Home > Publications database > HDAC and PI3K Antagonists Cooperate to Inhibit Growth of MYC-Driven Medulloblastoma. > print

001     130304
005     20240228143423.0
024 7 _ |a 10.1016/j.ccell.2016.02.011
|2 doi
024 7 _ |a pmid:26977882
|2 pmid
024 7 _ |a pmc:PMC4794752
|2 pmc
024 7 _ |a 1535-6108
|2 ISSN
024 7 _ |a 1878-3686
|2 ISSN
024 7 _ |a altmetric:6188781
|2 altmetric
037 _ _ |a DKFZ-2017-05383
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Pei, Yanxin
|b 0
245 _ _ |a HDAC and PI3K Antagonists Cooperate to Inhibit Growth of MYC-Driven Medulloblastoma.
260 _ _ |a Cambridge, Mass.
|c 2016
|b Cell Press
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1522135521_18537
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Medulloblastoma (MB) is a highly malignant pediatric brain tumor. Despite aggressive therapy, many patients succumb to the disease, and survivors experience severe side effects from treatment. MYC-driven MB has a particularly poor prognosis and would greatly benefit from more effective therapies. We used an animal model of MYC-driven MB to screen for drugs that decrease viability of tumor cells. Among the most effective compounds were histone deacetylase inhibitors (HDACIs). HDACIs potently inhibit survival of MYC-driven MB cells in vitro, in part by inducing expression of the FOXO1 tumor suppressor gene. HDACIs also synergize with phosphatidylinositol 3-kinase inhibitors to inhibit tumor growth in vivo. These studies identify an effective combination therapy for the most aggressive form of MB.
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 Forkhead Transcription Factors
|2 NLM Chemicals
650 _ 7 |a Histone Deacetylase Inhibitors
|2 NLM Chemicals
650 _ 7 |a Proto-Oncogene Proteins c-myc
|2 NLM Chemicals
650 _ 7 |a Phosphatidylinositol 3-Kinases
|0 EC 2.7.1.-
|2 NLM Chemicals
650 _ 7 |a Histone Deacetylases
|0 EC 3.5.1.98
|2 NLM Chemicals
700 1 _ |a Liu, Kun-Wei
|b 1
700 1 _ |a Wang, Jun
|b 2
700 1 _ |a Garancher, Alexandra
|b 3
700 1 _ |a Tao, Ran
|b 4
700 1 _ |a Esparza, Lourdes A
|b 5
700 1 _ |a Maier, Donna L
|b 6
700 1 _ |a Udaka, Yoko T
|b 7
700 1 _ |a Murad, Najiba
|b 8
700 1 _ |a Morrissy, Sorana
|b 9
700 1 _ |a Seker-Cin, Huriye
|0 P:(DE-HGF)0
|b 10
700 1 _ |a Brabetz, Sebastian
|0 P:(DE-He78)b0b3740107f746e09dc23fdf25eb0629
|b 11
|u dkfz
700 1 _ |a Qi, Lin
|b 12
700 1 _ |a Kogiso, Mari
|b 13
700 1 _ |a Schubert, Simone
|b 14
700 1 _ |a Olson, James M
|b 15
700 1 _ |a Cho, Yoon-Jae
|b 16
700 1 _ |a Li, Xiao-Nan
|b 17
700 1 _ |a Crawford, John R
|b 18
700 1 _ |a Levy, Michael L
|b 19
700 1 _ |a Kool, Marcel
|0 P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8
|b 20
|u dkfz
700 1 _ |a Pfister, Stefan
|0 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9
|b 21
|u dkfz
700 1 _ |a Taylor, Michael D
|b 22
700 1 _ |a Wechsler-Reya, Robert J
|b 23
773 _ _ |a 10.1016/j.ccell.2016.02.011
|g Vol. 29, no. 3, p. 311 - 323
|0 PERI:(DE-600)2074034-7
|n 3
|p 311 - 323
|t Cancer cell
|v 29
|y 2016
|x 1535-6108
909 C O |o oai:inrepo02.dkfz.de:130304
|p VDB
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 10
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 11
|6 P:(DE-He78)b0b3740107f746e09dc23fdf25eb0629
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 20
|6 P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 21
|6 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9
913 1 _ |a DE-HGF
|l Krebsforschung
|1 G:(DE-HGF)POF3-310
|0 G:(DE-HGF)POF3-312
|2 G:(DE-HGF)POF3-300
|v Functional and structural genomics
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
|b Gesundheit
914 1 _ |y 2016
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b CANCER CELL : 2015
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Thomson Reuters Master Journal List
915 _ _ |a WoS
|0 StatID:(DE-HGF)0110
|2 StatID
|b Science Citation Index
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
915 _ _ |a IF >= 20
|0 StatID:(DE-HGF)9920
|2 StatID
|b CANCER CELL : 2015
920 1 _ |0 I:(DE-He78)B062-20160331
|k B062
|l Pädiatrische Neuroonkologie
|x 0
920 1 _ |0 I:(DE-He78)L101-20160331
|k L101
|l DKTK Heidelberg
|x 1
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)B062-20160331
980 _ _ |a I:(DE-He78)L101-20160331
980 _ _ |a UNRESTRICTED

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21