Verónica Rendo – Targeting brain tumour evolution and treatment resistance
Our research group aims to uncover the mechanisms by which brain tumour cells evolve and become resistant to treatment. Our goal is to translate these findings into therapeutic strategies that more effectively and specifically kill cancer cells.
Despite decades of research, brain tumours remain one of the most lethal cancer types. The greatest challenge is that no curative treatment exists, and all patients eventually develop resistance against the limited amount of treatment options available.
Our lab aims to study the genetic and cell plasticity mechanisms that enable malignant brain tumour cells to develop, grow, and become resistant to treatment. To this end, we leverage cutting-edge genomic, functional genetics and computational approaches to explore these translational questions in clinical samples and preclinical models, which include patient-derived cell lines, organoids, and mouse xenografts.
Our overall goal is to identify and validate novel therapeutic strategies that extend the life of patients diagnosed with a malignant brain tumour.

Overview of our lab’s research.
More information is also available at www.rendolab.org
Group members
Publications
A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer
Part of Nature Communications, 2025
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Part of Science Translational Medicine, 2025
NAT2 activity increases cytotoxicity of anthracycline antibiotics and HDAC inhibitors
Part of Biochimica et Biophysica Acta - Molecular Basis of Disease, 2025
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p21-Dependent Senescence Induction by BMP4 Renders Glioblastoma Cells Vulnerable to Senolytics
Part of International Journal of Molecular Sciences, 2025
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Recurrent breakpoints in the BRD4 locus reduce toxicity associated with gene amplification
Part of Cell Genomics, 2025
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Comparison of high-throughput single-cell RNA-seq methods for ex vivo drug screening
Part of NAR Genomics and Bioinformatics, 2024
- DOI for Comparison of high-throughput single-cell RNA-seq methods for ex vivo drug screening
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Part of Biochemical Pharmacology, 2022
- DOI for Enhanced cytotoxicity of a novel family of ATPase inhibitors in colorectal cancer cells with high NAT2 activity
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Part of Journal of Experimental & Clinical Cancer Research, 2021
- DOI for Common and mutation specific phenotypes of KRAS and BRAF mutations in colorectal cancer cells revealed by integrative -omics analysis
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Defining eligible patients for allele-selective chemotherapies targeting NAT2 in colorectal cancer
Part of Scientific Reports, 2020
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Exploiting loss of heterozygosity for allele-selective colorectal cancer chemotherapy
Part of Nature Communications, 2020
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Unexpected Acetylation of Endogenous Aliphatic Amines by Arylamine N-Acetyltransferase NAT2
Part of Angewandte Chemie International Edition, p. 14342-14346, 2020
- DOI for Unexpected Acetylation of Endogenous Aliphatic Amines by Arylamine N-Acetyltransferase NAT2
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Targeting allelic loss in colorectal cancer
2018
Somatic Ephrin Receptor Mutations Are Associated with Metastasis in Primary Colorectal Cancer
Part of Cancer Research, p. 1730-1740, 2017
Part of Oncotarget, p. 98646-98659, 2017
Novel anti-cancer agents targeting NAT2 loss in colorectal cancer