% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Seiboldt:291417,
author = {T. Seiboldt$^*$ and C. Zeiser$^*$ and D. Nguyen$^*$ and S.
Celikyürekli$^*$ and S. Herter$^*$ and S. Najafi$^*$ and A.
Stroh-Dege$^*$ and C. Meulenbroeks and N. Mack$^*$ and R.
Salem-Altintas$^*$ and F. Westermann$^*$ and M.
Schlesner$^*$ and T. Milde$^*$ and M. Kool$^*$ and T.
Holland-Letz$^*$ and M. Vogler$^*$ and H. Peterziel$^*$ and
O. Witt$^*$ and I. Oehme$^*$},
title = {{S}ynergy of retinoic acid and {BH}3 mimetics in
{MYC}({N})-driven embryonal nervous system tumours.},
journal = {British journal of cancer},
volume = {131},
number = {4},
issn = {0007-0920},
address = {Edinburgh},
publisher = {Nature Publ. Group},
reportid = {DKFZ-2024-01391},
pages = {763-777},
year = {2024},
note = {#EA:B310#LA:B310# / 2024 Sep;131(4):763-777},
abstract = {Certain paediatric nervous system malignancies have dismal
prognoses. Retinoic acid (RA) is used in neuroblastoma
treatment, and preclinical data indicate potential benefit
in selected paediatric brain tumour entities. However,
limited single-agent efficacy necessitates combination
treatment approaches.We performed drug sensitivity profiling
of 76 clinically relevant drugs in combination with RA in 16
models (including patient-derived tumouroids) of the most
common paediatric nervous system tumours. Drug responses
were assessed by viability assays, high-content imaging, and
apoptosis assays and RA relevant pathways by RNAseq from
treated models and patient samples obtained through the
precision oncology programme INFORM (n = 2288).
Immunoprecipitation detected BCL-2 family interactions, and
zebrafish embryo xenografts were used for in vivo efficacy
testing.Group 3 medulloblastoma (MBG3) and neuroblastoma
models were highly sensitive to RA treatment. RA induced
differentiation and regulated apoptotic genes. RNAseq
analysis revealed high expression of BCL2L1 in MBG3 and BCL2
in neuroblastomas. Co-treatments with RA and BCL-2/XL
inhibitor navitoclax synergistically decreased viability at
clinically achievable concentrations. The combination of RA
with navitoclax disrupted the binding of BIM to BCL-XL in
MBG3 and to BCL-2 in neuroblastoma, inducing apoptosis in
vitro and in vivo.RA treatment primes MBG3 and NB cells for
apoptosis, triggered by navitoclax cotreatment.},
cin = {B310 / HD01 / W610 / B062 / B087 / C060 / FM01},
ddc = {610},
cid = {I:(DE-He78)B310-20160331 / I:(DE-He78)HD01-20160331 /
I:(DE-He78)W610-20160331 / I:(DE-He78)B062-20160331 /
I:(DE-He78)B087-20160331 / I:(DE-He78)C060-20160331 /
I:(DE-He78)FM01-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:38942989},
doi = {10.1038/s41416-024-02740-5},
url = {https://inrepo02.dkfz.de/record/291417},
}