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Sökning: WFRF:(Nelander Sven) > (2015-2019) > Epigenetic Regulati...

Epigenetic Regulation of ZBTB18 Promotes Glioblastoma Progression

Fedele, Vita (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Dai, Fangping (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Masilamani, Anie P. (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
visa fler...
Heiland, Dieter H. (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Kling, Eva (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Gätjens-Sanchez, Ana M. (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Ferrarese, Roberto (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Platania, Leonardo (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Soroush, Doostkam (författare)
Univ Freiburg, Neuroctr, Inst Neuropathol, Freiburg, Germany.;Univ Freiburg, Ctr Comprehens Canc, Freiburg, Germany.;Univ Freiburg, BIOSS Ctr Biol Signalling Studies, Freiburg, Germany.
Kim, Hyunsoo (författare)
Jackson Lab Genom Med, Farmington, CT USA.
Nelander, Sven (författare)
Uppsala universitet,Institutionen för immunologi, genetik och patologi,Science for Life Laboratory, SciLifeLab
Weyerbrock, Astrid (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
Prinz, Marco (författare)
Univ Freiburg, Neuroctr, Inst Neuropathol, Freiburg, Germany.;Univ Freiburg, Ctr Comprehens Canc, Freiburg, Germany.;Univ Freiburg, BIOSS Ctr Biol Signalling Studies, Freiburg, Germany.
Califano, Andrea (författare)
Columbia Univ, Inst Canc Genet, New York, NY USA.;Columbia Univ, Dept Biomed Informat, New York, NY USA.;Columbia Univ, Dept Syst Biol, New York, NY USA.
Iavarone, Antonio (författare)
Columbia Univ, Inst Canc Genet, New York, NY USA.;Columbia Univ, Med Ctr, Dept Pathol, New York, NY USA.;Columbia Univ, Med Ctr, Dept Neurol, New York, NY USA.
Bredel, Markus (författare)
Univ Alabama Birmingham, Sch Med, Ctr Comprehens Canc, Dept Radiat Oncol, Birmingham, AL USA.;Stanford Univ, Sch Med, Stanford Canc Inst, Dept Neurosurg, Stanford, CA 94305 USA.
Carro, Maria S. (författare)
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany.;Univ Freiburg, Fac Med, Freiburg, Germany.
visa färre...
Univ Freiburg, Med Ctr, Dept Neurosurg, Freiburg, Germany;Univ Freiburg, Fac Med, Freiburg, Germany. Univ Freiburg, Neuroctr, Inst Neuropathol, Freiburg, Germany.;Univ Freiburg, Ctr Comprehens Canc, Freiburg, Germany.;Univ Freiburg, BIOSS Ctr Biol Signalling Studies, Freiburg, Germany. (creator_code:org_t)
AMER ASSOC CANCER RESEARCH, 2017
2017
Engelska.
Ingår i: Molecular Cancer Research. - : AMER ASSOC CANCER RESEARCH. - 1541-7786 .- 1557-3125. ; 15:8, s. 998-1011
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Glioblastoma (GBM) comprises distinct subtypes characterized by their molecular profile. Mesenchymal identity in GBM has been associated with a comparatively unfavorable prognosis, primarily due to inherent resistance of these tumors to current therapies. The identification of molecular determinants of mesenchymal transformation could potentially allow for the discovery of new therapeutic targets. Zinc Finger and BTB Domain Containing 18 (ZBTB18/ZNF238/RP58) is a zinc finger transcriptional repressor with a crucial role in brain development and neuronal differentiation. Here, ZBTB18 is primarily silenced in the mesenchymal subtype of GBM through aberrant promoter methylation. Loss of ZBTB18 contributes to the aggressive phenotype of glioblastoma through regulation of poor prognosis-associated signatures. Restitution of ZBTB18 expression reverses the phenotype and impairs tumor-forming ability. These results indicate that ZBTB18 functions as a tumor suppressor in GBM through the regulation of genes associated with phenotypically aggressive properties.

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