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  1. Article ; Online: netboxr

    Eric Minwei Liu / Augustin Luna / Guanlan Dong / Chris Sander

    PLoS ONE, Vol 15, Iss 11, p e

    Automated discovery of biological process modules by network analysis in R.

    2020  Volume 0234669

    Abstract: Summary Large-scale sequencing projects, such as The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC), have generated high throughput sequencing and molecular profiling data sets, but it is still challenging to identify ... ...

    Abstract Summary Large-scale sequencing projects, such as The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC), have generated high throughput sequencing and molecular profiling data sets, but it is still challenging to identify potentially causal changes in cellular processes in cancer as well as in other diseases in an automated fashion. We developed the netboxr package written in the R programming language, which makes use of the NetBox algorithm to identify candidate cancer-related functional modules. The algorithm makes use of a data-driven, network-based approach that combines prior knowledge with a network clustering algorithm, obviating the need for and the limitation of independently curated functionally labeled gene sets. The method can combine multiple data types, such as mutations and copy number alterations, leading to more reliable identification of functional modules. We make the tool available in the Bioconductor R ecosystem for applications in cancer research and cell biology. Availability and implementation The netboxr package is free and open-sourced under the GNU GPL-3 license R package available at https://www.bioconductor.org/packages/release/bioc/html/netboxr.html.
    Keywords Medicine ; R ; Science ; Q
    Subject code 004
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Identification of novel prostate cancer drivers using RegNetDriver

    Priyanka Dhingra / Alexander Martinez-Fundichely / Adeline Berger / Franklin W. Huang / Andre Neil Forbes / Eric Minwei Liu / Deli Liu / Andrea Sboner / Pablo Tamayo / David S. Rickman / Mark A. Rubin / Ekta Khurana

    Genome Biology, Vol 18, Iss 1, Pp 1-

    a framework for integration of genetic and epigenetic alterations with tissue-specific regulatory network

    2017  Volume 23

    Abstract: Abstract We report a novel computational method, RegNetDriver, to identify tumorigenic drivers using the combined effects of coding and non-coding single nucleotide variants, structural variants, and DNA methylation changes in the DNase I ... ...

    Abstract Abstract We report a novel computational method, RegNetDriver, to identify tumorigenic drivers using the combined effects of coding and non-coding single nucleotide variants, structural variants, and DNA methylation changes in the DNase I hypersensitivity based regulatory network. Integration of multi-omics data from 521 prostate tumor samples indicated a stronger regulatory impact of structural variants, as they affect more transcription factor hubs in the tissue-specific network. Moreover, crosstalk between transcription factor hub expression modulated by structural variants and methylation levels likely leads to the differential expression of target genes. We report known prostate tumor regulatory drivers and nominate novel transcription factors (ERF, CREB3L1, and POU2F2), which are supported by functional validation.
    Keywords Tissue-specific regulatory network ; Cancer drivers ; Single nucleotide variants ; Structural variants ; DNA methylation ; Prostate cancer ; Biology (General) ; QH301-705.5 ; Genetics ; QH426-470
    Subject code 570
    Language English
    Publishing date 2017-07-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Whole-genome characterization of lung adenocarcinomas lacking alterations in the RTK/RAS/RAF pathway

    Jian Carrot-Zhang / Xiaotong Yao / Siddhartha Devarakonda / Aditya Deshpande / Jeffrey S. Damrauer / Tiago Chedraoui Silva / Christopher K. Wong / Hyo Young Choi / Ina Felau / A. Gordon Robertson / Mauro A.A. Castro / Lisui Bao / Esther Rheinbay / Eric Minwei Liu / Tuan Trieu / David Haan / Christina Yau / Toshinori Hinoue / Yuexin Liu /
    Ofer Shapira / Kiran Kumar / Karen L. Mungall / Hailei Zhang / Jake June-Koo Lee / Ashton Berger / Galen F. Gao / Binyamin Zhitomirsky / Wen-Wei Liang / Meng Zhou / Sitapriya Moorthi / Alice H. Berger / Eric A. Collisson / Michael C. Zody / Li Ding / Andrew D. Cherniack / Gad Getz / Olivier Elemento / Christopher C. Benz / Josh Stuart / J.C. Zenklusen / Rameen Beroukhim / Jason C. Chang / Joshua D. Campbell / D. Neil Hayes / Lixing Yang / Peter W. Laird / John N. Weinstein / David J. Kwiatkowski / Ming S. Tsao / William D. Travis

    Cell Reports, Vol 34, Iss 8, Pp 108784- (2021)

    2021  

    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: A new drug design targeting the adenosinergic system for Huntington's disease.

