Liming Yang
A5100662128- Cancer Genomics and Diagnostics
- Plant Stress Responses and Tolerance
- Plant Gene Expression Analysis
- Photosynthetic Processes and Mechanisms
- Genomics and Phylogenetic Studies
- Plant Molecular Biology Research
- RNA modifications and cancer
- CRISPR and Genetic Engineering
- Mycotoxins in Agriculture and Food
- Plant-Microbe Interactions and Immunity
- Epigenetics and DNA Methylation
- Cancer-related molecular mechanisms research
- Chromosomal and Genetic Variations
- Plant biochemistry and biosynthesis
- Genomics and Rare Diseases
- Genetic factors in colorectal cancer
- Cancer-related Molecular Pathways
- Plant Disease Resistance and Genetics
- Fungal and yeast genetics research
- RNA Research and Splicing
- Advanced Proteomics Techniques and Applications
- Genomics and Chromatin Dynamics
- Bioinformatics and Genomic Networks
- Plant tissue culture and regeneration
- Gene expression and cancer classification
Nanjing Forestry University
2017-2025
First Hospital of Jilin University
2024-2025
Jilin University
2025
Nanjing University of Science and Technology
2024
Gansu Agricultural University
2024
National Institutes of Health
2002-2023
National Cancer Institute
1999-2023
Guangzhou University of Chinese Medicine
2023
Center for Information Technology
2002-2023
Zoucheng People's Hospital
2023
Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined. The relationships between patterns and epigenetic phenotypes not yet clear. We analyzed genomes 200 clinically annotated adult cases de novo AML, using either whole-genome sequencing (50 cases) or whole-exome (150 cases), along with RNA microRNA DNA-methylation analysis. AML have fewer than most other cancers, an average only 13 found in genes. Of these, 5 genes recurrently mutated AML. A total...
We performed an extensive immunogenomic analysis of more than 10,000 tumors comprising 33 diverse cancer types by utilizing data compiled TCGA. Across types, we identified six immune subtypes—wound healing, IFN-γ dominant, inflammatory, lymphocyte depleted, immunologically quiet, and TGF-β dominant—characterized differences in macrophage or signatures, Th1:Th2 cell ratio, extent intratumoral heterogeneity, aneuploidy, neoantigen load, overall proliferation, expression immunomodulatory genes,...
For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical contain key features representing the democratized nature collection process. To ensure proper use this large dataset associated genomic features, we developed standardized named Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major outcome endpoints. In...
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...
We conducted comprehensive integrative molecular analyses of the complete set tumors in The Cancer Genome Atlas (TCGA), consisting approximately 10,000 specimens and representing 33 types cancer. performed clustering using data on chromosome-arm-level aneuploidy, DNA hypermethylation, mRNA, miRNA expression levels reverse-phase protein arrays, which all, except for revealed primarily organized by histology, tissue type, or anatomic origin. influence cell type was evident...
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...
Cancer chromatin accessibility landscape The Genome Atlas (TCGA) provides a high-quality resource of molecular data on large variety human cancers. Corces et al. used recently modified assay to profile determine the accessible in 410 TCGA samples from 23 cancer types (see Perspective by Taipale). When were integrated with other omics available for same tumor samples, inherited risk loci predisposition revealed, transcription factors and enhancers driving subtypes patient survival differences...
<h2>Summary</h2> DNA damage repair (DDR) pathways modulate cancer risk, progression, and therapeutic response. We systematically analyzed somatic alterations to provide a comprehensive view of DDR deficiency across 33 types. Mutations with accompanying loss heterozygosity were observed in over 1/3 genes, including <i>TP53</i> <i>BRCA1/2</i>. Other prevalent included epigenetic silencing the direct genes <i>EXO5</i>, <i>MGMT</i>, <i>ALKBH3</i> ∼20% samples. Homologous recombination (HRD) was...
Aneuploidy, whole chromosome or arm imbalance, is a near-universal characteristic of human cancers. In 10,522 cancer genomes from The Cancer Genome Atlas, aneuploidy was correlated with TP53 mutation, somatic mutation rate, and expression proliferation genes. Aneuploidy anti-correlated immune signaling genes, due to decreased leukocyte infiltrates in high-aneuploidy samples. Chromosome arm-level alterations show cancer-specific patterns, including loss 3p squamous We applied genome...
Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings tumor-infiltrating lymphocytes (TILs) based on H&E from 13 tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches images. Affinity propagation revealed local spatial structure in patterns correlation with overall survival. map...
Our comprehensive analysis of alternative splicing across 32 The Cancer Genome Atlas cancer types from 8,705 patients detects events and tumor variants by reanalyzing RNA whole-exome sequencing data. Tumors have up to 30% more than normal samples. Association somatic with confirmed known trans associations in SF3B1 U2AF1 identified additional trans-acting (e.g., TADA1, PPP2R1A). Many tumors thousands not detectable samples; on average, we ≈930 exon-exon junctions ("neojunctions") typically...
