Author

Bismark Appiah

University of FreiburgORCID 0000-0003-4670-3951Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 1 Developmental Biology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

Andreas VlachosiD· 1 shared Ariane LehmanniD· 1 shared Arquimedes ChefferiD· 1 shared Asma Y. AlrawashdehiD· 1 shared Bertram BengschiD· 1 shared Camilla L. FullioiD· 1 shared Christiane HaffneriD· 1 shared Dietrich Alexander RuessiD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCancer Biology

Andreas VlachosORCID

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2 papers

Recent·Most cited

Cancer BiologySignal Transduction and Targeted TherapyPeer-reviewedJan 16, 2026

Vertical RAS-pathway inhibition in pancreatic cancer drives therapeutically exploitable mitochondrial alterations

Philipp Hafner, Steffen Johannes Keller, Xun Chen…·Dietrich Alexander Ruess

This study shows that dual SHP2/MEK inhibition in pancreatic cancer causes mitochondrial changes and ROS elevation, leading to a therapy-resistant state that can be targeted with GPX4 inhibition.

9 citationstop 1%

humanbulk RNA-seq

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Developmental BiologybioRxivPreprintApr 8, 2022

DOT1L activity affects cell lineage progression in the developing brain by controlling metabolic programs

Bismark Appiah, Camilla L. Fullio, Christiane Haffner…·Tanja Vogel

This study shows that DOT1L activity regulates AP lineage progression in the developing mouse neocortex by controlling metabolic programs and gene expression.

DOI 10.1101/2022.04.08.487591

mousescRNA-seq

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