Author

Bertram Bengsch

University of FreiburgORCID 0000-0003-2552-740XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Organism:human· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Luciana HannibaliD· 2 shared Robert ZeiseriD· 2 shared Alberto Anastacio AmarillaiD· 1 shared Alejandro Rojas‐FernándeziD· 1 shared Alexander A. KhromykhiD· 1 shared Alexander TyshkovskiyiD· 1 shared Alexandra Emilia SchlaakiD· 1 shared Alireza A. BaradariD· 1 shared

Activity by Year

2023-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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Focal author (center)Selected co-authorORCID co-authorUnlinked name

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2 shared papersCancer Biology

Luciana HannibalORCID

Mutual co-authors in cluster

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3 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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Cancer BiologybioRxivPreprintOct 1, 2025

Oncogenic PTPN11/SHP2 drives immune escape in juvenile myelomonocytic leukemia (JMML) through activation of ectonucleotidase/adenosine signaling

Jovana Rajak, Ke Meng, Anna Lena Stippel…·Miriam Erlacher

This study identifies PTPN11/SHP2-driven adenosine signaling as a mechanism of immune escape in JMML, showing that CD39 inhibition can enhance T cell responses and reduce myeloproliferation.

DOI 10.1101/2025.10.01.679664

mousebulk RNA-seq

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NeuroscienceNature AgingPeer-reviewedNov 13, 2023

Senolytic therapy alleviates physiological human brain aging and COVID-19 neuropathology.

Julio Aguado, Alberto Anastacio Amarilla, Atefeh Taherian Fard…·Ernst Jurgen Wolvetang

This study shows senolytic drugs reduce brain aging and COVID-19-related neuropathology by targeting senescent cells in human brain organoids and mice.

80 citationstop 1%

humanmouse

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