Author

C. M. Blakely

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

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Cancer Biology· 5

Signature Assays, Organisms & Methods

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Organism:human· 5 Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:drug response / drug discovery· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

C. E. McCoach· 4 shared T. G. Bivona· 4 shared W. Wu· 4 shared F. Haderk· 3 shared J. K. Rotow· 3 shared P. Gui· 3 shared V. Olivas· 3 shared B. C. Bastian· 2 shared

Activity by Year

2016-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 42 mutual co-author links

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4 shared papersCancer Biology

C. E. McCoach

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5 papers

Recent·Most cited

A focal adhesion kinase-YAP signaling axis drives drug tolerant persister cells and residual disease in lung cancer

F. Haderk, C. Fernandez-Mendez, L. Cech, J. Yu, I. M. Meraz, V. Olivas, D. Barbosa Rabago, D. L. Kerr, C. Gomez, D. V. Allegakoen, J. Guan, K. N. Shah, K. A. Herrington, O. M. Gbenedio, S. Nanjo, , T. G. Bivona

This study identifies a FAK-YAP signaling axis that drives drug-tolerant persister cells and residual disease in lung cancer, showing that inhibiting this axis improves tumor response to targeted therapies.

bioRxiv · Oct 23, 2021Cancer Biology

Targeted cancer therapy induces APOBEC fuelling the evolution of drug resistance

D. R. Caswell, M. K. Mayekar, P. Gui, E. K. Law, N. I. Vokes, C. M. Ruiz, M. Dietzen, M. Angelova, C. Bailey, O. Pich, B. Bakker, W. Wu, T. J. Humpton, D. L. Kerr, W. Hill, , Argyr

This study shows that targeted cancer therapy induces APOBEC-mediated mutagenesis, promoting drug resistance by increasing genetic diversity through mechanisms involving NF-κB activation and reduced DNA repair.

bioRxiv · Dec 18, 2020Cancer Biology

Heterogeneity and targeted therapy-induced adaptations in lung cancer revealed by longitudinal single-cell RNA sequencing

A. Maynard, C. E. McCoach, J. K. Rotow, L. Harris, F. Haderk, L. D. Kerr, E. A. Yu, E. L. Schenk, W. Tan, A. Zee, M. Tan, P. Gui, T. Lea, W. Wu, A. Urisman, , T. G. Bivona

This study uses longitudinal single-cell RNA sequencing to reveal therapy-induced adaptations in lung cancer, identifying cell state transitions and pathways associated with treatment response and resistance.

bioRxiv · Dec 8, 2019 · PreprintCancer Biology

Co-occurring alterations in the RAS-MAPK pathway limit response to MET inhibitor treatment in MET exon 14 skipping mutation positive lung cancer

J. K. Rotow, P. Gui, W. Wu, V. M. Raymond, R. B. Lanman, F. J. Kaye, N. Peled, F. Fece de la Cruz, B. Nadres, R. B. Corcoran, I. Yeh, B. C. Bastian, P. Starostik, K. Newsom, V. R. Olivas, , C. M. Blakely

The paper identifies co-occurring RAS-MAPK pathway alterations in MET exon 14 skipping mutation positive lung cancers that limit response to MET inhibitors and suggests combining MET and MEK inhibitors to overcome resistance.

bioRxiv · May 24, 2019Cancer Biology

Novel computational method for predicting polytherapy switching strategies to overcome tumor heterogeneity and evolution

V. D. Jonsson, C. M. Blakely, L. Lin, S. Asthana, V. Olivas, M. A. Gubens, N. Matni, B. C. Bastian, B. S. Taylor, J. C. Doyle, T. G. Bivona

This paper develops a computational framework to predict dynamic polytherapy switching strategies to address tumor heterogeneity and evolution in lung adenocarcinoma.

bioRxiv · Nov 8, 2016Cancer Biology