Wen-Wei Liang
A5081854684- Cancer Genomics and Diagnostics
- Osteoarthritis Treatment and Mechanisms
- RNA modifications and cancer
- Ferroptosis and cancer prognosis
- Cell Adhesion Molecules Research
- Lung Cancer Treatments and Mutations
- Bioinformatics and Genomic Networks
- Ubiquitin and proteasome pathways
- Silk-based biomaterials and applications
- Epigenetics and DNA Methylation
- Radiomics and Machine Learning in Medical Imaging
- RNA Research and Splicing
- Bone Tissue Engineering Materials
- Total Knee Arthroplasty Outcomes
- Tendon Structure and Treatment
- Genetics, Bioinformatics, and Biomedical Research
- Melanoma and MAPK Pathways
- Cancer-related Molecular Pathways
- Single-cell and spatial transcriptomics
- interferon and immune responses
- Orthopaedic implants and arthroplasty
- Orthopedic Infections and Treatments
- Chemokine receptors and signaling
- Immune cells in cancer
- Mitochondrial Function and Pathology
Nanjing Medical University
2011-2024
Jiangsu Province Hospital
2015-2024
New York Genome Center
2024
New York University
2024
Washington University in St. Louis
2017-2023
James S. McDonnell Foundation
2016-2023
Ministry of Agriculture and Rural Affairs
2022
South China Agricultural University
2022
Jilin University
2021
State Key Laboratory on Integrated Optoelectronics
2021
Highlights•Alteration map of 10 signaling pathways across 9,125 samples from 33 cancer types•Reusable, curated pathway templates that include a catalogue driver genes•57% tumors have at least one potentially actionable alteration in these pathways•Co-occurrence alterations suggests combination therapy opportunitiesSummaryGenetic control cell-cycle progression, apoptosis, and cell growth are common hallmarks cancer, but the extent, mechanisms, co-occurrence differ between individual tumor...
Identifying molecular cancer drivers is critical for precision oncology. Multiple advanced algorithms to identify now exist, but systematic attempts combine and optimize them on large datasets are few. We report a PanCancer PanSoftware analysis spanning 9,423 tumor exomes (comprising all 33 of The Cancer Genome Atlas projects) using 26 computational tools catalog driver genes mutations. 299 with implications regarding their anatomical sites cancer/cell types. Sequence- structure-based...
To explore the biology of lung adenocarcinoma (LUAD) and identify new therapeutic opportunities, we performed comprehensive proteogenomic characterization 110 tumors 101 matched normal adjacent tissues (NATs) incorporating genomics, epigenomics, deep-scale proteomics, phosphoproteomics, acetylproteomics. Multi-omics clustering revealed four subgroups defined by key driver mutations, country, gender. Proteomic phosphoproteomic data illuminated downstream copy number aberrations, somatic...
Gene fusions represent an important class of somatic alterations in cancer. We systematically investigated 9,624 tumors across 33 cancer types using multiple fusion calling tools. identified a total 25,664 fusions, with 63% validation rate. Integration gene expression, copy number, and annotation data revealed that involving oncogenes tend to exhibit increased whereas tumor suppressors have the opposite effect. For kinases, we found 1,275 intact kinase domain, proportion which varied...
Glioblastoma (GBM) is the most aggressive nervous system cancer. Understanding its molecular pathogenesis crucial to improving diagnosis and treatment. Integrated analysis of genomic, proteomic, post-translational modification metabolomic data on 99 treatment-naive GBMs provides insights GBM biology. We identify key phosphorylation events (e.g., phosphorylated PTPN11 PLCG1) as potential switches mediating oncogenic pathway activation, well targets for EGFR-, TP53-, RB1-altered tumors. Immune...
We present a proteogenomic study of 108 human papilloma virus (HPV)-negative head and neck squamous cell carcinomas (HNSCCs). Proteomic analysis systematically catalogs HNSCC-associated proteins phosphosites, prioritizes copy number drivers, highlights an oncogenic role for RNA processing genes. investigation mutual exclusivity between FAT1 truncating mutations 11q13.3 amplifications reveals dysregulated actin dynamics as common functional consequence. Phosphoproteomics characterizes two...
For the past decade, cancer genomic studies have focused on mutations leading to splice-site disruption, overlooking those having splice-creating potential. Here, we applied a bioinformatic tool, MiSplice, for large-scale discovery of splice-site-creating (SCMs) across 8,656 TCGA tumors. We report 1,964 originally mis-annotated clear evidence creating alternative splice junctions. TP53 and GATA3 26 18 SCMs, respectively, ATRX has 5 from lower-grade gliomas. Mutations in 11 genes, including...
