Author

O. Demerdash

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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Assay:bulk RNA-seq· 2 Approach:experimental assay· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell-cell communication· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

C. Vakoc· 2 shared O. Klingbeil· 2 shared D. Maia-Silva· 1 shared D. Tuveson· 1 shared E. Adelman· 1 shared E. Hodges· 1 shared G. Biffi· 1 shared J. C. Smith· 1 shared

Activity by Year

2019-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersCancer Biology

C. Vakoc

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Author profile →

3 papers

Recent·Most cited

TCR-H: Machine Learning Prediction of T-cell Receptor Epitope Binding on Unseen Datasets

R. R. Tatikonda, O. Demerdash, J. C. Smith

TCR-H is a SVM model trained on experimentally validated non-binders to predict TCR epitope binding, achieving high AUC on unseen test sets.

bioRxiv · Nov 28, 2023 · PreprintImmunology

In vivo genetic screen identifies a SLC5A3-dependent myo-inositol auxotrophy in acute myeloid leukemia

Y. Wei, S. Iyer, S. Costa, Z. Yang, M. Kramer, E. Adelman, O. Klingbeil, O. Demerdash, S. Polyanskaya, K. Chang, S. Goodwin, E. Hodges, W. R. McCombie, M. Figueroa, C. Vakoc

The paper identifies SLC5A3-dependent myo-inositol auxotrophy in AML through genetic screening and shows synthetic lethality between ISYNA1 and SLC5A3.

bioRxiv · Dec 22, 2020 · PreprintCancer Biology

Squamous trans-differentiation of pancreatic cancer cells promotes stromal inflammation

T. Somerville, G. Biffi, J. Dassler-Plenker, K. Miyabayashi, Y. Xu, D. Maia-Silva, O. Klingbeil, O. Demerdash, M. Egeblad, D. Tuveson, C. Vakoc

This study shows that squamous trans-differentiation of pancreatic cancer cells promotes stromal inflammation by converting pancreatic stellate cells into inflammatory CAFs via TP63-dependent mechanisms.

bioRxiv · Nov 6, 2019Cancer Biology