A5037828313- Cancer Genomics and Diagnostics
- Prostate Cancer Treatment and Research
- Bladder and Urothelial Cancer Treatments
- Prostate Cancer Diagnosis and Treatment
- Renal cell carcinoma treatment
- Genetic factors in colorectal cancer
- Cancer Immunotherapy and Biomarkers
- Sarcoma Diagnosis and Treatment
- Neurofibromatosis and Schwannoma Cases
- Epigenetics and DNA Methylation
- Radiomics and Machine Learning in Medical Imaging
- Urinary and Genital Oncology Studies
- Soft tissue tumors and treatment
- Magnesium Oxide Properties and Applications
- Radiopharmaceutical Chemistry and Applications
- Neuroblastoma Research and Treatments
- Single-cell and spatial transcriptomics
- Ferroptosis and cancer prognosis
- Cancer-related molecular mechanisms research
- Migration and Labor Dynamics
- Genetic Mapping and Diversity in Plants and Animals
- Multiferroics and related materials
- Viral-associated cancers and disorders
- Recycling and utilization of industrial and municipal waste in materials production
- Supramolecular Self-Assembly in Materials
Weifang Medical University
2023-2025
Washington University in St. Louis
2020-2024
Ningbo University
2023-2024
Ocean University of China
2024
China Light Industry Press (China)
2024
Saint Louis University
2019
Abstract Circulating tumor DNA (ctDNA) sensitivity remains subpar for molecular residual disease (MRD) detection in bladder cancer patients. To remedy this problem, we focused on the biofluid most proximal to disease, urine, and analyzed urine 74 localized We integrated ultra-low-pass whole genome sequencing (ULP-WGS) with personalized profiling by deep (uCAPP-Seq) achieve sensitive MRD predict overall survival. Variant allele frequency, inferred mutational burden, copy number-derived...
Background The standard of care treatment for muscle-invasive bladder cancer (MIBC) is radical cystectomy, which typically preceded by neoadjuvant chemotherapy. However, the inability to assess minimal residual disease (MRD) noninvasively limits our ability offer bladder-sparing treatment. Here, we sought develop a liquid biopsy solution via urine tumor DNA (utDNA) analysis. Methods and findings We applied Cancer Personalized Profiling Deep Sequencing (uCAPP-Seq), targeted next-generation...
Background The leading cause of mortality for patients with the neurofibromatosis type 1 (NF1) cancer predisposition syndrome is development malignant peripheral nerve sheath tumor (MPNST), an aggressive soft tissue sarcoma. In setting NF1, this frequently arises from within its common and benign precursor, plexiform neurofibroma (PN). Transformation PN to MPNST challenging diagnose due difficulties in distinguishing cross-sectional imaging results intralesional heterogeneity resulting...
We hypothesized that circulating tumor DNA (ctDNA) molecular residual disease (MRD) analysis without prior mutational knowledge could be performed after neoadjuvant chemotherapy to assess oligometastatic colorectal cancer (CRC) treated surgically with curative intent. also investigated urine as an alternative analyte for ctDNA MRD detection in this nongenitourinary setting.
<p>Supplementary Figure S3. Kaplan-Meier analysis of an additional cohort 27 patients with oligometastatic mCRPC, stratified by <i>AR</i> enhancer amplification status in plasma cell-free DNA. (A) Progression-free survival, (B) radiographic progression-free and (C) overall survival. p values were calculated the log-rank test.</p>
<p>Supplementary Figure S1. Genomic landscape of metastatic castration-resistant prostate cancer (mCRPC) samples profiled using EnhanceAR-Seq. EnhanceAR-Seq, Enhancer and neighboring loci Androgen Receptor Sequencing.</p>
<p>Supplementary Figure S9. Cell-free DNA methylation analysis of differentially accessible transcription factor binding sites. The box and whisker plots summarize levels in plasma cfDNA from <i>AR</i>/enhancer altered versus wild-type mCRPC patients after z-score transformation the 10,000 TF sites corresponding to each top 20 TFs that are (A) most (B) least lethal high-risk patients. p values were calculated by Mann-Whitney U test. cfDNA, cell-free DNA; mCRPC, metastatic...
<p>Supplementary Figure S11. Cell-free DNA methylation levels of the top 10 least stem-like signature genes in plasma. The box and whisker plots summarize promoter rates for plasma cfDNA from <i>AR</i>/enhancer altered versus wild-type mCRPC patients. p values were calculated by Student’s t test. cfDNA, cell-free DNA; mCRPC, metastatic castration-resistant prostate cancer; TF, transcription factor.</p>
<p>Supplementary Figure S2. Kaplan-Meier analysis based on plasma collected prior to first-line androgen receptor-signaling inhibitor (ARSI) treatment according (A,B) Androgen receptor (<i>AR</i>) gene body status and (C,D) <i>AR</i> enhancer region in 63 patients with metastatic castration-resistant prostate cancer (mCRPC). p values were calculated by the log-rank test hazard ratios (HRs) Mantel-Haenszel method.</p>
<p>Supplementary Figure S7. Distribution of differentially methylated regions in mCRPC plasma cell-free DNA. (A) hypomethylated and hypermethylated genic DMRs pre-treatment cfDNA <i>AR</i>/enhancer altered lethal (compared to wild-type mCRPC). (B) Genomic annotation based on their location the genome. (C) Top 50 found from patients cfDNA, DNA; CDS, coding sequence; DMRs, regions; mCRPC, metastatic castration-resistant prostate cancer; UTR, untranslated region.</p>
<div>AbstractPurpose:<p>Metastatic castration-resistant prostate cancer (mCRPC) resistant to androgen receptor signaling inhibitors (ARSI) is often lethal. Liquid biopsy biomarkers for this deadly form of disease remain under investigation, and underpinning mechanisms ill-understood.</p>Experimental Design:<p>We applied targeted cell-free DNA (cfDNA) sequencing 126 patients with mCRPC from three academic centers separately performed genome-wide cfDNA methylation on 43...
