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  1. Article: A Novel Oncogenic Driver in a Lung Adenocarcinoma Patient Harboring an

    Chen, Dong / Li, Xing-Liang / Wu, Biao / Zheng, Xiao-Bin / Wang, Wen-Xian / Chen, Hua-Fei / Dong, Yi-Yu / Xu, Chun-Wei / Fang, Mei-Yu

    Frontiers in oncology

    2020  Volume 10, Page(s) 867

    Abstract: Introduction: ...

    Abstract Introduction:
    Language English
    Publishing date 2020-06-16
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2020.00867
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Integrated Genomic Analysis of Hürthle Cell Cancer Reveals Oncogenic Drivers, Recurrent Mitochondrial Mutations, and Unique Chromosomal Landscapes.

    Ganly, Ian / Makarov, Vladimir / Deraje, Shyamprasad / Dong, YiYu / Reznik, Ed / Seshan, Venkatraman / Nanjangud, Gouri / Eng, Stephanie / Bose, Promita / Kuo, Fengshen / Morris, Luc G T / Landa, Inigo / Carrillo Albornoz, Pedro Blecua / Riaz, Nadeem / Nikiforov, Yuri E / Patel, Kepal / Umbricht, Christopher / Zeiger, Martha / Kebebew, Electron /
    Sherman, Eric / Ghossein, Ronald / Fagin, James A / Chan, Timothy A

    Cancer cell

    2018  Volume 34, Issue 2, Page(s) 256–270.e5

    Abstract: The molecular foundations of Hürthle cell carcinoma (HCC) are poorly understood. Here we describe a comprehensive genomic characterization of 56 primary HCC tumors that span the spectrum of tumor behavior. We elucidate the mutational profile and driver ... ...

    Abstract The molecular foundations of Hürthle cell carcinoma (HCC) are poorly understood. Here we describe a comprehensive genomic characterization of 56 primary HCC tumors that span the spectrum of tumor behavior. We elucidate the mutational profile and driver mutations and show that these tumors exhibit a wide range of recurrent mutations. Notably, we report a high number of disruptive mutations to both protein-coding and tRNA-encoding regions of the mitochondrial genome. We reveal unique chromosomal landscapes that involve whole-chromosomal duplications of chromosomes 5 and 7 and widespread loss of heterozygosity arising from haploidization and copy-number-neutral uniparental disomy. We also identify fusion genes and disrupted signaling pathways that may drive disease pathogenesis.
    MeSH term(s) Chromosome Aberrations ; DNA Repair ; DNA, Mitochondrial/genetics ; Haploidy ; Humans ; Loss of Heterozygosity ; Mutation ; Signal Transduction ; TOR Serine-Threonine Kinases/physiology ; Telomerase/genetics ; Thyroid Neoplasms/genetics
    Chemical Substances DNA, Mitochondrial ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; TERT protein, human (EC 2.7.7.49) ; Telomerase (EC 2.7.7.49)
    Language English
    Publishing date 2018-09-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2018.07.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5650: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 104: Show issues

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  3. Article ; Online: Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts.

    Li, Shunqiang / Shen, Dong / Shao, Jieya / Crowder, Robert / Liu, Wenbin / Prat, Aleix / He, Xiaping / Liu, Shuying / Hoog, Jeremy / Lu, Charles / Ding, Li / Griffith, Obi L / Miller, Christopher / Larson, Dave / Fulton, Robert S / Harrison, Michelle / Mooney, Tom / McMichael, Joshua F / Luo, Jingqin /
    Tao, Yu / Goncalves, Rodrigo / Schlosberg, Christopher / Hiken, Jeffrey F / Saied, Laila / Sanchez, Cesar / Giuntoli, Therese / Bumb, Caroline / Cooper, Crystal / Kitchens, Robert T / Lin, Austin / Phommaly, Chanpheng / Davies, Sherri R / Zhang, Jin / Kavuri, Megha Shyam / McEachern, Donna / Dong, Yi Yu / Ma, Cynthia / Pluard, Timothy / Naughton, Michael / Bose, Ron / Suresh, Rama / McDowell, Reida / Michel, Loren / Aft, Rebecca / Gillanders, William / DeSchryver, Katherine / Wilson, Richard K / Wang, Shaomeng / Mills, Gordon B / Gonzalez-Angulo, Ana / Edwards, John R / Maher, Christopher / Perou, Charles M / Mardis, Elaine R / Ellis, Matthew J

    Cell reports

    2013  Volume 4, Issue 6, Page(s) 1116–1130

    Abstract: To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained ... ...

    Abstract To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained with high fidelity. However, at the single-nucleotide level, variable numbers of PDX-specific somatic events were documented, although they were only rarely functionally significant. Variant allele frequencies were often preserved in the PDXs, demonstrating that clonal representation can be transplantable. Estrogen-receptor-positive PDXs were associated with ESR1 ligand-binding-domain mutations, gene amplification, or an ESR1/YAP1 translocation. These events produced different endocrine-therapy-response phenotypes in human, cell line, and PDX endocrine-response studies. Hence, deeply sequenced PDX models are an important resource for the search for genome-forward treatment options and capture endocrine-drug-resistance etiologies that are not observed in standard cell lines. The originating tumor genome provides a benchmark for assessing genetic drift and clonal representation after transplantation.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Alleles ; Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Drug Resistance, Neoplasm ; Estradiol/pharmacology ; Estrogen Receptor alpha/genetics ; Female ; Gene Amplification ; Genomic Instability ; Heterografts ; Humans ; Mice ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Neoplasm Staging ; Phosphoproteins/genetics ; Point Mutation ; RNA, Neoplasm/biosynthesis ; RNA, Neoplasm/genetics ; Transcription Factors ; Translocation, Genetic
    Chemical Substances Adaptor Proteins, Signal Transducing ; ESR1 protein, human ; Estrogen Receptor alpha ; Neoplasm Proteins ; Phosphoproteins ; RNA, Neoplasm ; Transcription Factors ; YAP1 protein, human ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2013-09-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2013.08.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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