Author

J. N. Singh

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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Assay:bulk RNA-seq· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:clustering· 1 Research Focus:differential expression· 1

Frequent Co-Authors

D. L. Burkhart· 2 shared K. L. Morel· 2 shared L. Ellis· 2 shared A. A. Hamid· 1 shared A. G. Sowalsky· 1 shared A. M. Bergman· 1 shared A. Sheahan· 1 shared A. T. Ku· 1 shared

Activity by Year

2022-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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2 shared papersCancer Biology

D. L. Burkhart

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2 papers

Recent·Most cited

MYBL2 drives prostate cancer plasticity and identifies CDK2 as a therapeutic vulnerability in RB1-loss and neuroendocrine prostate cancer

L. Ellis, B. German, J. N. Singh, D. L. Burkhart, A. Sheahan, H. Bergom, K. L. Morel, H. Beltran, J. Hwang, K. Lawrenson

This study identifies MYBL2 as a master regulator of phenotypic plasticity in prostate cancer and shows CDK2 inhibition as a potential therapeutic strategy for MYBL2-driven tumors.

bioRxiv · Jan 31, 2024 · PreprintCancer Biology

Loss of tristetraprolin activates NF-κB induced phenotypic plasticity and primes transition to lethal prostate cancer

K. L. Morel, A. A. Hamid, B. G. Falcon, J. N. Singh, S. Linder, A. M. Bergman, H. G. van der Poel, I. Hofland, E. M. Bekers, S. Trostel, S. Wilkinson, A. T. Ku, D. L. Burkhart, M. Kim, J. Kim, , L. Ellis

This study shows that loss of ZFP36 promotes NF-κB activation and phenotypic plasticity in prostate cancer, leading to aggressive disease and castration resistance, which can be reversed by NF-κB inhibition.

bioRxiv · Aug 5, 2022 · PreprintCancer Biology