LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 2 of total 2

Search options

  1. Article ; Online: The ATR inhibitor ceralasertib potentiates cancer checkpoint immunotherapy by regulating the tumor microenvironment.

    Hardaker, Elizabeth L / Sanseviero, Emilio / Karmokar, Ankur / Taylor, Devon / Milo, Marta / Michaloglou, Chrysis / Hughes, Adina / Mai, Mimi / King, Matthew / Solanki, Anisha / Magiera, Lukasz / Miragaia, Ricardo / Kar, Gozde / Standifer, Nathan / Surace, Michael / Gill, Shaan / Peter, Alison / Talbot, Sara / Tohumeken, Sehmus /
    Fryer, Henderson / Mostafa, Ali / Mulgrew, Kathy / Lam, Carolyn / Hoffmann, Scott / Sutton, Daniel / Carnevalli, Larissa / Calero-Nieto, Fernando J / Jones, Gemma N / Pierce, Andrew J / Wilson, Zena / Campbell, David / Nyoni, Lynet / Martins, Carla P / Baker, Tamara / Serrano de Almeida, Gilberto / Ramlaoui, Zainab / Bidar, Abdel / Phillips, Benjamin / Boland, Joseph / Iyer, Sonia / Barrett, J Carl / Loembé, Arsene-Bienvenu / Fuchs, Serge Y / Duvvuri, Umamaheswar / Lou, Pei-Jen / Nance, Melonie A / Gomez Roca, Carlos Alberto / Cadogan, Elaine / Critichlow, Susan E / Fawell, Steven / Cobbold, Mark / Dean, Emma / Valge-Archer, Viia / Lau, Alan / Gabrilovich, Dmitry I / Barry, Simon T

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1700

    Abstract: The Ataxia telangiectasia and Rad3-related (ATR) inhibitor ceralasertib in combination with the PD-L1 antibody durvalumab demonstrated encouraging clinical benefit in melanoma and lung cancer patients who progressed on immunotherapy. Here we show that ... ...

    Abstract The Ataxia telangiectasia and Rad3-related (ATR) inhibitor ceralasertib in combination with the PD-L1 antibody durvalumab demonstrated encouraging clinical benefit in melanoma and lung cancer patients who progressed on immunotherapy. Here we show that modelling of intermittent ceralasertib treatment in mouse tumor models reveals CD8
    MeSH term(s) Humans ; Animals ; Mice ; CD8-Positive T-Lymphocytes ; B7-H1 Antigen ; Tumor Microenvironment ; Cell Line, Tumor ; Immunotherapy ; Disease Models, Animal ; Neoplasms ; Ataxia Telangiectasia Mutated Proteins ; Indoles ; Morpholines ; Pyrimidines ; Sulfonamides
    Chemical Substances ceralasertib (85RE35306Z) ; B7-H1 Antigen ; ATR protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Indoles ; Morpholines ; Pyrimidines ; Sulfonamides
    Language English
    Publishing date 2024-02-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-45996-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Clinical Validation of Coexisting Activating Mutations Within EGFR, Mitogen-Activated Protein Kinase, and Phosphatidylinositol 3-Kinase Pathways in Lung Cancers.

    De Marchi, Federico / Haley, Lisa / Fryer, Henderson / Ibrahim, Junaid / Beierl, Katie / Zheng, Gang / Gocke, Christopher D / Eshleman, James R / Belchis, Deborah / Illei, Peter / Lin, Ming-Tseh

    Archives of pathology & laboratory medicine

    2018  Volume 143, Issue 2, Page(s) 174–182

    Abstract: Context.—: Mutations within the same signature transduction pathway are redundant and, therefore, most are mutually exclusive. Laboratory errors, however, may introduce unexpected coexisting mutations.: Objective.—: To validate coexisting mutations ... ...

    Abstract Context.—: Mutations within the same signature transduction pathway are redundant and, therefore, most are mutually exclusive. Laboratory errors, however, may introduce unexpected coexisting mutations.
    Objective.—: To validate coexisting mutations within epidermal growth factor receptor (EGFR), mitogen-activated protein kinase, and phosphatidylinositol 3-kinase pathways.
    Design.—: In this retrospective study for quality assessment of next-generation sequencing in a clinical diagnostics setting, coexisting mutations within EGFR, KRAS, NRAS, BRAF, AKT1, and PIK3CA genes were examined in 1208 non-small cell lung cancers.
    Results.—: EGFR mutations did not coexist with BRAF mutations, neither kinase-activated nor kinase-impaired mutations. There was a low but similar incidence (3.3%-5.1%) of PIK3CA mutations in BRAF-, EGFR-, and KRAS-mutated lung cancers and a rare incidence of coexisting KRAS and EGFR mutations detected in 1 of 1208 lung cancers (0.08%) or 1 of 226 EGFR-mutated lung cancers (0.4%). Coexisting BRAF p.V600E mutation was observed in 3 of 4 AKT1 p.E17K-mutated lung cancers. Mutational profiling of DNA reisolated from subareas with the same or different histomorphology, using an alternative assay, confirmed that coexisting mutations might present within the same (whole or subclonal) population or different populations and clarified that the so-called coexisting activating KRAS and BRAF mutations originally reported in a specimen were indeed present in separate lung nodules submitted in the same block.
    Conclusions.—: The results supported that EGFR and BRAF mutations are early driver mutations in lung cancers. Guidelines from official organizations to establish standard operating procedures are warranted to validate unexpected coexisting mutations and, if clinically indicated, to determine their presence in the same or different tumor populations.
    MeSH term(s) Carcinoma, Non-Small-Cell Lung/genetics ; DNA Mutational Analysis/methods ; ErbB Receptors/genetics ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Lung Neoplasms/genetics ; MAP Kinase Signaling System/genetics ; Phosphatidylinositol 3-Kinase/genetics
    Chemical Substances Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2018-09-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Validation Study
    ZDB-ID 194119-7
    ISSN 1543-2165 ; 0363-0153 ; 0096-8528 ; 0003-9985
    ISSN (online) 1543-2165
    ISSN 0363-0153 ; 0096-8528 ; 0003-9985
    DOI 10.5858/arpa.2017-0495-OA
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.36: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top