Chromatin accessibility is essential in regulating gene expression and cellular identity, alterations have been implicated driving cancer initiation, progression metastasis
Post-translational modifications (PTMs) play key roles in regulating cell signaling and physiology both normal cancer cells. Advances mass spectrometry enable high-throughput, accurate, sensitive measurement of PTM levels to better understand their role, prevalence, crosstalk. Here, we analyze the largest collection proteogenomics data from 1,110 patients with profiles across 11 types (10 National Cancer Institute's Clinical Proteomic Tumor Analysis Consortium [CPTAC]). Our study reveals...
Cancer driver events refer to key genetic aberrations that drive oncogenesis; however, their exact molecular mechanisms remain insufficiently understood. Here, our multi-omics pan-cancer analysis uncovers insights into the impacts of cancer drivers by identifying significant cis-effects and distal trans-effects quantified at RNA, protein, phosphoprotein levels. Salient observations include association point mutations copy-number alterations with rewiring protein interaction networks,...
DNA methylation plays a critical role in establishing and maintaining cellular identity. However, it is frequently dysregulated during tumor development closely intertwined with other genetic alterations. Here, we leveraged multi-omic profiling of 687 tumors matched non-involved adjacent tissues from the kidney, brain, pancreas, lung, head neck, endometrium to identify aberrant associated RNA protein abundance changes build Pan-Cancer catalog. We uncovered lineage-specific epigenetic drivers...
The DEAD-box RNA helicase Prp5 is required for the formation of prespliceosome through an ATP-dependent function to remodel U2 small nuclear ribonucleoprotein particles (snRNPs) and ATP-independent unknown mechanism. has also been implicated in proofreading branch site sequence, but molecular mechanism not well characterized. Using actin precursor mRNA (pre-mRNA) carrying mutations, we identified a Prp5-containing with directly bound (snRNA). contact regions on near branchpoint-interacting...
Abstract The Cancer Genome Atlas (TCGA) and International Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) genome (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis Whole Genomes (PCAWG) Consortium, which aggregated data from 2,658 cancers across 38 tumour types, we compare WES WGS side-by-side 746 TCGA samples, finding that ~80% mutations overlap in covered exonic regions. We estimate low variant allele fraction (VAF <...
NAC transcription factors are one of the largest families transcriptional regulators in plants, and members gene family play vital roles regulating plant growth development processes including biotic/abiotic stress responses. However, little information is available about pitaya. In this study, we conducted a genome-wide analysis total 64 NACs (named HuNAC1-HuNAC64) were identified pitaya (Hylocereus). These genes grouped into fifteen subgroups with diversities proportions, exon-intron...
We introduce a pioneering approach that integrates pathology imaging with transcriptomics and proteomics to identify predictive histology features associated critical clinical outcomes in cancer. utilize 2,755 H&E-stained histopathological slides from 657 patients across 6 cancer types CPTAC. Our models effectively recapitulate distinctions readily made by human pathologists: tumor vs. normal (AUROC = 0.995) tissue-of-origin 0.979). further investigate power on tasks not normally performed...
Background/Aims: The biological effects of periodic mechanical stress on chondrocytes have been studied extensively over the past few years. However, mechanisms underlying chondrocyte mechanosensing and signaling in response to remain be determined. In current study, we examined focal adhesion kinase (FAK) stress-induced proliferation matrix synthesis. Methods Results: Periodic significantly induced sustained phosphorylation FAK at Tyr397 Tyr576/577. Reduction with targeted shRNA via...
RTK/RAS/RAF pathway alterations (RPAs) are a hallmark of lung adenocarcinoma (LUAD). In this study, we use whole-genome sequencing (WGS) 85 cases found to be RPA(-) by previous studies from The Cancer Genome Atlas (TCGA) characterize the minority LUADs lacking apparent in pathway. We show that WGS analysis uncovers RPA(+) 28 (33%) samples. Among remaining 57 cases, observe focal deletions targeting promoter or transcription start site STK11 (n = 7) KEAP1 3), and mutations associated with...
Abstract Summary MIRMMR predicts microsatellite instability status in cancer samples using methylation and mutation information, contrast to existing methods that rely on observed microsatellites. Additionally, highlights those genetic alterations contributing instability. Availability implementation Source code is freely available at https://github.com/ding-lab/MIRMMR under the MIT license, implemented R supported Unix/OS X operating systems. Supplementary information data are Bioinformatics online.
Repair of articular cartilage defects using bilayered scaffolds is problematic because tissue-engineered prone to overgrowth toward subchondral bone, resulting in structural abnormalities and bone. A "twice freeze-drying" technique was used construct a dense isolation layer between the bone layers an integrated scaffold prevent from excessive downgrowth. Briefly, beta-tricalcium phosphate for scaffold, high-concentration chitosan/gelatin solution layer, low-concentration layer. As controls,...