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@ARTICLE{Birocchi:180727,
author = {F. Birocchi and M. Cusimano and F. Rossari and S. Beretta
and P. M. V. Rancoita and A. Ranghetti and S. Colombo and B.
M. Costa$^*$ and P. Angel$^*$ and F. Sanvito and M. Callea
and R. Norata and L. Chaabane and T. Canu and A. Spinelli
and M. Genua and R. Ostuni and I. Merelli and N. Coltella
and L. Naldini},
title = {{T}argeted inducible delivery of immunoactivating cytokines
reprograms glioblastoma microenvironment and inhibits growth
in mouse models.},
journal = {Science translational medicine},
volume = {14},
number = {653},
issn = {1946-6234},
address = {Washington, DC},
publisher = {AAAS},
reportid = {DKFZ-2022-01518},
pages = {eabl4106},
year = {2022},
note = {DKFZ-ZMBH Alliance},
abstract = {Glioblastoma multiforme (GBM) is the most common and lethal
brain tumor characterized by a strongly immunosuppressive
tumor microenvironment (TME) that represents a barrier also
for the development of effective immunotherapies. The
possibility to revert this hostile TME by immunoactivating
cytokines is hampered by the severe toxicity associated with
their systemic administration. Here, we exploited a
lentiviral vector-based platform to engineer hematopoietic
stem cells ex vivo with the aim of releasing, via their
tumor-infiltrating monocyte/macrophage progeny,
interferon-α (IFN-α) or interleukin-12 (IL-12) at the
tumor site with spatial and temporal selectivity. Taking
advantage of a syngeneic GBM mouse model, we showed that
inducible release of IFN-α within the TME achieved robust
tumor inhibition up to eradication and outperformed systemic
treatment with the recombinant protein in terms of efficacy,
tolerability, and specificity. Single-cell RNA sequencing of
the tumor immune infiltrate revealed reprogramming of the
immune microenvironment toward a proinflammatory and
antitumoral state associated with loss of a macrophage
subpopulation shown to be associated with poor prognosis in
human GBM. The spatial and temporal control of IL-12 release
was critical to overcome an otherwise lethal hematopoietic
toxicity while allowing to fully exploit its antitumor
activity. Overall, our findings demonstrate a potential
therapeutic approach for GBM and set the bases for a
recently launched first-in-human clinical trial in patients
with GBM.},
cin = {A100},
ddc = {500},
cid = {I:(DE-He78)A100-20160331},
pnm = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
pid = {G:(DE-HGF)POF4-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35857642},
doi = {10.1126/scitranslmed.abl4106},
url = {https://inrepo02.dkfz.de/record/180727},
}