Author

J. K. Rotow

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 Approach:experimental assay· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:clustering· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

C. E. McCoach· 3 shared C. M. Blakely· 3 shared T. G. Bivona· 3 shared W. Wu· 3 shared F. Haderk· 2 shared P. Gui· 2 shared A. Gupta· 1 shared A. M. Wolff· 1 shared

Activity by Year

2019-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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3 shared papersCancer Biology

C. E. McCoach

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Author profile →

3 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

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