Author

H.-c. Ting

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:cell type annotation· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Assay:proteomics· 1 Assay:scRNA-seq· 1

Frequent Co-Authors

Y. Park· 2 shared A. Deschenes· 1 shared A. Doshi· 1 shared B. Alagesan· 1 shared C. R. Vakoc· 1 shared C. Tonelli· 1 shared D. A. Tuveson· 1 shared D. J. Pappin· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersCancer Biology

Y. Park

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2 papers

Recent·Most cited

SPDEF promotes the classical subtype of pancreatic ductal adenocarcinoma.

C. Tonelli, G. N. Yordanov, Y. Hao, A. Deschenes, O. Klingbeil, H.-C. Ting, E. Brosnan, A. Doshi, Y. Park, C. R. Vakoc, J. Preall, D. Tuveson

The paper identifies SPDEF as a key driver of the classical subtype of pancreatic ductal adenocarcinoma, showing its role in tumor progression and dependence on specific target genes.

bioRxiv · Mar 18, 2022 · PreprintCancer Biology

Oncogenic KRAS engages an RSK1/NF1 complex in pancreatic cancer

D. K. Cheng, T. E. Oni, Y. Park, J. S. Thalappillil, H.-c. Ting, N. Prasad, B. Alagesan, K. D. Rivera, D. J. Pappin, L. Van Aelst, D. A. Tuveson

This study identifies RSK1 as a KRASG12D-specific interactor in PDAC and shows RSK1 mediates negative feedback on wild-type KRAS.

bioRxiv · Sep 14, 2020 · PreprintCancer Biology