TY  - JOUR
A1  - Feldheim, Jonas
A1  - Kessler, Almuth F.
A1  - Feldheim, Julia J.
A1  - Schmitt, Dominik
A1  - Oster, Christoph
A1  - Lazaridis, Lazaros
A1  - Glas, Martin
A1  - Ernestus, Ralf-Ingo
A1  - Monoranu, Camelia M.
A1  - Löhr, Mario
A1  - Hagemann, Carsten
T1  - BRMS1 in gliomas — an expression analysis
JF  - Cancers
N2  - The metastatic suppressor BRMS1 interacts with critical steps of the metastatic cascade in many cancer entities. As gliomas rarely metastasize, BRMS1 has mainly been neglected in glioma research. However, its interaction partners, such as NFκB, VEGF, or MMPs, are old acquaintances in neurooncology. The steps regulated by BRMS1, such as invasion, migration, and apoptosis, are commonly dysregulated in gliomas. Therefore, BRMS1 shows potential as a regulator of glioma behavior. By bioinformatic analysis, in addition to our cohort of 118 specimens, we determined BRMS1 mRNA and protein expression as well as its correlation with the clinical course in astrocytomas IDH mutant, CNS WHO grade 2/3, and glioblastoma IDH wild-type, CNS WHO grade 4. Interestingly, we found BRMS1 protein expression to be significantly decreased in the aforementioned gliomas, while BRMS1 mRNA appeared to be overexpressed throughout. This dysregulation was independent of patients’ characteristics or survival. The protein and mRNA expression differences cannot be finally explained at this stage. However, they suggest a post-transcriptional dysregulation that has been previously described in other cancer entities. Our analyses present the first data on BRMS1 expression in gliomas that can provide a starting point for further investigations.
KW  - glioblastoma
KW  - metastasis
KW  - suppressor
KW  - behavior
KW  - mRNA
KW  - protein
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-319225
SN  - 2072-6694
VL  - 15
IS  - 11
ER  - 
TY  - JOUR
A1  - Salvador, Ellaine
A1  - Köppl, Theresa
A1  - Hörmann, Julia
A1  - Schönhärl, Sebastian
A1  - Bugaeva, Polina
A1  - Kessler, Almuth F.
A1  - Burek, Malgorzata
A1  - Ernestus, Ralf-Ingo
A1  - Löhr, Mario
A1  - Hagemann, Carsten
T1  - Tumor Treating Fields (TTFields) induce cell junction alterations in a human 3D in vitro model of the blood-brain barrier
JF  - Pharmaceutics
N2  - In a recent study, we showed in an in vitro murine cerebellar microvascular endothelial cell (cerebEND) model as well as in vivo in rats that Tumor-Treating Fields (TTFields) reversibly open the blood–brain barrier (BBB). This process is facilitated by delocalizing tight junction proteins such as claudin-5 from the membrane to the cytoplasm. In investigating the possibility that the same effects could be observed in human-derived cells, a 3D co-culture model of the BBB was established consisting of primary microvascular brain endothelial cells (HBMVEC) and immortalized pericytes, both of human origin. The TTFields at a frequency of 100 kHz administered for 72 h increased the permeability of our human-derived BBB model. The integrity of the BBB had already recovered 48 h post-TTFields, which is earlier than that observed in cerebEND. The data presented herein validate the previously observed effects of TTFields in murine models. Moreover, due to the fact that human cell-based in vitro models more closely resemble patient-derived entities, our findings are highly relevant for pre-clinical studies.
KW  - blood-brain barrier
KW  - Tumor-Treating Fields (TTFields)
KW  - CNS disorders
KW  - human brain microvascular endothelial cells (HBMVEC)
KW  - human cells
KW  - 3D in vitro model
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-304830
SN  - 1999-4923
VL  - 15
IS  - 1
ER  -