Author

A. Vedder

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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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1 Assay:proteomics· 1 Assay:whole-exome sequencing· 1

Frequent Co-Authors

E. Padron· 3 shared M. Binder· 2 shared M. E. Balasis· 2 shared M. E. Fernandez-Zapico· 2 shared M. M. Patnaik· 2 shared A. A. Mangaonkar· 1 shared A. Buradkar· 1 shared A. E. Gaspar-Maia· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersCancer Biology

E. Padron

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Author profile →

3 papers

Recent·Most cited

Targeting BET Proteins downregulates miR-33a to promote synergy with PIM inhibitors in CMML

C. Letson, M. E. Balasis, H. Newman, M. Binder, A. Vedder, F. Kinose, M. Ball, T. Kruer, A. Quintana, T. L. Lasho, C. M. Finke, L. L. Almada, J. M. Grants, G. Zhang, M. E. Fernandez-Zapico, , E. Padron

This study identifies PIM inhibitors as synergistic with BET inhibitors in myeloid leukemia, showing miR-33a downregulation drives PIM1 upregulation and GM-CSF hypersensitivity as a biomarker for combination therapy.

bioRxiv · Nov 1, 2022Cancer Biology

CBL mutations promote activation of PI3K/AKT signaling via LYN kinase

R. Belizaire, S. H. J. Koochaki, N. Udeshi, A. Vedder, L. Sun, T. Svinkina, C. Hartigan, C. Stanclift, M. Schenone, S. A. Carr, E. Padron, B. L. Ebert

The paper investigates how CBL mutations drive oncogenesis by enhancing LYN kinase activity and PI3K/AKT signaling, suggesting LYN inhibition as a therapeutic strategy.

bioRxiv · Apr 13, 2020 · PreprintCancer Biology

RAS mutations drive proliferative chronic myelomonocytic leukemia via activation of a novel KMT2A-PLK1 axis

R. M. Carr, D. Vorobyev, T. Lasho, D. L. Marks, E. J. Tolosa, A. Vedder, L. Almada, A. Yurchenko, I. Padioleau, B. Alver, G. Coltro, M. Binder, S. L. Safgren, I. Horn, X. You, , M. M. Patnaik

This study identifies RAS mutations as drivers of proliferative CMML through a novel KMT2A-PLK1 axis, showing PLK1 inhibition can improve disease outcomes in patient-derived xenografts.

bioRxiv · Dec 23, 2019 · PreprintCancer Biology