Author

A. S. Lamort

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 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

G. T. Stathopoulos· 3 shared M. A. Pepe· 3 shared R. A. Hatz· 3 shared A. Marazioti· 2 shared G. Ntaliarda· 2 shared I. Giopanou· 2 shared I. Koch· 2 shared I. Lilis· 2 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersCancer Biology

G. T. Stathopoulos

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Author profile →

3 papers

Recent·Most cited

Tumor-secreted versican co-opts myeloid IKKβ during metastasis

M. Spella, A. S. Lamort, M. Vreka, A. Marazioti, I. Lilis, G. Ntaliarda, G. Skiadas, E. Bouloukou, G. A. Giotopoulou, M. A. Pepe, S. A. Weiss, A. Petrera, S. M. Hauck, I. Koch, M. Lindner, , G. T. Stathopoulos

This study identifies tumor-secreted versican as a driver of myeloid IKKβ activation during metastasis, showing its role in promoting inflammation and metastasis through IL-1β release.

bioRxiv · May 20, 2021 · PreprintCancer Biology

KRAS signalling in malignant pleural mesothelioma

A. Marazioti, A. Krontira, M. A. Pepe, M. Iliopoulou, D. E. Wagner, H. Papadaki, S. G. Antimisiaris, I. Psallidas, M. Spella, I. Lilis, I. Giopanou, M. Vreka, C. Blanquart, M. Gregoire, S. Deshayes, , G. T. Stathopoulos

This study identifies KRAS mutations as a significant driver in human malignant pleural mesothelioma and demonstrates their role in disease initiation and treatment response in mouse models.

bioRxiv · Oct 22, 2020 · PreprintPhysiology

An in vivo inflammatory loop potentiates KRAS blockade

K. A. Arendt, G. Ntaliarda, V. Armenis, D. Kati, C. Henning, G. Giotopoulou, M. A. Pepe, L. V. Klotz, A. S. Lamort, R. A. Hatz, S. Kobold, G. T. Stathopoulos

The paper shows that KRAS-mutant tumors rely on an inflammatory loop involving C-C-motif chemokine ligand 2/interleukin-1β signaling, making them resistant to KRAS inhibitors in vivo but responsive in certain transplant models.

bioRxiv · Apr 19, 2020Cancer Biology