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@ARTICLE{Mller:170569,
author = {M. Müller$^*$ and L. Rösch$^*$ and S. Najafi$^*$ and C.
Gatzweiler$^*$ and J. Ridinger$^*$ and X. F. Gerloff$^*$ and
D. T. W. Jones$^*$ and J. Baßler and S. Kreth$^*$ and S.
Stainczyk$^*$ and K. Frese and B. Meder and F.
Westermann$^*$ and T. Milde$^*$ and H. Peterziel$^*$ and O.
Witt$^*$ and I. Oehme$^*$},
title = {{C}ombining {APR}-246 and {HDAC}-{I}nhibitors: {A} {N}ovel
{T}argeted {T}reatment {O}ption for {N}euroblastoma.},
journal = {Cancers},
volume = {13},
number = {17},
issn = {2072-6694},
address = {Basel},
publisher = {MDPI},
reportid = {DKFZ-2021-02020},
pages = {4476},
year = {2021},
note = {#EA:B310#LA:B310#},
abstract = {APR-246 (Eprenetapopt/PRIMA-1Met) is a very potent
anti-cancer drug in clinical trials and was initially
developed as a p53 refolding agent. As an alternative mode
of action, the elevation of reactive oxygen species (ROS)
has been proposed. Through an in silico analysis, we
investigated the responses of approximately 800 cancer cell
lines (50 entities; Cancer Therapeutics Response Portal,
CTRP) to APR-246 treatment. In particular, neuroblastoma,
lymphoma and acute lymphocytic leukemia cells were highly
responsive. With gene expression data from the Cancer Cell
Line Encyclopedia (CCLE; n = 883) and patient samples (n =
1643) from the INFORM registry study, we confirmed that
these entities express low levels of SLC7A11, a previously
described predictive biomarker for APR-246 responsiveness.
Combining the CTRP drug response data with the respective
CCLE gene expression profiles, we defined a novel gene
signature, predicting the effectiveness of APR-246 treatment
with a sensitivity of $90\%$ and a specificity of $94\%.$ We
confirmed the predicted APR-246 sensitivity in 8/10 cell
lines and in ex vivo cultures of patient samples. Moreover,
the combination of ROS detoxification-impeding APR-246 with
approved HDAC-inhibitors, known to elevate ROS,
substantially increased APR-246 sensitivity in cell cultures
and in vivo in two zebrafish neuroblastoma xenograft models.
These data provide evidence that APR-246, in combination
with HDAC-inhibitors, displays a novel potent targeted
treatment option for neuroblastoma patients.},
keywords = {ROS (Other) / TP53 (Other) / histone deacetylases (Other) /
pediatric tumors of the nervous system (Other) / precision
medicine (Other) / response prediction biomarker (Other) /
small molecule inhibitors (Other)},
cin = {B310 / B360 / HD01 / B087},
ddc = {610},
cid = {I:(DE-He78)B310-20160331 / I:(DE-He78)B360-20160331 /
I:(DE-He78)HD01-20160331 / I:(DE-He78)B087-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34503286},
doi = {10.3390/cancers13174476},
url = {https://inrepo02.dkfz.de/record/170569},
}