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@ARTICLE{Vanner:132541,
author = {R. J. Vanner and M. Remke and M. Gallo and H. J. Selvadurai
and F. Coutinho and L. Lee and M. Kushida and R. Head and S.
Morrissy and X. Zhu and T. Aviv and V. Voisin and I. D.
Clarke and Y. Li and A. J. Mungall and R. A. Moore and Y. Ma
and S. J. M. Jones and M. A. Marra and D. Malkin and P. A.
Northcott and M. Kool$^*$ and S. Pfister$^*$ and G. Bader
and K. Hochedlinger and A. Korshunov$^*$ and M. D. Taylor
and P. B. Dirks},
title = {{Q}uiescent sox2(+) cells drive hierarchical growth and
relapse in sonic hedgehog subgroup medulloblastoma.},
journal = {Cancer cell},
volume = {26},
number = {1},
issn = {1535-6108},
address = {Cambridge, Mass.},
publisher = {Cell Press},
reportid = {DKFZ-2018-00223},
pages = {33 - 47},
year = {2014},
abstract = {Functional heterogeneity within tumors presents a
significant therapeutic challenge. Here we show that
quiescent, therapy-resistant Sox2(+) cells propagate sonic
hedgehog subgroup medulloblastoma by a mechanism that
mirrors a neurogenic program. Rare Sox2(+) cells produce
rapidly cycling doublecortin(+) progenitors that, together
with their postmitotic progeny expressing NeuN, comprise
tumor bulk. Sox2(+) cells are enriched following
anti-mitotic chemotherapy and Smoothened inhibition,
creating a reservoir for tumor regrowth. Lineage traces from
Sox2(+) cells increase following treatment, suggesting that
this population is responsible for relapse. Targeting
Sox2(+) cells with the antineoplastic mithramycin abrogated
tumor growth. Addressing functional heterogeneity and
eliminating Sox2(+) cells presents a promising therapeutic
paradigm for treatment of sonic hedgehog subgroup
medulloblastoma.},
keywords = {Antigens, Nuclear (NLM Chemicals) / Antineoplastic Agents
(NLM Chemicals) / Biomarkers, Tumor (NLM Chemicals) /
Hedgehog Proteins (NLM Chemicals) / Microtubule-Associated
Proteins (NLM Chemicals) / Nerve Tissue Proteins (NLM
Chemicals) / NeuN protein, mouse (NLM Chemicals) /
Neuropeptides (NLM Chemicals) / Nuclear Proteins (NLM
Chemicals) / Patched Receptors (NLM Chemicals) / Receptors,
Cell Surface (NLM Chemicals) / Receptors, G-Protein-Coupled
(NLM Chemicals) / SHH protein, human (NLM Chemicals) / SMO
protein, human (NLM Chemicals) / SOX2 protein, human (NLM
Chemicals) / SOXB1 Transcription Factors (NLM Chemicals) /
Shh protein, mouse (NLM Chemicals) / Smo protein, mouse (NLM
Chemicals) / Smoothened Receptor (NLM Chemicals) / Sox2
protein, mouse (NLM Chemicals) / doublecortin protein (NLM
Chemicals) / neuronal nuclear antigen NeuN, human (NLM
Chemicals) / Plicamycin (NLM Chemicals)},
cin = {B062 / G380},
ddc = {610},
cid = {I:(DE-He78)B062-20160331 / I:(DE-He78)G380-20160331},
pnm = {312 - Functional and structural genomics (POF3-312)},
pid = {G:(DE-HGF)POF3-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:24954133},
pmc = {pmc:PMC4441014},
doi = {10.1016/j.ccr.2014.05.005},
url = {https://inrepo02.dkfz.de/record/132541},
}