Author

Victor R. Olivas

University of California, San Francisco

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 3

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Beatrice GiniiD· 3 shared Wei WuiD· 3 shared Collin M. Blakely· 2 shared Dora Barbosa· 2 shared Paul Allegakoen· 2 shared Sarah Elmes· 2 shared Trever Grant BivonaiD· 2 shared Aleah F. Caulin· 1 shared

Activity by Year

2017-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersCancer Biology

Beatrice GiniORCID

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Author profile →

3 papers

Recent·Most cited

Actionable biological programs to enhance EGFR-targeted therapy response unveiled by single-cell lineage tracing in clinically relevant lung cancer models

Beatrice Gini, Whitney Tamaki, Johnny X. Yu, Dora Barbosa, Wei Wu, Yashar Pourmoghadam, Paul Allegakoen, Donghwa Kim, Sohit Miglani, Sarah Elmes, Victor R. Olivas, Hani Goodarzi, Trever Grant Bivona

This study uses single-cell lineage tracing and RNAseq to identify pre-existing resistant tumor subclones in lung cancer models and their transcriptional programs, revealing mechanisms of therapy resistance.

bioRxiv · May 19, 2025 · PreprintCancer Biology

CDK4 or CDK6 upregulation induces DNA replication stress and genomic instability to cause EGFR targeted therapy resistance in lung cancer

Beatrice Gini, Philippe Gui, Wei Wu, Daniel Lucas Kerr, Lisa Tan, Dora Barbosa, Victor R. Olivas, Paul Allegakoen, Carlos Gomez, Patrick R. Halliday, Sarah Elmes, Veronica Steri, Turja Chakrabarti, Trever Grant Bivona, Collin M. Blakely

This study shows that CDK4/6 upregulation causes DNA replication stress and genomic instability, leading to resistance to EGFR inhibitors in lung cancer, and suggests combining CDK4/6 and EGFR inhibitors as a treatment.

bioRxiv · Mar 12, 2024 · PreprintCancer Biology

Evolution and clinical impact of genetic epistasis within EGFR-mutant lung cancers

Collin M. Blakely, Thomas B.K. Watkins, Wei Wu, Beatrice Gini, Jacob J. Chabon, Caroline E. McCoach, Nicholas McGranahan, Gareth A. Wilson, Nicolai J. Birkbak, Victor R. Olivas, Julia Rotow, Ashley Maynard, Victoria Wang, Matthew A. Gubens, Kimberly C. Banks, , Trever G. Bivona

The paper investigates genetic epistasis in EGFR-mutant lung cancers using over 2,000 cases, showing that genetic combinations, not single drivers, dominate tumor progression and clinical outcomes.

bioRxiv · Mar 16, 2017 · PreprintCancer Biology