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· 2

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Wei WuiD· 2 shared Aleah F. Caulin· 1 shared Anibal R. Cordero· 1 shared Ashley Maynard· 1 shared Beatrice GiniiD· 1 shared Boyko S. AtanassoviD· 1 shared Bradley Balk· 1 shared Caroline E. McCoach· 1 shared

Activity by Year

2017-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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2 shared papersCancer Biology

Wei WuORCID

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2 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

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