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Showing 1–13 of 13 results
Advanced filters: Author: Amaia Lujambio Clear advanced filters

  • In this Review, Lujambio and colleagues provide an overview of the use of in vitro and in vivo precision models for hepatocellular carcinoma, their strengths and limitations, and how they can be used to identify and test precision therapies and biomarkers.

    • Marina Barcena-Varela
    • Satdarshan P. Monga
    • Amaia Lujambio
    Reviews
    Nature Reviews Gastroenterology & Hepatology
    Volume: 22, P: 191-205

  • Liver metastases lead to resistance to immunotherapy through the ‘siphoning’ of tumor antigen–specific CD8+ T cells into the liver, which results in a systemic ‘immune desert’ incapable of controlling tumor burden.

    • Katherine E. Lindblad
    • Amaia Lujambio
    News & Views
    Nature Medicine
    Volume: 27, P: 25-27

  • In 2021, our understanding of resistance to therapy in primary liver tumours improved drastically. By taking a holistic approach, three independent studies have characterized the tumour cell biodiversity across space, time and aetiologies in primary liver cancer, decoding the crosstalk between different cell types within the tumour ecosystem and their individual contributions to therapy resistance.

    • Chantal Desdouets
    • Amaia Lujambio
    News & Views
    Nature Reviews Gastroenterology & Hepatology
    Volume: 19, P: 83-84

  • Multiomics analysis of tumor samples from the phase 1b GO30140 and phase 3 IMbrave150 trials reveals baseline immune and genetic features that might identify patients with advanced hepatocellular carcinoma who will benefit from atezolizumab and bevacizumab combination therapy.

    • Andrew X. Zhu
    • Alexander R. Abbas
    • Yulei Wang
    Research
    Nature Medicine
    Volume: 28, P: 1599-1611

  • Cellular senescence, a cell-autonomous growth arrest program, also executes pleiotropic non-cell-autonomous activities through the senescence-associated secretory phenotype (SASP). The innate cGAS–STING DNA-sensing pathway is now shown to regulate senescence by recognizing cytosolic DNA and inducing SASP factors, uncovering an unexpected link between these two previously unrelated pathways.

    • Marina Ruiz de Galarreta
    • Amaia Lujambio
    News & Views
    Nature Cell Biology
    Volume: 19, P: 1008-1009

  • Gain-of-function mutations in CTNNB1 (encoding for b-catenin) leading to deregulated Wnt/β-catenin signaling are frequently observed in patients with hepatocellular carcinoma (HCC). Here the authors show that inhibiting b-catenin with lipid nanoparticles encapsulating siRNA targeting CTNNB1 impairs tumor growth and promotes anti-tumor immunity in preclinical HCC models.

    • Brandon M. Lehrich
    • Evan R. Delgado
    • Satdarshan P. Monga
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-26

  • In hepatocellular carcinoma driven by non-alcoholic steatohepatitis, aberrant T cell activation and impaired immune surveillance seem to make hepatocellular carcinoma less responsive to anti-PD1 or anti-PDL1 immunotherapy.

    • Dominik Pfister
    • Nicolás Gonzalo Núñez
    • Mathias Heikenwalder
    ResearchOpen Access
    Nature
    Volume: 592, P: 450-456

  • Myeloid cells are the predominant cell type in the tumor microenvironment of human and murine glioblastoma (GBM). By generating a mouse model deficient for all monocyte chemoattractant proteins, here the authors show that blocking monocyte recruitment promotes a compensatory neutrophil influx and that concomitant neutrophil inhibition is required to improve survival in GBM preclinical models.

    • Zhihong Chen
    • Nishant Soni
    • Dolores Hambardzumyan
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-24

  • Senescence of hematopoietic progenitor cells, enforced by the BRAFV600E mutation, underlies the development of Langerhans cell histiocytosis and could be a new target for drug development and therapy of this disease in patients.

    • Camille Bigenwald
    • Jessica Le Berichel
    • Miriam Merad
    Research
    Nature Medicine
    Volume: 27, P: 851-861

  • A systematic screen identifies FGFR1 signalling reactivation as an adaptive resistance mechanism after MEK inhibition specific for KRAS tumours, which can be targeted by combined inhibition with the clinically approved drugs trametinib and ponatinib.

    • Eusebio Manchado
    • Susann Weissmueller
    • Scott W. Lowe
    Research
    Nature
    Volume: 534, P: 647-651