Author

L. Post

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 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:perturbation response prediction· 1

Frequent Co-Authors

A. Kulkarni· 1 shared B. Huang· 1 shared B. L. Parker· 1 shared C. E. McCoach· 1 shared C. Fernandez-Mendez· 1 shared C. Gomez· 1 shared C. J. Kuo· 1 shared C. M. Blakely· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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1 shared paperCancer Biology

A. Kulkarni

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Author profile →

2 papers

Recent·Most cited

Identification of resistance mechanisms to small-molecule inhibition of TEAD-regulated transcription

A. Kulkarni, V. Mohan, T. Tang, L. Post, M. Manning, N. Thio, B. L. Parker, J. Rosenbluh, J. H. A. Vissers, K. F. Harvey

This study identifies resistance mechanisms to TEAD inhibitors by showing MAPK hyperactivation can counteract their effects and suggests combining TEAD and MEK inhibition as a therapeutic strategy.

bioRxiv · Aug 16, 2023Cancer Biology

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