlying reduced T and NK cell activity in RCC remain unclear. Here,…
View article: Atypical memory B cells acquire Breg phenotypes in hepatocellular carcinoma
Atypical memory B cells acquire Breg phenotypes in hepatocellular carcinoma Open
The functional plasticity of tumor-infiltrating lymphocyte B-cells (TIL-B) spans from antitumor responses to noncanonical immune suppression. Yet, how the tumor microenvironment (TME) influences TIL-B development is still underappreciated.…
View article: Revolutionizing cancer treatment: the emerging potential and potential challenges of <i>in vivo</i> self-processed CAR cell therapy
Revolutionizing cancer treatment: the emerging potential and potential challenges of <i>in vivo</i> self-processed CAR cell therapy Open
Chimeric antigen receptor (CAR) cell immunotherapies, including CAR-T, CAR-Macrophages, CAR-Natural Killer, CAR-γδ T, etc., have demonstrated significant advancements in the treatment of both hematologic malignancies and solid tumors. Desp…
View article: Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin isoform imbalance on survival of patients with metastatic melanoma.
View article: Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of combination treatment on p53-activation in skin melanoma malignant phenotype in in vitro 3D models
View article: Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of combination treatment on p53-activation in skin melanoma malignant phenotype in in vitro 3D models
View article: Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Rescue-validation of β-arrestin imbalance effects on MDM2-dependent IGF1R expression.
View article: Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Specificity of β-arrestin1/2 siRNA effectson MDM2 localization.
View article: Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Table S1. Cell lines used in this study.
View article: Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on IGF1R expression
View article: Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Rescue-validation of β-arrestin imbalance effects on MDM2-dependent IGF1R expression.
View article: Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on response to dacarbazine (DTIC)
View article: Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin isoform imbalance on survival of patients with metastatic melanoma.
View article: Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Specificity of β-arrestin1/2 siRNA effectson MDM2 localization.
View article: Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on MDM2 localization
View article: Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Table S2. Antibodies used in this study.