David
Santamaría Velilla
Dana–Farber Cancer Institute
Boston, Estados UnidosPublicacións en colaboración con investigadores/as de Dana–Farber Cancer Institute (13)
2024
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Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy
Nature, Vol. 629, Núm. 8013, pp. 919-926
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In vivo vulnerabilities to GPX4 and HDAC inhibitors in drug-persistent versus drug-resistant BRAFV600E lung adenocarcinoma
Cell Reports Medicine, Vol. 5, Núm. 8
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RAS-ON inhibition overcomes clinical resistance to KRAS G12C-OFF covalent blockade
Nature Communications, Vol. 15, Núm. 1
2022
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Comparative Analysis and Isoform-Specific Therapeutic Vulnerabilities of KRAS Mutations in Non-Small Cell Lung Cancer
Clinical Cancer Research, Vol. 28, Núm. 8, pp. 1640-1650
2021
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Targeting Infrequent Driver Alterations in Non-Small Cell Lung Cancer
Trends in Cancer, Vol. 7, Núm. 5, pp. 410-429
2020
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Inhibition of DDR1 enhances in vivo chemosensitivity in KRAS-mutant lung adenocarcinoma
JCI Insight, Vol. 5, Núm. 15
2019
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Myc stimulates cell cycle progression through the activation of Cdk1 and phosphorylation of p27
Scientific Reports, Vol. 9, Núm. 1
2018
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A putative role for Discoidin Domain Receptor 1 in cancer chemoresistance
Cell Adhesion and Migration, Vol. 12, Núm. 4, pp. 394-397
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KRAS Dimerization Impacts MEK Inhibitor Sensitivity and Oncogenic Activity of Mutant KRAS
Cell, Vol. 172, Núm. 4, pp. 857-868.e15
2017
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A Braf kinase-inactive mutant induces lung adenocarcinoma
Nature, Vol. 548, Núm. 7666, pp. 239-243
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In vivo oncogenic conflict triggered by co-existing KRAS and EGFR activating mutations in lung adenocarcinoma
Oncogene, Vol. 36, Núm. 16, pp. 2309-2318
2016
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KRAS-driven lung adenocarcinoma: Combined DDR1/Notch inhibition as an effective therapy
ESMO Open, Vol. 1, Núm. 5
2014
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Genetic characterization of the role of the Cip/Kip family of proteins as cyclin-dependent kinase inhibitors and assembly factors
Molecular and Cellular Biology, Vol. 34, Núm. 8, pp. 1452-1459