Ignacio Melero

ORCID: 0000-0002-1360-348X
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About
Contact & Profiles
Research Areas
  • Cancer Immunotherapy and Biomarkers
  • Immunotherapy and Immune Responses
  • CAR-T cell therapy research
  • Immune Cell Function and Interaction
  • Monoclonal and Polyclonal Antibodies Research
  • Radiopharmaceutical Chemistry and Applications
  • Immune cells in cancer
  • T-cell and B-cell Immunology
  • Cancer Research and Treatments
  • Virus-based gene therapy research
  • HER2/EGFR in Cancer Research
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Nanoplatforms for cancer theranostics
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Nanoparticle-Based Drug Delivery
  • Cancer Genomics and Diagnostics
  • RNA Interference and Gene Delivery
  • Peptidase Inhibition and Analysis
  • Viral Infections and Vectors
  • Cancer Cells and Metastasis
  • Chemokine receptors and signaling
  • Mosquito-borne diseases and control
  • S100 Proteins and Annexins
  • Colorectal Cancer Treatments and Studies
  • interferon and immune responses

Clinica Universidad de Navarra
2016-2025

Centro de Investigación Biomédica en Red de Cáncer
2017-2025

Universidad de Navarra
2016-2025

Navarre Institute of Health Research
2016-2025

University of Oxford
2023-2025

Chartered Institute of Management Accountants
2011-2023

University of Chieti-Pescara
2023

Instituto de Salud Carlos III
2018-2023

Roche (Switzerland)
2022

Bipar
2014-2021

<h3>Importance</h3> Most patients with hepatocellular carcinoma (HCC) are diagnosed advanced disease not eligible for potentially curative therapies; therefore, new treatment options needed. Combining nivolumab ipilimumab may improve clinical outcomes compared monotherapy. <h3>Objective</h3> To assess efficacy and safety of plus in HCC who were previously treated sorafenib. <h3>Design, Setting, Participants</h3> CheckMate 040 is a multicenter, open-label, multicohort, phase 1/2 study. In the...

10.1001/jamaoncol.2020.4564 article EN cc-by-nc-nd JAMA Oncology 2020-10-02

Mechanisms of acquired resistance to immune checkpoint inhibitors (ICI) are poorly understood. We leveraged a collection 14 ICI-resistant lung cancer samples investigate whether alterations in genes encoding HLA Class I antigen processing and presentation machinery (APM) components or interferon signaling play role PD-1 PD-L1 antagonistic antibodies. Recurrent mutations copy-number changes were not detected our cohort. In one case, we found homozygous loss B2M that caused lack cell-surface...

10.1158/2159-8290.cd-17-0593 article EN Cancer Discovery 2017-10-13

Weak and ineffective antitumor cytotoxic T lymphocyte (CTL) responses can be rescued by immunomodulatory mAbs targeting PD-1 or CD137. Using Batf3(-/-) mice, which are defective for cross-presentation of cell-associated antigens, we show that BATF3-dependent dendritic cells (DC) essential the response to therapy with anti-CD137 anti-PD-1 mAbs. mice failed prime an endogenous CTL-mediated immune toward tumor-associated including neoantigens. As a result, could not amplify any therapeutically...

10.1158/2159-8290.cd-15-0510 article EN Cancer Discovery 2015-10-23

Abstract Summary: Cancer immunotherapy has great promise, but is limited by diverse mechanisms used tumors to prevent sustained antitumor immune responses. Tumors disrupt antigen presentation, T/NK–cell activation, and homing through soluble cell-surface mediators, the vasculature, immunosuppressive cells such as myeloid-derived suppressor regulatory T cells. However, many molecular preventing efficacy of immunity have been identified can be disrupted combination immunotherapy. Here, we...

10.1158/2159-8290.cd-13-0985 article EN Cancer Discovery 2014-05-01
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