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The Casanova/Moll/Uras Lab: Cancer Research

Emilio Casanova

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Herwig Moll

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Iris Uras

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Research interests

Our main research goal is to unravel the contribution of key cellular signaling pathways to tumorigenesis. Our research tools are: Genetically modified mice modeling human cancer, genetically manipulated human and mouse cancer cell lines, tumor transplant models and human tumor samples.

KRAS driven lung adenocarcinoma

Lung cancer is the most frequent cancer with an aggressive clinical course and high mortality rates. Most cases are diagnosed at advanced stages when treatment options are limited and the efficacy of chemotherapy is poor. The disease has a complex and heterogeneous background with non-small-cell lung cancer (NSCLC) accounting for 85% of patients and lung adenocarcinoma being the most common histological subtype. Almost 30% of adenocarcinomas of the lung are driven by an activating Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation. The ability to inhibit the oncogenic KRAS has been the holy grail of cancer research and the search for inhibitors is immensely ongoing as KRAS-mutated tumors are among the most aggressive and refractory to treatment. We are interested in therapeutic strategies tailored for KRAS driven NSCLC relying on the blockage of KRAS functional output, cellular dependencies, metabolic features and immunotherapy.

Selected publications

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Uras, IZ, et al., KRAS mutated lung adenocarcinoma responds to pan-ERBB and Aurora kinase inhibitors. 2026. NPJ Precis Oncol. Available at: https://doi.org/10.1038/s41698-025-01242-8

Luca, AC, et al., Loss of SPHK1 fuels inflammation to drive KRAS-mutated lung adenocarcinoma. 2025. Cancer Letters. Available at: https://doi.org/10.1016/j.canlet.2025.217733

Caratti, B. et al., 2022. The glucocorticoid receptor associates with RAS complexes to inhibit cell proliferation and tumor growth. Science Signaling. Available at: DOI: 10.1126/scisignal.abm4452

Breitenecker, K. et al., 2021. Downregulation of A20 promotes immune escape of lung adenocarcinomas. Science Translational Medicine. Available at: https://doi.org/10.1126/scitranslmed.abc3911

Mohrherr, J. et al., 2019. JAK-STAT inhibition impairs K-RAS-driven lung adenocarcinoma progression. International Journal of Cancer. Available at: https://doi.org/10.1002/ijc.32624

Moll, H.P. et al., 2018. Afatinib restrains K-RAS-driven lung tumorigenesis. Science Translational Medicine. Available at: http://dx.doi.org/10.1126/scitranslmed.aao2301

Grabner, B. et al., 2015. Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis. Nature Communications. Available at: http://dx.doi.org/10.1038/ncomms7285

Musteanu, M. et al., 2012. A mouse model to identify cooperating signaling pathways in cancer. Nature Methods. Available at: https://doi.org/10.1038/nmeth.2130

Group members

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From left to right: Ritesh Narwal, Sadaf Keshavarz, Emilio Casanova, Faith David, Eva Putz, Lena Vlasitz, Masa Beres, Christoph Trenk, Marija Trkulja, Jaqueline Horvath, Herwig Moll, Sarah Trouvilliez, Aaron Rauscher, Pauline Sieger, Iris Uras, Michael Machtinger and Monika Homolya