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@ARTICLE{Komljenovic:284364,
author = {Komljenovic, Dorde and Bäuerle, Tobias and Alves-de-Lima,
Jessica and Trigueros, Laura and Dietz, Cara and Winter,
Zoltan and Araceli, Tommaso and Strotzer, Quirin and Wendl,
Christina and Brendel, Matthias and Proescholdt, Martin A
and Harter, Patrick N and Evert, Katja and Pukrop, Tobias
and Blazquez, Raquel},
title = {{L}ocal metastatic expansion versus secondary intra-organ
dissemination: two causes of neurological death explained by
fundamentally different metastatic colonization patterns.},
journal = {Molecular cancer},
volume = {25},
number = {1},
issn = {1476-4598},
address = {London},
publisher = {Biomed Central},
reportid = {DZNE-2026-00132},
pages = {17},
year = {2026},
abstract = {Neurological failure contributes to $15-50\%$ of deaths in
patients with brain metastases, yet the underlying
mechanisms remain poorly understood. Clinical causes range
from local compression to meningeal metastasis. In this
context, a link between infiltrative histopathological
growth patterns (HGPs) and meningeal metastasis was recently
described and prompted this reverse translation study.We
conducted a retrospective postmortem histological assessment
and a prospective MRI-based proof-of-concept study to
explore neurological decline mechanisms in two experimental
brain metastasis models with different HGPs: (i) the
non-infiltrative TUBO model, characterized by well-defined
tumor borders and a multilayered astrocytic capsule; and
(ii) the infiltrative E0771-LG model, exhibiting diffuse
infiltration and widespread astrogliosis.In the TUBO model,
neurological death resulted from local metastatic expansion
compressing vital structures, while the E0771-LG model
caused mortality mainly through widespread secondary
dissemination. We provide the first direct evidence of
contralateral recolonization by secondary
metastasis-initiating cells (secMICs), and highlight the
high efficiency of secondary spread. Additionally, we show
that secMICs exploit distinct anatomical structures to reach
distant brain regions, bypassing classical vascular
dissemination routes. Notably, the HGP and its associated
features are intrinsic to tumor cells and are established
early during metastatic colonization.This study identifies
the HGP as a potential surrogate for predicting the
underlying cause of organ failure in brain metastases.
Additionally, it highlights the significant role of
secondary dissemination and recolonization in brain
metastasis, processes that have been largely overlooked in
clinical practice. These findings address a critical
knowledge gap and may inform future treatment strategies.},
keywords = {Brain Neoplasms: secondary / Brain Neoplasms: pathology /
Brain Neoplasms: diagnostic imaging / Animals / Humans /
Mice / Neoplasm Metastasis / Disease Models, Animal / Female
/ Retrospective Studies / Male / Magnetic Resonance Imaging
/ Nervous System Diseases: etiology / Nervous System
Diseases: pathology / Brain metastasis (Other) / Cause of
death (Other) / Histological growth pattern (Other) /
Infiltration (Other) / Local metastatic expansion (Other) /
MMPI (Other) / Meningeal metastasis (Other) / Neurological
decline (Other) / Recolonization (Other) / Secondary
dissemination (Other)},
cin = {AG Haass},
ddc = {570},
cid = {I:(DE-2719)1110007},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41580751},
pmc = {pmc:PMC12849154},
doi = {10.1186/s12943-026-02574-0},
url = {https://pub.dzne.de/record/284364},
}