Publications by authors named "Huating Yuan"

Background: TMPRSS2-ERG (T2E) fusion is highly related to aggressive clinical features in prostate cancer (PC), which guides individual therapy. However, current fusion prediction tools lacked enough accuracy and biomarkers were unable to be applied to individuals across different platforms due to their quantitative nature. This study aims to identify a transcriptome signature to detect the T2E fusion status of PC at the individual level.

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Glioblastoma stem cells (GSCs) contributed to the progression, treatment resistance, and relapse of glioblastoma (GBM). However, current researches on GSCs were performed usually outside the human tumor microenvironment, ignoring the importance of the cellular states of primary GSCs. In this study, we leveraged single-cell transcriptome sequencing data of 6 independent GBM cohorts from public databases, and combined lineage and stemness features to identify primary GSCs.

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Objectives: Systematically identifying cancer cell functional states, especially their associations, is key to understanding the pathogenesis of cancers.

Materials And Methods: Here, we systematically identified six cancer-related states, including epithelial-mesenchymal transition (EMT), immune response, epithelial differentiation, stress, G1/S and G2/M phases, in head and neck squamous cell carcinoma (HNSCC) based on single-cell RNA-sequencing (scRNA-seq).

Results And Conclusion: We defined the association patterns between these functional states and found the patterns were correlated with the state activity.

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T cells exhibit heterogeneous functional states, which correlate with responsiveness to immune checkpoint blockade and prognosis of tumor patients. However, the molecular regulatory mechanisms underlying the dynamic process of T cell state transition remain largely unknown. Based on single-cell transcriptome data of T cells in non-small cell lung cancer, we combined cell states and pseudo-times to propose a pipeline to construct dynamic regulatory networks for dissecting the process of T cell dysfunction.

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Single-cell RNA sequencing presents the sophisticated delineation of cell transcriptomes in many cancer types and highlights the tumor heterogeneity at higher resolution, which provides a new chance to explore the molecular mechanism in a minority of cells. In this study, we utilized publicly available single-cell RNA-seq data to discover and comprehensively dissect rare genes existing in few glioblastoma (GBM) cells. Moreover, we designed a framework to systematically identify 51 rare protein-coding genes (PCGs) and 47 rare long non-coding RNAs (lncRNAs) in GBM.

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High functional heterogeneity of cancer cells poses a major challenge for cancer research. Single-cell sequencing technology provides an unprecedented opportunity to decipher diverse functional states of cancer cells at single-cell resolution, and cancer scRNA-seq datasets have been largely accumulated. This emphasizes the urgent need to build a dedicated resource to decode the functional states of cancer single cells.

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Substantial cancer genome sequencing efforts have discovered many important driver genes contributing to tumorigenesis. However, very little is known about the genetic alterations of long non-coding RNAs (lncRNAs) in cancer. Thus, there is a need for systematic surveys of driver lncRNAs.

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Breast cancer is a very complex and heterogeneous disease with variable molecular mechanisms of carcinogenesis and clinical behaviors. The identification of prognostic risk factors may enable effective diagnosis and treatment of breast cancer. In particular, numerous gene-expression-based prognostic signatures were developed and some of them have already been applied into clinical trials and practice.

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: Systematically tracking the tumor immunophenotype is required to understand the mechanisms of cancer immunity and improve clinical benefit of cancer immunotherapy. However, progress in current research is hindered by the lack of comprehensive immune activity resources and easy-to-use tools for biologists, clinicians, and researchers to conveniently evaluate immune activity during the "cancer-immunity cycle." We developed a user-friendly one-stop shop web tool called TIP to comprehensively resolve tumor immunophenotype.

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Increasing evidence suggests that the abnormality of microRNAs (miRNAs) and their downstream targets is frequently implicated in the pathogenesis of human cancers, however, the clinical benefit of causal miRNA-target interactions has been seldom studied. Here, we proposed a computational method to optimize prognosis-related key miRNA-target interactions by combining transcriptome and clinical data from thousands of TCGA tumors across 16 cancer types. We obtained a total of 1,956 prognosis-related key miRNA-target interactions between 112 miRNAs and 1,443 their targets.

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Large-scale sequencing studies discovered substantial genetic variants occurring in enhancers which regulate genes via long range chromatin interactions. Importantly, such variants could affect enhancer regulation by changing transcription factor bindings or enhancer hijacking, and in turn, make an essential contribution to disease progression. To facilitate better usage of published data and exploring enhancer deregulation in various human diseases, we created DiseaseEnhancer (http://biocc.

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