Junjie Zhao
- Renal cell carcinoma treatment
- Epigenetics and DNA Methylation
- Phagocytosis and Immune Regulation
- Cancer Immunotherapy and Biomarkers
- Protein Hydrolysis and Bioactive Peptides
- Architecture and Computational Design
- Food composition and properties
- Phytochemicals and Antioxidant Activities
- Piperaceae Chemical and Biological Studies
- Proteins in Food Systems
- Pancreatic and Hepatic Oncology Research
- Healthcare and Venom Research
- Essential Oils and Antimicrobial Activity
Sichuan University
2024-2025
West China Hospital of Sichuan University
2025
Hunan University of Traditional Chinese Medicine
2024
Computer Algorithms for Medicine
2020
Abstract Purpose: Fumarate hydratase–deficient renal cell carcinoma (FH-deficient RCC) is a rare and lethal subtype of kidney cancer. However, the optimal treatments molecular correlates benefits for FH-deficient RCC are currently lacking. Experimental Design: A total 91 patients with from 15 medical centers between 2009 2022 were enrolled in this study. Genomic bulk RNA-sequencing (RNA-seq) performed on 88 45 untreated RCCs, respectively. Single-cell RNA-seq was to identify biomarkers...
544 Background: Non-clear cell renal carcinoma (nccRCC) accounts for approximately 25% of all (RCC) and lacks standards care. More recent data suggests the efficacy anti-PD-(L)1 plus anti-CTLA-4 immune checkpoint inhibitors combined with tyrosine-kinase in RCC. Cadonilimab (AK104) is a first-in-class tetravalent bispecific antibody that targets both PD-1 CTLA-4, showing manageable safety profile favorable clinical benefits. Here we explore cadonilimab combination axitinib patients advanced...
<div>AbstractPurpose:<p>Fumarate hydratase–deficient renal cell carcinoma (FH-deficient RCC) is a rare and lethal subtype of kidney cancer. However, the optimal treatments molecular correlates benefits for FH-deficient RCC are currently lacking.</p>Experimental Design:<p>A total 91 patients with from 15 medical centers between 2009 2022 were enrolled in this study. Genomic bulk RNA-sequencing (RNA-seq) performed on 88 45 untreated RCCs, respectively. Single-cell...
<p>Supplementary Figure 2. Treatment details and survival outcomes of patients with metastatic FH-deficient RCC. (A) Swimmer plot showing the treatment response duration each patient receiving first-line systemic treatments; (B) Progression-free for (C) Overall (OS) treatments.</p>
<p>Supplementary Figure 6. Validation of the FH-deficient RCC immune signature. (A) UMAP plot showing expression selected genes; (B) Correlations between six genes in signature and treatment response, significance differential (q value) was determined by two-sided Wilcoxon rank-sum test with Bonferroni FDR correction; (C) several related hallmark pathways, correction. *, q<0.05; **, q<0.01; ***, q<0.001; ****, q<0.0001.</p>
<p>Supplementary Figure 3. Forest plot showing the prognostic value of clinicopathologic and molecular features in patients treated with first-line ICI+TKI combination therapy. HR<1 indicates better survival comparator group, while HR>1 control group. TMB, tumor mutation burden; MUT, mutation; WT, wild type; TPS, proportion score; CCP, cell cycle progression; Sig., signature.</p>
<p>Supplementary Figure 6. Validation of the FH-deficient RCC immune signature. (A) UMAP plot showing expression selected genes; (B) Correlations between six genes in signature and treatment response, significance differential (q value) was determined by two-sided Wilcoxon rank-sum test with Bonferroni FDR correction; (C) several related hallmark pathways, correction. *, q<0.05; **, q<0.01; ***, q<0.001; ****, q<0.0001.</p>
<p>Supplementary Figure 5. Cell clusters and their distribution in a validation cohort by Dong et al.. (A) UMAP plot showing the sample of T cells; (B) all cells collected from four samples; (C) Dot marker gene expression for clusters; (D) Bar plots tissue (E) Tissue prevalence cell estimated Ro/e score.</p>
<p>Supplementary Figure 2. Treatment details and survival outcomes of patients with metastatic FH-deficient RCC. (A) Swimmer plot showing the treatment response duration each patient receiving first-line systemic treatments; (B) Progression-free for (C) Overall (OS) treatments.</p>
<p>Supplementary Figure 1. Survival outcomes of patients with synchronous and metachronous metastatic disease treatment flows. Overall survival (OS) for FH-deficient RCC in the overall systemic setting (A), ICI+TKI (B), TKI monotherapy (C); (D) Sankey diagram showing flows RCC.</p>
<p>Supplementary Figure 5. Cell clusters and their distribution in a validation cohort by Dong et al.. (A) UMAP plot showing the sample of T cells; (B) all cells collected from four samples; (C) Dot marker gene expression for clusters; (D) Bar plots tissue (E) Tissue prevalence cell estimated Ro/e score.</p>
<p>Supplementary Figure 1. Survival outcomes of patients with synchronous and metachronous metastatic disease treatment flows. Overall survival (OS) for FH-deficient RCC in the overall systemic setting (A), ICI+TKI (B), TKI monotherapy (C); (D) Sankey diagram showing flows RCC.</p>