Lorea Jordana-Urriza

ORCID: 0000-0003-2323-817X
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About
Contact & Profiles
Research Areas
  • Immune cells in cancer
  • CAR-T cell therapy research
  • Epigenetics and DNA Methylation
  • Chemokine receptors and signaling
  • T-cell and B-cell Immunology
  • Angiogenesis and VEGF in Cancer
  • Immune Cell Function and Interaction
  • Advanced biosensing and bioanalysis techniques
  • Biosimilars and Bioanalytical Methods
  • Kruppel-like factors research
  • Immunotherapy and Immune Responses

German Cancer Research Center
2022-2023

Heidelberg University
2022-2023

Universidad de Navarra
2022-2023

Navarre Institute of Health Research
2022

Understanding the mechanisms that drive chimeric antigen receptor (CAR) T cell function and persistence in multiple myeloma (MM) remains a critical challenge for improving therapeutic outcomes. In this study, we applied single-cell multiomics gene regulatory network (GRN) analysis to characterize transcriptional dynamics clonal evolution of BCMA-targeted CAR cells longitudinally collected bone marrow (BM) peripheral blood (PB) samples from MM patients. Our results revealed infiltrating BM...

10.1101/2025.04.01.646378 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-04-06

Abstract Epithelial ovarian cancer (EOC) is one of the most lethal gynecologic cancers worldwide. EOC cells educate tumor-associated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironment (TME). In addition, frequently activate Notch1 receptors on endothelial (EC) facilitate metastasis. However, further work required establish whether endothelium also influences education recruited monocytes. Here, we report that canonical Notch...

10.1158/0008-5472.can-22-0076 article EN Cancer Research 2022-10-06

<div>Abstract<p>Epithelial ovarian cancer (EOC) is one of the most lethal gynecologic cancers worldwide. EOC cells educate tumor-associated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironment (TME). In addition, frequently activate Notch1 receptors on endothelial (EC) facilitate metastasis. However, further work required establish whether endothelium also influences education recruited monocytes. Here, we report...

10.1158/0008-5472.c.6514245 preprint EN 2023-03-31

<div>Abstract<p>Epithelial ovarian cancer (EOC) is one of the most lethal gynecologic cancers worldwide. EOC cells educate tumor-associated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironment (TME). In addition, frequently activate Notch1 receptors on endothelial (EC) facilitate metastasis. However, further work required establish whether endothelium also influences education recruited monocytes. Here, we report...

10.1158/0008-5472.c.6514245.v1 preprint EN 2023-03-31
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