@article{CeteciXuCetecietal.2011,
  author    = {Ceteci, Fatih and Xu, Jiajia and Ceteci, Semra and Zanucco, Emanuele and Thakur, Chitra and Rapp, Ulf R.},
  title     = {Conditional Expression of Oncogenic C-RAF in Mouse Pulmonary Epithelial Cells Reveals Differential Tumorigenesis and Induction of Autophagy Leading to Tumor Regression},
  series = {Neoplasia},
  volume    = {13},
  journal   = {Neoplasia},
  number    = {11},
  doi       = {10.1593/neo.11652},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134347},
  pages     = {1005-1018},
  year      = {2011},
  abstract  = {Here we describe a novel conditional mouse lung tumor model for investigation of the pathogenesis of human lung cancer. On the basis of the frequent involvement of the Ras-RAF-MEK-ERK signaling pathway in human non-small cell lung carcinoma (NSCLC), we have explored the target cell availability, reversibility, and cell type specificity of transformation by oncogenic C-RAF. Targeting expression to alveolar type II cells or to Clara cells, the two likely precursors of human NSCLC, revealed differential tumorigenicity between these cells. Whereas expression of oncogenic C-RAF in alveolar type II cells readily induced multifocal macroscopic lung tumors independent of the developmental state, few tumors with type II pneumocytes features and incomplete penetrance were found when targeted to Clara cells. Induced tumors did not progress and were strictly dependent on the initiating oncogene. Deinduction of mice resulted in tumor regression due to autophagy rather than apoptosis. Induction of autophagic cell death in regressing lung tumors suggests the use of autophagy enhancers as a treatment choice for patients with NSCLC.},
  language  = {en}
}
@article{SchneiderDittrichBoecketal.2016,
  author    = {Schneider, Eberhard and Dittrich, Marcus and B{\"o}ck, Julia and Nanda, Indrajit and M{\"u}ller, Tobias and Seidmann, Larissa and Tralau, Tim and Galetzka, Danuta and El Hajj, Nady and Haaf, Thomas},
  title     = {CpG sites with continuously increasing or decreasing methylation from early to late human fetal brain development},
  series = {Gene},
  volume    = {592},
  journal   = {Gene},
  number    = {1},
  doi       = {10.1016/j.gene.2016.07.058},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-186936},
  pages     = {110-118},
  year      = {2016},
  abstract  = {Normal human brain development is dependent on highly dynamic epigenetic processes for spatial and temporal gene regulation. Recent work identified wide-spread changes in DNA methylation during fetal brain development. We profiled CpG methylation in frontal cortex of 27 fetuses from gestational weeks 12-42, using Illumina 450K methylation arrays. Sites showing genome-wide significant correlation with gestational age were compared to a publicly available data set from gestational weeks 3-26. Altogether, we identified 2016 matching developmentally regulated differentially methylated positions (m-dDMPs): 1767 m-dDMPs were hypermethylated and 1149 hypomethylated during fetal development. M-dDMPs are underrepresented in CpG islands and gene promoters, and enriched in gene bodies. They appear to cluster in certain chromosome regions. M-dDMPs are significantly enriched in autism-associated genes and CpGs. Our results promote the idea that reduced methylation dynamics during fetal brain development may predispose to autism. In addition, m-dDMPs are enriched in genes with human-specific brain expression patterns and/or histone modifications. Collectively, we defined a subset of dDMPs exhibiting constant methylation changes from early to late pregnancy. The same epigenetic mechanisms involving methylation changes in cis-regulatory regions may have been adopted for human brain evolution and ontogeny.},
  language  = {en}
}