Author

Julia Strangmann

University of Freiburg

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

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:metabolomics· 1 Assay:proteomics· 1

Frequent Co-Authors

Akanksha AnandiD· 2 shared Andrea Proaño-VascoiD· 2 shared Katrin BöttcheriD· 2 shared Linus R. SchömigiD· 2 shared Michael QuanteiD· 2 shared Robert ThimmeiD· 2 shared Roland Michael SchmidiD· 2 shared Theresa BaumeisteriD· 2 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCancer Biology

Akanksha AnandORCID

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2 papers

Recent·Most cited

Microbiota metabolized Bile Acids accelerate Gastroesophageal Adenocarcinoma via FXR inhibition

Theresa Baumeister, Andrea Proaño-Vasco, Amira Metwaly, Karin Kleigrewe, Alexander Kuznetsov, Linus R. Schömig, Martin Borgmann, Mohammed Khiat, Akanksha Anand, Julia Strangmann, Katrin Böttcher, Dirk Haller, Andreas Dunkel, Veronika Somoza, Sinah Reiter, , Michael Quante

This study shows that high-fat diets promote GEAC by altering the microbiota-Bile Acid axis and inhibiting FXR, with FXR agonists like OCA slowing disease progression.

Cellular and Molecular Gastroenterology and Hepatology · Jan 1, 2025Peer-reviewedCancer Biology

KRas, in addition to Tp53 is a driver for early carcinogenesis and a molecular target in a mouse model of invasive gastro-esophageal adenocarcinoma

Akanksha Anand, Linus R. Schömig, Sebastian Lange, Li Tran, Krzysztof Flisikowski, Rupert Öllinger, Roland Rad, Michael W. Vieth, Katja Steiger, Theresa Baumeister, Julia Strangmann, Hana Algül, Katrin J. Ciecielski, Katrin Böttcher, Hsin‐Yu Fang, , Michael Quante

This study identifies KRAS mutation as a driver of invasive gastro-esophageal adenocarcinoma in a mouse model, showing its synergistic role with Tp53 or Rb1 loss and potential as a therapeutic target.

bioRxiv · May 7, 2024 · PreprintCancer Biology