Author

E. Still

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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Research Focus:cancer & tumor microenvironment· 3 Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1 Assay:proteomics· 1 Assay:whole-genome sequencing· 1

Frequent Co-Authors

A. Kentsis· 3 shared R. Koche· 3 shared S. Armstrong· 3 shared A. Krivtsov· 2 shared C. Reed· 2 shared E. de Stanchina· 2 shared F. Brown· 2 shared A. Blackford· 1 shared

Activity by Year

2017-2017 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersCancer Biology

A. Kentsis

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3 papers

Recent·Most cited

Peptidomimetic blockade of MYB in acute myeloid leukemia

K. Ramaswamy, L. Forbes, G. Minuesa, T. Gindin, F. Brown, M. Kharas, A. Krivtsov, S. Armstrong, E. Still, E. de Stanchina, B. Knoechel, R. Koche, A. Kentsis

This study develops a peptidomimetic inhibitor, MYBMIM, that blocks MYB:CBP/P300 complex assembly in AML cells, leading to apoptosis and reduced tumor growth in mice.

bioRxiv · Nov 20, 2017Cancer Biology

Human PGBD5 DNA transposase promotes site-specific oncogenic mutations in rhabdoid tumors

A. Henssen, R. Koche, J. Zhuang, E. Jiang, C. Reed, A. Eisenberg, E. Still, I. MacArthur, E. Rodriguez-Fos, S. Gonzalez, M. Puiggros, A. Blackford, C. Mason, E. De Stanchina, M. Gonen, , A. Kentsis

This study identifies PGBD5 as an oncogenic DNA transposase in rhabdoid tumors, causing site-specific genomic rearrangements through PSS sequences and end-joining repair.

bioRxiv · Feb 23, 2017Cancer Biology

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

F. Brown, E. Still, P. Cifani, S. Takao, C. Reed, S. Ficarro, R. Koche, P. Romanienko, W. Mark, C. O'Donnell, B. Spitzer, C. Stutzke, A. Krivtsov, G. Pouliot, J. Marto, , A. Kentsis

This study identifies MEF2C phosphorylation as a marker of chemotherapy resistance in AML and shows that inhibiting this phosphorylation can overcome resistance in MEF2C-activated cells.

bioRxiv · Feb 9, 2017Cancer Biology