ALK Inhibition Prolongs Survival in a Mouse Model of <i>ALK</i> -Positive Anaplastic Thyroid Cancer
Our data demonstrate that the combination of ALK<sup>F1174L</sup> mutation with <i>Trp53</i> loss leads to the development of ATC. This study provides the first functional data supporting the use of ALK inhibitors in patients with <i>ALK</i>-driven ATC. Our novel ATC mouse model and the derived cell lines offer valuable tools to explore the molecular characteristics of ATC, especially signaling pathway activation and tumor microenvironment, and to test novel therapeutics for the treatment of advanced thyroid cancers.
Authors
- Lars C. Moeller (ORCID: https://orcid.org/0000-0002-9330-9036)
- Johannes Köster (ORCID: https://orcid.org/0000-0001-9818-9320)
- Jukka Kero (ORCID: https://orcid.org/0000-0001-8767-7222)
- Dagmar Fuehrer
- Christoph Hoppe (ORCID: https://orcid.org/0000-0001-9364-9201)
- Yara Maria Machlah (ORCID: https://orcid.org/0009-0001-9441-3046)
- Tim Brandenburg
- Johannes H. Schulte (ORCID: https://orcid.org/0000-0003-0671-1201)
- Feyza Cansiz (ORCID: https://orcid.org/0009-0006-6526-990X)
- Hendrik J Undeutsch (ORCID: https://orcid.org/0009-0009-1527-6273)
- Georg Sebastian Hönes (ORCID: https://orcid.org/0000-0002-5080-7166)
- Adrian D Prinz
- Sarah Theurer
- Jens Siveke
Institutions
- University of Turku (FI)
- Essen University Hospital (DE)
- University of Duisburg-Essen (DE)
- Charité - Universitätsmedizin Berlin (DE)
Publication Details
- Journal
- Thyroid
- Published
- 2025-12-30
- DOI
- https://doi.org/10.1177/10507256251409070
- Primary Topic
- Thyroid Cancer Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00