Author

Collin M. Blakely

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

Frequent Co-Authors

Wei WuiD· 3 shared Beatrice GiniiD· 2 shared Trever Grant BivonaiD· 2 shared Victor R. Olivas· 2 shared Aleah F. Caulin· 1 shared Anibal R. Cordero· 1 shared Ashley Maynard· 1 shared Boyko S. AtanassoviD· 1 shared

Activity by Year

2017-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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3 shared papersCancer Biology

Wei WuORCID

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3 papers

Recent·Most cited

Reversible therapeutic resistance in EGFR mutant lung cancer caused by RB1 loss induced lineage plasticity

Letian Zhang, Meenalakshmi Chinnam, Bradley Balk, Xiaojing Zhang, Yanqing Wang, Tatiana Shaurova, Shamshad Alam, Saraswati Pokharel, Prashant Singh, Justine J. Jacobi, Jianmin Wang, Eduardo Cortes Gomez, Michael Habitzruther, Mukund Seshadri, Boyko S. Atanassov, , David W. Goodrich

This study shows RB1 loss in EGFR mutant lung cancer leads to reversible lineage plasticity, accelerating resistance to EGFR TKI therapy through non-genetic mechanisms.

bioRxiv · Aug 4, 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