Author

E. M. Kerr

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 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

P. D. Dunne· 3 shared A. E. Ryan· 2 shared C. McCann· 2 shared D. B. Longley· 2 shared L. J. Egan· 2 shared N. T. Crawford· 2 shared S. S. McDade· 2 shared T. Sessler· 2 shared

Activity by Year

2019-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersCancer Biology

P. D. Dunne

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Stromal cell sialylation suppresses T cells in inflammatory tumour microenvironments: A new tumour stromal cell immune checkpoint?

H. Egan, O. Treacy, K. Lynch, N. A. Leonard, G. O'Malley, K. DeVeirman, K. Vanderkerken, M. Craughwell, L. J. Egan, T. Ritter, A. M. Hogan, K. Redmond, M. Sheehan, A. Canney, S. Hynes, , A. E. Ryan

This study shows that sialylation of stromal cells in tumors enhances immunosuppression and that targeting this process can reverse immune cell exhaustion.

bioRxiv · Jun 18, 2021 · PreprintImmunology

Clinical positioning of the IAP antagonist tolinapant (ASTX660) in colorectal cancer

D. B. Longley, N. T. Crawford, K. J. Stott, T. Sessler, C. McCann, W. McDaid, C. Latimer, J. Fox, J. M. Munck, T. Smyth, A. Shah, V. Martins, M. Lawler, P. D. Dunne, E. M. Kerr, , V. M. Coyle

This study shows tolinapant, an IAP inhibitor, enhances chemotherapy-induced apoptosis in colorectal cancer by modulating FLIP and HDACs, suggesting its clinical use in poor prognosis MSS CRC with elevated cIAP1/2.

bioRxiv · Nov 20, 2020Cancer Biology

FLIP(L) determines p53 induced life or death

A. Lees, A. J. McIntyre, F. Falcone, N. T. Crawford, C. McCann, G. P. Quinn, J. Z. Roberts, T. Sessler, P. F. Gallagher, K. McAllister, K. McLaughlin, W. L. Allen, C. Holohan, L. J. Egan, A. E. Ryan, , S. S. McDade

This study identifies FLIP(L) as a p53 target that determines cell fate by promoting cell cycle arrest and inhibiting apoptosis.

bioRxiv · Nov 28, 2019 · PreprintCancer Biology