<p>Supplementary Figure S8. Transcription factor analysis in localized prostate cancer versus blood. Log2 fold change of the 20 TFs with most accessible and least binding sites plasma cell-free DNA (see Fig. 4E, Table S12 S13) adenocarcinoma tumors from TCGA (n = 496) blood samples GTEX 337) (Methods). p value was calculated by Student’s t test. GTEX, Genotype-Tissue Expression project; TCGA, The Cancer Atlas Genome TF, transcription factor.</p>
<p>Supplementary Figure S5. Kaplan-Meier survival analysis based on plasma collected prior to first-line androgen receptor-signaling inhibitor (ARSI) treatment in 63 mCRPC patients according (A,B) <i>PTEN</i> copy number loss status cfDNA, (C,D) or mutation and (E,F) alteration <i>AR</i>/Enhancer cfDNA. p values were calculated by the log-rank test hazard ratios (HRs) Mantel-Haenszel method. cell-free DNA; mCRPC; metastatic castration-resistant prostate cancer.</p>
<p>Supplementary Figure S6. Kaplan–Meier survival analysis of the 43-patient mCRPC cohort that also underwent genome-wide EM-seq, according to (A,B) <i>AR</i>/enhancer alteration status and (C,D) median-split ichorCNA-based median tumor fraction. p values were calculated by log-rank test hazard ratios (HRs) Mantel-Haenszel method. cfDNA, cell-free DNA; mCRPC; metastatic castration-resistant prostate cancer.</p>
<p>Supplementary Figure S4. Summary of alterations in biologically relevant pathways found pre-ARSI plasma cell-free DNA 63 metastatic castration-resistant prostate cancer patients. ARSI, androgen receptor-signaling inhibitors.</p>
<p>Supplementary Figure S10. Cell-free DNA methylation levels of the top 10 most stem-like signature genes in plasma. The box and whisker plots summarize promoter rates for plasma cfDNA from <i>AR</i>/enhancer altered versus wild-type mCRPC patients. p values were calculated by Student’s t test. cfDNA, cell-free DNA; mCRPC, metastatic castration-resistant prostate cancer; TF, transcription factor.</p>
Objectives Lower respiratory infections are the most significant health threat to children under 5 years old, leading highest disease burden across all age groups. This study aims provide an up-to-date assessment of global lower in age. Methods utilizes data and methodologies from Global Burden Disease Study 2021 analyze changes 1990 2021, focusing on incidence, mortality, disability-adjusted life years. A jointpoint model is employed calculate trends average annual percentage change among...
Objective To assess the global burden of chronic obstructive pulmonary disease (COPD) and cross-country inequalities from 1990 to 2021 project changes until 2045. Methods Data on prevalence, mortality, disability-adjusted life-years (DALYs) for COPD were extracted Global Burden Disease Study ( https://vizhub.healthdata.org/gbd-results/ ). Trends analyzed globally, regionally, nationally, considering population growth, aging, epidemiological changes. Inequalities quantified using World Health...
Metastatic castration-resistant prostate cancer (mCRPC) resistant to androgen receptor signaling inhibitors (ARSI) is often lethal. Liquid biopsy biomarkers for this deadly form of disease remain under investigation, and underpinning mechanisms ill-understood.
PURPOSE Cell-free DNA (cfDNA) and circulating tumor cell (CTC)–based liquid biopsies have emerged as potential tools to predict responses androgen receptor (AR)–directed therapy in metastatic prostate cancer. However, because of complex mechanisms incomplete understanding genomic events involved cancer resistance, current assays (eg, CTC AR-V7) demonstrate low sensitivity remain underutilized. The recent discovery AR enhancer amplification > 80% patients with disease its association...
Abstract Background The leading cause of mortality for patients with the Neurofibromatosis type 1 (NF1) cancer predisposition syndrome is development Malignant Peripheral Nerve Sheath Tumor (MPNST), an aggressive soft tissue sarcoma. In setting NF1, this frequently arises from within its common and benign precursor, plexiform neurofibroma (PN). Transformation PN to MPNST challenging diagnose due difficulties in distinguishing cross-sectional imaging results intralesional heterogeneity...
Abstract Motivation Detection of genomic alterations in circulating tumor DNA (ctDNA) is currently used for active clinical monitoring cancer progression and treatment response. While methods analysis small mutations are more developed, strategies detecting structural variants (SVs) ctDNA limited. Additionally, reproducibly calling small-scale mutations, copy number alterations, SVs challenging due to the lack unified tools these different classes variants. Results We developed a pipeline...
Abstract Background Universal social medical insurance coverage is viewed as a major factor in promoting integration, but insufficient evidence exists on the integration of elderly rural migrants (ERM), generally aged 60 years and above, low- middle-income countries. To address this problem, we explore relationship between location (SMI), such host city, context Chinese ERM. Methods This study based data from 2017 National Internal Migrant Dynamic Monitoring Survey China. The participants...