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@ARTICLE{Berberich:140856,
author = {A. Berberich$^*$ and T. Kessler$^*$ and C. Thome$^*$ and S.
Pusch$^*$ and T. Hielscher$^*$ and F. Sahm$^*$ and I.
Oezen$^*$ and L.-M. Schmitt$^*$ and S. Ciprut$^*$ and N.
Hucke$^*$ and P. Rübmann$^*$ and M. Fischer$^*$ and D.
Lemke$^*$ and M. Breckwoldt$^*$ and A. von Deimling$^*$ and
M. Bendszus and M. Platten$^*$ and W. Wick$^*$},
title = {{T}argeting resistance against the {MDM}2 inhibitor
{RG}7388 in glioblastoma cells by the {MEK} inhibitor
trametinib.},
journal = {Clinical cancer research},
volume = {25},
number = {1},
issn = {1557-3265},
address = {Philadelphia, Pa. [u.a.]},
publisher = {AACR},
reportid = {DKFZ-2018-01611},
pages = {253-265},
year = {2019},
abstract = {Resistance is an obstacle of glioma therapy. Despite
targeted interventions, tumors harbor primary resistance or
become resistant over short course of treatment. This study
examined the mouse double minute 2 (MDM2) inhibitor RG7388
together with radiotherapy and analyzed strategies to
overcome acquired MDM2 inhibitor resistance in
glioblastoma.Effects of RG7388 and radiotherapy were
analyzed in p53 wild-type glioblastoma cell lines and
glioma-initiating cells. RG7388 resistant cells were
generated by increasing RG7388 doses over three months.
Regulated pathways were investigated by microarray, qRT-PCR
and immunoblot analysis and specifically inhibited to
evaluate rational salvage therapies at RG7388 resistance.
Effects of RG7388 and trametinib treatment were challenged
in an orthotopical mouse model with RG7388 resistant U87MG
glioblastoma cells.MDM2 inhibition required functional p53
and showed synergistic activity with radiotherapy in
first-line treatment. Long-term exposure to RG7388 induced
resistance by activation of the extracellular
signal-regulated kinases 1/2 (ERK1/2) - insulin growth
factor binding protein 1 (IGFBP1) signaling cascade, which
was specifically overcome by ERK1/2 pathway inhibition with
trametinib and knockdown of IGFBP1. Combining trametinib
with continued RG7388 treatment enhanced anti-tumor effects
at RG7388 resistance in vitro and in vivo.These data provide
a rationale for combining RG7388 and radiotherapy as
first-line therapy with a specific relevance for tumors
insensitive to alkylating standard chemotherapy and for the
addition of trametinib to continued RG7388 treatment as
salvage therapy after acquired resistance against RG7388 for
clinical practice.},
cin = {B320 / C060 / B300 / D170 / L101},
ddc = {610},
cid = {I:(DE-He78)B320-20160331 / I:(DE-He78)C060-20160331 /
I:(DE-He78)B300-20160331 / I:(DE-He78)D170-20160331 /
I:(DE-He78)L101-20160331},
pnm = {312 - Functional and structural genomics (POF3-312)},
pid = {G:(DE-HGF)POF3-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30274984},
doi = {10.1158/1078-0432.CCR-18-1580},
url = {https://inrepo02.dkfz.de/record/140856},
}