The Cancer Genome Atlas (TCGA) cancer genomics dataset includes over 10,000 tumor-normal exome pairs across 33 different types, in total >400 TB of raw data files requiring analysis. Here we describe the Multi-Center Mutation Calling Multiple Cancers project, our effort to generate a comprehensive encyclopedia somatic mutation calls for TCGA enable robust cross-tumor-type analyses. Our approach accounts variance and batch effects introduced by rapid advancement DNA extraction,...
Highlights•871 predisposition variants/CNVs discovered in 8% of 10,389 cases 33 cancers•Pan-cancer approach identified shared variants and genes across cancers•33 affecting activating domains oncogenes showed high expression•47 VUSs prioritized using cancer enrichment, LOH, expression other evidenceSummaryWe conducted the largest investigation to date, discovering 853 pathogenic or likely from types. Twenty-one single cross-cancer associations, including novel associations SDHA melanoma...
We analyzed molecular data on 2,579 tumors from The Cancer Genome Atlas (TCGA) of four gynecological types plus breast. Our aims were to identify shared and unique features, clinically significant subtypes, potential therapeutic targets. found 61 somatic copy-number alterations (SCNAs) 46 significantly mutated genes (SMGs). Eleven SCNAs 11 SMGs had not been identified in previous TCGA studies the individual tumor types. functionally estrogen receptor-regulated long non-coding RNAs (lncRNAs)...
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...
Hippo signaling has been recognized as a key tumor suppressor pathway. Here, we perform comprehensive molecular characterization of 19 core genes in 9,125 samples across 33 cancer types using multidimensional "omic" data from The Cancer Genome Atlas. We identify somatic drivers among and the related microRNA (miRNA) regulators, functional genomic approaches, experimentally characterize YAP TAZ mutation effects miR-590 miR-200a regulation for TAZ. pathway activity is best characterized by...
We characterized the epigenetic landscape of genes encoding long noncoding RNAs (lncRNAs) across 6,475 tumors and 455 cancer cell lines. In stark contrast to CpG island hypermethylation phenotype in cancer, we observed a recurrent hypomethylation 1,006 lncRNA including EPIC1 (epigenetically-induced lncRNA1). Overexpression is associated with poor prognosis luminal B breast patients enhances tumor growth vitro vivo. Mechanistically, promotes cell-cycle progression by interacting MYC through...
Hotspot mutations in splicing factor genes have been recently reported at high frequency hematological malignancies, suggesting the importance of RNA cancer. We analyzed whole-exome sequencing data across 33 tumor types The Cancer Genome Atlas (TCGA), and we identified 119 with significant non-silent mutation patterns, including over-representation, recurrent loss function (tumor suppressor-like), or hotspot profile (oncogene-like). Furthermore, analysis revealed altered events associated...
Highlights•MYC paralogs are significantly amplified (28% of all samples)•MYC antagonists mutated (MGA, 4% samples) or deleted (MNT, 10% alterations mutually exclusive with PIK3CA, PTEN, APC, BRAF alterations•Expression analysis reveals pan-cancer and tumor-specific MYC-associated pathwaysSummaryAlthough the MYC oncogene has been implicated in cancer, a systematic assessment MYC, related transcription factors, co-regulatory proteins, forming proximal network (PMN), across human cancers is...
Highlights•An overview of PanCancer Atlas analyses on oncogenic molecular processes•Germline genome affects somatic genomic landscape in a pathway-dependent fashion•Genome mutations impact expression, signaling, and multi-omic profiles•Mutation burdens drivers influence immune-cell composition microenvironmentSummaryThe Cancer Genome (TCGA) has catalyzed systematic characterization diverse alterations underlying human cancers. At this historic junction marking the completion over 11,000...
Fusarium species cause serious diseases in cereal staple food crops such as wheat and maize. Currently, the mechanisms underlying resistance to Fusarium-caused are still largely unknown. In present study, we employed a combined proteomic transcriptomic approach investigate genes responding F. graminearum infection that causes head blight (FHB). We found total of 163 37 proteins were induced by infection. These associated with signaling pathways mediated salicylic acid (SA), jasmonic (JA),...
The role of enhancers, a key class non-coding regulatory DNA elements, in cancer development has increasingly been appreciated. Here, we present the detection and characterization large number expressed enhancers genome-wide analysis 8928 tumor samples across 33 types using TCGA RNA-seq data. Compared with matched normal tissues, global enhancer activation was observed most cancers. Across types, activity positively associated aneuploidy, but not mutation load, suggesting hypothesis centered...