    Nai-Kuei Huang / Jung-Hsin Lin / Jiun-Tsai Lin / Chia-I Lin / Eric Minwei Liu / Chun-Jung Lin / Wan-Ping Chen / Yuh-Chiang Shen / Hui-Mei Chen / Jhih-Bin Chen / Hsing-Lin Lai / Chieh-Wen Yang / Ming-Chang Chiang / Yu-Shuo Wu / Chen Chang / Jiang-Fan Chen / Jim-Min Fang / Yun-Lian Lin / Yijuang Chern

    PLoS ONE, Vol 6, Iss 6, p e

    2011  Volume 20934

    Abstract: BACKGROUND: Huntington's disease (HD) is a neurodegenerative disease caused by a CAG trinucleotide expansion in the Huntingtin (Htt) gene. The expanded CAG repeats are translated into polyglutamine (polyQ), causing aberrant functions as well as aggregate ...

    Abstract BACKGROUND: Huntington's disease (HD) is a neurodegenerative disease caused by a CAG trinucleotide expansion in the Huntingtin (Htt) gene. The expanded CAG repeats are translated into polyglutamine (polyQ), causing aberrant functions as well as aggregate formation of mutant Htt. Effective treatments for HD are yet to be developed. METHODOLOGY/PRINCIPAL FINDINGS: Here, we report a novel dual-function compound, N(6)-(4-hydroxybenzyl)adenine riboside (designated T1-11) which activates the A(2A)R and a major adenosine transporter (ENT1). T1-11 was originally isolated from a Chinese medicinal herb. Molecular modeling analyses showed that T1-11 binds to the adenosine pockets of the A(2A)R and ENT1. Introduction of T1-11 into the striatum significantly enhanced the level of striatal adenosine as determined by a microdialysis technique, demonstrating that T1-11 inhibited adenosine uptake in vivo. A single intraperitoneal injection of T1-11 in wildtype mice, but not in A(2A)R knockout mice, increased cAMP level in the brain. Thus, T1-11 enters the brain and elevates cAMP via activation of the A(2A)R in vivo. Most importantly, addition of T1-11 (0.05 mg/ml) to the drinking water of a transgenic mouse model of HD (R6/2) ameliorated the progressive deterioration in motor coordination, reduced the formation of striatal Htt aggregates, elevated proteasome activity, and increased the level of an important neurotrophic factor (brain derived neurotrophic factor) in the brain. These results demonstrate the therapeutic potential of T1-11 for treating HD. CONCLUSIONS/SIGNIFICANCE: The dual functions of T1-11 enable T1-11 to effectively activate the adenosinergic system and subsequently delay the progression of HD. This is a novel therapeutic strategy for HD. Similar dual-function drugs aimed at a particular neurotransmitter system as proposed herein may be applicable to other neurotransmitter systems (e.g., the dopamine receptor/dopamine transporter and the serotonin receptor/serotonin transporter) and may facilitate the ...
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2011-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Transforming Fusions of FGFR and TACC Genes in Human Glioblastoma

    Singh, Devendra / Abhijit Guha / Angelica Castano / Anna Lasorella / Antonio Iavarone / Daniel J. Brat / David Zagzag / Eric Minwei Liu / Francesco Niola / Gaetano Finocchiaro / John G. Golfinos / Jonathan Reichel / Joseph Minhow Chan / Ken Aldape / Kunlong Qiu / Michele Ceccarelli / Paola Porrati / Pietro Zoppoli / Raul Rabadan /
    Riccardo Riccardi / Ryan Sullivan / Serena Pellegatta / Tom Mikkelsen / Zhibo Gao

    Science. 2012 Sept. 7, v. 337, no. 6099

    2012  

    Abstract: Oncogenic TACC-tics Human cancers exhibit many types of genomic rearrangements—including some that juxtapose sequences from two unrelated genes—thereby creating fusion proteins with oncogenic activity. Functional analysis of these fusion genes can ... ...

    Abstract Oncogenic TACC-tics Human cancers exhibit many types of genomic rearrangements—including some that juxtapose sequences from two unrelated genes—thereby creating fusion proteins with oncogenic activity. Functional analysis of these fusion genes can provide mechanistic insights into tumorigenesis and potentially lead to effective drugs, as famously illustrated by the BCR-ABL gene in chronic myelogenous leukemia. Singh et al. (p. 1231, published online 26 July) identify and characterize a fusion gene present in 3% of human glioblastomas, a deadly brain cancer. In the resultant fusion protein, the tyrosine kinase region of the fibroblast growth factor receptor (FGFR) is joined to a domain from a transforming acidic coiled-coil (TACC) protein. The TACC-FGFR protein is oncogenic, shows unregulated kinase activity, localizes to the mitotic spindle, and disrupts chromosome segregation. In mice, FGFR inhibitors slowed the growth of tumors driven by the TACC-FGFR gene, suggesting that a subset of glioblastoma patients may benefit from these types of drugs.
    Keywords brain ; carcinogenesis ; chromosome segregation ; drugs ; fibroblast growth factor receptors ; genes ; humans ; leukemia ; mice ; mitotic spindle apparatus ; patients ; proteins ; tyrosine
    Language English
    Dates of publication 2012-0907
    Size p. 1231-1235.
    Publishing place American Association for the Advancement of Science
    Document type Article
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1220834
    Database NAL-Catalogue (AGRICOLA)

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