001     132541
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024 7 _ |a 10.1016/j.ccr.2014.05.005
|2 doi
024 7 _ |a pmid:24954133
|2 pmid
024 7 _ |a pmc:PMC4441014
|2 pmc
024 7 _ |a 1535-6108
|2 ISSN
024 7 _ |a 1878-3686
|2 ISSN
024 7 _ |a altmetric:2449834
|2 altmetric
037 _ _ |a DKFZ-2018-00223
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Vanner, Robert J
|b 0
245 _ _ |a Quiescent sox2(+) cells drive hierarchical growth and relapse in sonic hedgehog subgroup medulloblastoma.
260 _ _ |a Cambridge, Mass.
|c 2014
|b Cell Press
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1520341977_24409
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
|0 0
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520 _ _ |a 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.
536 _ _ |a 312 - Functional and structural genomics (POF3-312)
|0 G:(DE-HGF)POF3-312
|c POF3-312
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Antigens, Nuclear
|2 NLM Chemicals
650 _ 7 |a Antineoplastic Agents
|2 NLM Chemicals
650 _ 7 |a Biomarkers, Tumor
|2 NLM Chemicals
650 _ 7 |a Hedgehog Proteins
|2 NLM Chemicals
650 _ 7 |a Microtubule-Associated Proteins
|2 NLM Chemicals
650 _ 7 |a Nerve Tissue Proteins
|2 NLM Chemicals
650 _ 7 |a NeuN protein, mouse
|2 NLM Chemicals
650 _ 7 |a Neuropeptides
|2 NLM Chemicals
650 _ 7 |a Nuclear Proteins
|2 NLM Chemicals
650 _ 7 |a Patched Receptors
|2 NLM Chemicals
650 _ 7 |a Receptors, Cell Surface
|2 NLM Chemicals
650 _ 7 |a Receptors, G-Protein-Coupled
|2 NLM Chemicals
650 _ 7 |a SHH protein, human
|2 NLM Chemicals
650 _ 7 |a SMO protein, human
|2 NLM Chemicals
650 _ 7 |a SOX2 protein, human
|2 NLM Chemicals
650 _ 7 |a SOXB1 Transcription Factors
|2 NLM Chemicals
650 _ 7 |a Shh protein, mouse
|2 NLM Chemicals
650 _ 7 |a Smo protein, mouse
|2 NLM Chemicals
650 _ 7 |a Smoothened Receptor
|2 NLM Chemicals
650 _ 7 |a Sox2 protein, mouse
|2 NLM Chemicals
650 _ 7 |a doublecortin protein
|2 NLM Chemicals
650 _ 7 |a neuronal nuclear antigen NeuN, human
|2 NLM Chemicals
650 _ 7 |a Plicamycin
|0 NIJ123W41V
|2 NLM Chemicals
700 1 _ |a Remke, Marc
|b 1
700 1 _ |a Gallo, Marco
|b 2
700 1 _ |a Selvadurai, Hayden J
|b 3
700 1 _ |a Coutinho, Fiona
|b 4
700 1 _ |a Lee, Lilian
|b 5
700 1 _ |a Kushida, Michelle
|b 6
700 1 _ |a Head, Renee
|b 7
700 1 _ |a Morrissy, Sorana
|b 8
700 1 _ |a Zhu, Xueming
|b 9
700 1 _ |a Aviv, Tzvi
|b 10
700 1 _ |a Voisin, Veronique
|b 11
700 1 _ |a Clarke, Ian D
|b 12
700 1 _ |a Li, Yisu
|b 13
700 1 _ |a Mungall, Andrew J
|b 14
700 1 _ |a Moore, Richard A
|b 15
700 1 _ |a Ma, Yussanne
|b 16
700 1 _ |a Jones, Steven J M
|b 17
700 1 _ |a Marra, Marco A
|b 18
700 1 _ |a Malkin, David
|b 19
700 1 _ |a Northcott, Paul A
|0 P:(DE-HGF)0
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700 1 _ |a Kool, Marcel
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700 1 _ |a Pfister, Stefan
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700 1 _ |a Bader, Gary
|b 23
700 1 _ |a Hochedlinger, Konrad
|b 24
700 1 _ |a Korshunov, Andrey
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700 1 _ |a Taylor, Michael D
|b 26
700 1 _ |a Dirks, Peter B
|b 27
773 _ _ |a 10.1016/j.ccr.2014.05.005
|g Vol. 26, no. 1, p. 33 - 47
|0 PERI:(DE-600)2074034-7
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|p 33 - 47
|t Cancer cell
|v 26
|y 2014
|x 1535-6108
909 C O |o oai:inrepo02.dkfz.de:132541
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910 1 _ |a Deutsches Krebsforschungszentrum
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21