Zhenyu Ji
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View article: An artificial intelligence system for qualified mucosal observation time during colonoscopic withdrawal
An artificial intelligence system for qualified mucosal observation time during colonoscopic withdrawal Open
Colonoscopic withdrawal time is crucial for achieving a high adenoma detection rate (ADR) and reducing post-colonoscopy colorectal cancer risk. Enhanced qualified mucosal observation improves ADR, but manual quantification of qualified muc…
View article: Fabrication and functional validation of a hybrid biomimetic nanovaccine (HBNV) against Kit-mutant melanoma
Fabrication and functional validation of a hybrid biomimetic nanovaccine (HBNV) against Kit-mutant melanoma Open
Cancer nanovaccines hold the promise for personalization, precision, and pliability by integrating all the elements essential for effective immune stimulation. An effective immune response requires communication and interplay between antig…
View article: Geotemporal Analysis of Melanoma Incidence and Mortality Identifies Distinct Clusters of Trends within the United States Between 2001 and 2019
Geotemporal Analysis of Melanoma Incidence and Mortality Identifies Distinct Clusters of Trends within the United States Between 2001 and 2019 Open
View article: Molecular Analysis of Murine KitK641E Melanoma Progression
Molecular Analysis of Murine KitK641E Melanoma Progression Open
View article: Supplementary Figure S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S2. EphA2 inhibitor-kinase interaction maps.
View article: Supplementary Table S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Table S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Table S1. The information of the melanoma patients for EphA2 analysis.
View article: Supplementary Table S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Table S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Table S2. Combination indices per method of Chou and Talalay.
View article: Data from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Data from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
BRAFV600E is the most common oncogenic lesion in melanoma and results in constitutive activation of the MAPK pathway and uncontrolled cell growth. Selective BRAF inhibitors such as vemurafenib have been shown to neutralize oncog…
View article: Supplementary Table S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Table S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Table S2. Combination indices per method of Chou and Talalay.
View article: Supplementary Figure S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S1. Survival Curves for VEM resistant lines.
View article: Supplementary Figure S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S1. Survival Curves for VEM resistant lines.
View article: Supplementary Figure S4 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S4 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S4. EphA2 inhibitors suppressed the viability of VEM sensitive and resistant BRAF mutant cell lines and NRAS mutant cell lines.
View article: Supplementary Figure S5 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S5 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S5. ALW-II-41-27 suppresses in vivo tumor growth of both VEM sensitive and resistant melanomas.
View article: Supplementary Figure S4 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S4 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S4. EphA2 inhibitors suppressed the viability of VEM sensitive and resistant BRAF mutant cell lines and NRAS mutant cell lines.
View article: Supplementary Figure S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S2 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S2. EphA2 inhibitor-kinase interaction maps.
View article: Supplementary Figure S3 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S3 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S3. Fig. S3. Validation of EphA2 as the target of EphA2 inhibitors.
View article: Supplementary Table S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Table S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Table S1. The information of the melanoma patients for EphA2 analysis.
View article: Supplementary Figure S5 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S5 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S5. ALW-II-41-27 suppresses in vivo tumor growth of both VEM sensitive and resistant melanomas.
View article: Data from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Data from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
BRAFV600E is the most common oncogenic lesion in melanoma and results in constitutive activation of the MAPK pathway and uncontrolled cell growth. Selective BRAF inhibitors such as vemurafenib have been shown to neutralize oncog…
View article: Supplementary Figure Legends from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure Legends from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure Legends
View article: Supplementary Figure Legends from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure Legends from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure Legends
View article: Supplementary Figure S3 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
Supplementary Figure S3 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma Open
Supplementary Figure S3. Fig. S3. Validation of EphA2 as the target of EphA2 inhibitors.
View article: Supplementary Figure 2 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Figure 2 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 88K, Nutlin-3 induces p53 and Hdm2 but not Mdm4 even though the basal levels of Mdm4 is higher than Hdm2.
View article: Supplementary Table 1 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Table 1 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 89K, These are molecules that respond to vemurafenib.
View article: Supplementary Figure 1 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Figure 1 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 75K, Survival curves for A375 and A375(PLX-R) which have been induced into resistance.
View article: Supplementary Figure 3 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Figure 3 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 136K, Synergistic cytotoxicity between vemurafenib and Nt3. Green cells are live while dead cells are red in this assay.
View article: Supplementary Figure 4 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Figure 4 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 57K, Suppression of survivin levels by Nt3 (6 uM) in 4 melanoma lines.
View article: Supplementary Table 1 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Table 1 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 89K, These are molecules that respond to vemurafenib.
View article: Supplementary Figure 4 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Figure 4 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 57K, Suppression of survivin levels by Nt3 (6 uM) in 4 melanoma lines.
View article: Supplementary Figure 6 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth
Supplementary Figure 6 from Vemurafenib Synergizes with Nutlin-3 to Deplete Survivin and Suppresses Melanoma Viability and Tumor Growth Open
PDF file, 74K, Mean survival fraction upon exposure to 10uM vemurafenib among p53 mutated and p53WT cell lines.