Zilin Wang
A5010742228- Renal cell carcinoma treatment
- Epigenetics and DNA Methylation
- Phagocytosis and Immune Regulation
- Cancer Immunotherapy and Biomarkers
- Cytomegalovirus and herpesvirus research
- DNA Repair Mechanisms
- Enzyme Production and Characterization
- Animal Nutrition and Physiology
- Rabbits: Nutrition, Reproduction, Health
- Melanoma and MAPK Pathways
- Renal and related cancers
- Microbial Metabolic Engineering and Bioproduction
- Moringa oleifera research and applications
- Fungal and yeast genetics research
- Tuberous Sclerosis Complex Research
- Genomics and Chromatin Dynamics
- CRISPR and Genetic Engineering
- Liver physiology and pathology
- Microbial metabolism and enzyme function
- Cytokine Signaling Pathways and Interactions
- Microbial Community Ecology and Physiology
- DNA and Nucleic Acid Chemistry
- Cancer Mechanisms and Therapy
- Algal biology and biofuel production
Sichuan University
1993-2024
West China Hospital of Sichuan University
2024
Henan Agricultural University
2024
The Graduate Center, CUNY
1999
University of Kentucky
1999
DNA is frequently damaged by various physical and chemical agents. damage can lead to mutations during replication. In the yeast Saccharomyces cerevisiae, damage-induced mutagenesis pathway requires Rev1 protein. We have isolated a human cDNA homologous REV1 gene. The consists of 4255 bp codes for protein 1251 amino acid residues with calculated molecular weight 138 248 Da. gene localized between 2q11.1 2q11.2. show that dCMP transferase specifically inserts residue opposite template G....
In the yeast Saccharomyces cerevisiae, DNA polymerase ζ (Polζ) is required in a major lesion bypass pathway. To help understand role of Polζ bypass, we have performed vitro biochemical analyses this response to several lesions. Purified limited translesion synthesis opposite template TT (6-4) photoproduct, incorporating A or T with similar efficiencies (and less frequently G) 3′ T, and predominantly 5′ T. incorporated G an acetylaminofluorene (AAF)-adducted guanine. The lesion, however,...
Small-molecule inhibitors are an attractive therapeutic approach for most types of human cancers. SKLB-163, a novel benzothiazole-2-thiol derivative, was developed via computer-aided drug design and de novo synthesis. MTT assay showed it had potent anti-proliferative activity on various cancer cells. Treatment cells with SKLB-163 induced obvious apoptosis inhibited proliferation in vitro. administered p.o. marked antitumor vivo. Proteomic techniques were employed to identify possible target...
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...
Rationale: The different variants of renal angiomyolipoma pose diagnostic and therapeutic challenges in clinical practice. We report a rare case solid-cystic angiomyolipoma, with the aim offering new insights into preoperative imaging assessment masses. Patient concerns: A 72-year-old female was admitted to our hospital because mass discovered her right kidney during an abdominal computed tomography scan at another hospital. Her medical history includes 5-year hypertension treated...
Replacing corn with different levels of wheat in the iso-energy and -protein diet broilers impacts on growth performance intestinal homeostasis under condition supplying multienzyme complex were evaluated this study. A total 480 10-day-old male assigned randomly to low-level group (15% 35.18% corn), medium-level (30% 22.27%), high-level (55.77% without corn) until 21 d. The supplementation did not affect hepatic function, serum glycolipid profile, or bone turnover. replacement 55% increased...
<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>