Author

K. Honarnejad

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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Bioengineering· 1 Cancer Biology· 1 Pathology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Organism:human· 2 Organism:mouse· 2 Approach:statistical model· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

C. A. Klein· 2 shared J. Warfsmann· 2 shared S. Kirsch· 2 shared X. Lu· 2 shared A. Abaurrea· 1 shared A. Cigliano· 1 shared A. Cipitria· 1 shared A. Coluccio· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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2 shared papersBioengineering

C. A. Klein

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Dormancy-inducing 3D-engineered matrix uncovers mechanosensitive and drug protective FHL2-p21 signaling axis

S. Bakhshandeh, U. Heras, H. M. Taieb, A. R. Varadarajan, S. M. Lissek, S. M. Huecker, X. Lu, D. S. Garske, S. A. E. Young, A. Abaurrea, M. M. Caffarel, A. Riestra, P. Bragado, J. Contzen, M. Gossen, , A. Cipitria

The paper identifies a mechanosensitive FHL2-p21 signaling axis in dormant cancer cells using 3D-engineered matrices, showing its role in drug resistance and potential as a target for therapy.

bioRxiv · Jan 25, 2023Bioengineering

RASSF1A independence and early Galectin-1 upregulation in PIK3CA induced hepatocarcinogenesis: new therapeutic venues

A. Scheiter, K. Evert, L. Reibenspies, A. Cigliano, K. Annweiler, K. Mueller, L.-M.-G. Poehmerer, T. Itzel, S. Materna-Reichelt, A. Coluccio, K. Honarnejad, A. Teufel, C. Brochhausen, F. Dombrowski, X. Chen, , K. Utpatel

This study shows that PIK3CA mutations drive hepatocarcinogenesis independently of RASSF1A status, with early Galectin-1 upregulation and synergistic therapeutic effects of PIK3CA and Galectin-1 inhibitors.

bioRxiv · Jun 15, 2021Pathology

Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

M. Werner-Klein, A. Grujovic, C. Irlbeck, M. Obradovic, M. Hoffmann, H. Koerkel-Qu, X. Lu, S. Treitschke, C. Koestler, C. Botteron, K. Weidele, C. Werno, B. Polzer, S. Kirsch, M. Guzvic, , C. A. Klein

The paper identifies IL6 trans-signaling as a mechanism supporting DCC survival and outgrowth during clinical latency, with microenvironmental dependencies and PIK3CA mutations linked to metastatic progression.

bioRxiv · May 28, 2020Cancer Biology