Yunpeng Yang

Supplementary Table S3 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Table S3 shows that oligonucleotides used in this study.

Supplementary Table S2 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Table S2 shows that individual clinicopathologic data have been reported in NSCLC patients with EGFR-fusions that were treated with EGFR-TKIs.

Supplementary Figure S4 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Figure S4 shows that SRC mediates the phosphorylation of the C-terminal SHC1 at Y239/240, including molecular docking analysis of the EGFR-SHC1 and SRC interaction, along with immunoblotting validation in HEK-293T cells following SRC knockdown and in SYF cells reconstituted with wild-type …

Data from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Abstract Although epidermal growth factor receptor (EGFR) fusions in non–small cell lung cancer (NSCLC) typically show sensitivity to tyrosine kinase inhibitors (TKI), we identified an EGFR–SHC1 fusion subtype that exhibits intrinsic resistance to EGFR-TKI monotherapy through a dual-activation mechanism in the preclinical …

Supplementary Figure S2 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Figure S2 shows that inactivation of the N-terminal EGFR kinase domain only partially abrogates the tumorigenicity of EGFR-SHC1, as demonstrated by soft agar colony formation assays. It also presents dose-response curves comparing the sensitivity of EGFR-RAD51 and EGFR-SHC1 to three EGFR-TKIs, …

Supplementary Figure S3 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Figure S3 shows that both the N-terminal EGFR kinase domain and the C-terminal SHC1 phosphorylation sites contribute to the oncogenic properties of EGFR-SHC1, including analyses of SHC1 phosphorylation in response to EGF stimulation, TKI sensitivity in Ba/F3 cells, and functional assessments …

Supplementary Table S4 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Table S4 shows that list of genes included in the SYSUCC Personalized Diagnostics Panel (Tumor tissues).

Supplementary Table S1 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Table S1 shows that the transcription of fusion genes were detected by whole transcriptome sequencing (WTS) in patient #1's specimen.

Supplementary Figure S5 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Figure S5 shows that dual inhibition of afatinib plus SRC-TKIs represents a potential treatment strategy for EGFR-SHC1-driven tumors, including immunoblotting analyses of downstream signaling following combination treatment with afatinib and tirbanibulin, dose-response curves for the combination in Ba/F3-EGFR-SHC1 cells, and validation …

Supplementary Figure S1 from The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Supplementary Figure S1 shows the identification and validation of the EGFR-SHC1 fusion in NSCLC patients, including RT-PCR and Sanger sequencing confirmation, as well as the oncogenic potential of EGFR-SHC1 demonstrated through immunoblotting, flow cytometry, soft agar colony formation, and IL-3-independent proliferation assays …

The Oncogenic EGFR–SHC1 Fusion Confers Insensitivity to EGFR-TKIs via Dual Activation of N-EGFR Kinase Domain and C-SHC1 Phosphorylation Sites in Lung Cancer

Jiani Zheng, Shen Zhao, Jianhua Zhan, Weitao Zhuang et autres

Although epidermal growth factor receptor (EGFR) fusions in non-small cell lung cancer (NSCLC) typically show sensitivity to tyrosine kinase inhibitors (TKI), we identified an EGFR-SHC1 fusion subtype that exhibits intrinsic resistance to EGFR-TKI monotherapy through a dual-activation mechanism in the preclinical and …

cn (code pays fourni par la source)

Anti–LAG-3 Antibody LBL-007 plus Tislelizumab and Chemotherapy as First-Line Therapy for Advanced Nasopharyngeal Carcinoma: A Multicenter Phase 2 Trial

Dongchen Sun, Gang Chen, Yu Chen, Song Qu et autres

PURPOSE: Prior studies reported synergistic antitumor activity by dual inhibition of lymphocyte activation gene-3 (LAG-3) and PD-1. This study investigated the activity, safety, and biomarker of LAG-3/PD-1 co-blockade plus chemotherapy as first-line treatment for recurrent or metastatic nasopharyngeal carcinoma (RM-NPC). PATIENTS AND …

cn, gb (code pays fourni par la source)