Author

J. W. Riess

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

Frequent Co-Authors

F. Haderk· 2 shared I. M. Meraz· 2 shared J. A. Roth· 2 shared M. Majidi· 2 shared T. G. Bivona· 2 shared V. Olivas· 2 shared A. K. Simons· 1 shared A. Srivastava· 1 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 28 mutual co-author links

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2 shared papersCancer Biology

F. Haderk

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A Genomically and Clinically Annotated Patient Derived Xenograft (PDX) Resource for Preclinical Research in Non-Small Cell Lung Cancer

X. Y. Woo, A. Srivastava, P. C. Mack, J. H. Graber, B. J. Sanderson, M. W. Lloyd, M. Chen, S. Domanskyi, R. Gandour-Edwards, R. A. Tsai, J. Keck, M. Cheng, M. Bundy, E. L. Jocoy, J. W. Riess, , C. J. Bult

The paper describes a collection of 79 genomically and clinically annotated lung cancer PDX models that retain patient tumor features and treatment responses, available through MMHCdb.

bioRxiv · Mar 6, 2022Cancer Biology

3-Phosphoinositide-dependent kinase 1 drives acquired resistance to osimertinib

I. M. Meraz, M. Majidi, B. Fang, F. Meng, L. Gao, R. Shao, R. Song, F. Li, M. J. Ha, Q. Wang, J. Wang, E. J. Shpall, S. Y. Jung, F. Haderk, P. Gui, , J. A. Roth

This study identifies PDK1 as a driver of osimertinib resistance in NSCLC, showing its inhibition sensitizes resistant cells and correlates with disease progression.

bioRxiv · Dec 10, 2021Cancer 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