Author

J. Tse

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 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Assay:proteomics· 2 Research Focus:cancer & tumor microenvironment· 1 Approach:deep learning· 1 Approach:statistical model· 1

Frequent Co-Authors

N. Gray· 2 shared T. Zhang· 2 shared A. Boussioutas· 1 shared A. I. Azimpour· 1 shared A. Krokhotin· 1 shared A. L. Chand· 1 shared A. L. E. Carli· 1 shared A. S. Boghossian· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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2 shared papersCancer Biology

N. Gray

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Author profile →

3 papers

Recent·Most cited

Borrowing Transcriptional Kinases to Activate Apoptosis

R. C. Sarott, S. P. Gourisankar, B. A. Karim, S. Nettles, H. Yang, B. Dwyer, J. M. Simanauskaite, J. Tse, H. Abuzaid, A. Krokhotin, T. Zhang, S. M. Hinshaw, M. R. Green, G. R. Crabtree, N. Gray

The paper develops bivalent molecules that convert kinase inhibitors into activators of proapoptotic genes, achieving selective killing of DLBCL cells with low cytotoxicity.

bioRxiv · Oct 23, 2023 · PreprintCancer Biology

Covalent Disruptor of YAP-TEAD Association Suppresses Defective Hippo Signaling

M. Fan, W. Lu, J. Che, N. P. Kwiatkowski, Y. Gao, H.-S. Seo, S. B. Ficarro, P. C. Gokhale, Y. Liu, E. A. Geffken, J. Lakhani, K. Song, M. Kuljanin, W. Ji, J. Jiang, , N. Gray

This paper develops a covalent inhibitor of the YAP-TEAD complex, demonstrating its ability to suppress Hippo signaling defects and inhibit cancer cell growth.

bioRxiv · May 10, 2022Cancer Biology

The kinase activity of the cancer stem cell marker DCLK1 drives gastric cancer progression by reprogramming the stromal tumor landscape

S. Afshar-Sterle, A. L. E. Carli, R. O'Keefe, J. Tse, S. Fischer, A. I. Azimpour, D. Baloyan, L. Elias, P. Thilakasiri, O. Patel, F. M. Ferguson, M. F. Eissmann, A. L. Chand, N. S. Gray, R. Busuttil, , M. Buchert

This study identifies DCLK1 kinase activity as a driver of gastric cancer progression by reprogramming the tumor stroma and promoting invasiveness and metastasis.

bioRxiv · Apr 21, 2022 · PreprintCancer Biology