@article{YildirimSemerciBenayahuAdamovskietal.2015,
  author    = {Yildirim-Semerci, Cigdem and Benayahu, Dafna and Adamovski, Miriam and Wollenberger, Ursula},
  title     = {An Electrochemical Assay for Monitoring Differentiation of the Osteoblastic Cell Line (MBA-15) on the Sensor Chip},
  series = {Electroanalysis : an international journal devoted to fundamental and practical aspects of electroanalysis},
  volume    = {27},
  journal   = {Electroanalysis : an international journal devoted to fundamental and practical aspects of electroanalysis},
  number    = {6},
  publisher = {Wiley-VCH},
  address   = {Weinheim},
  issn      = {1040-0397},
  doi       = {10.1002/elan.201400684},
  pages     = {1350 -- 1358},
  year      = {2015},
  abstract  = {An electrochemical assay for the indication of the activity of the cell bound differentiation marker alkaline phosphatase (ALP) is proposed using voltammetry on an in-vitro cell culture. The basis of the assay is cultivation of cells on gold microelectrodes in wells of a microplate, catalytic hydrolysis of p-aminophenyl phosphate by ALP and indication of p-aminophenol oxidation by square wave voltammetry (SWV) with the sensors onto which the cells attached. The morphology of the bone marrow stromal cell line (MBA-15) on the electrode surface was investigated and it exhibited in vitro osteogenic characteristics. Since ALP is expressed on the cell surface in early differentiation stage of osteoblastic cells, its activity was followed after different culture times over a period of 144 h by recording repetitive voltammograms at different time points upon addition of the substrate p-aminophenyl phosphate. The ALP activity was estimated from the signal increase related to formation rate of p-aminophenol and the number of cells. The highest value was measured at 120 h, when the cells reached confluence. The results of the electrochemical activity assay are consistent with the colorimetric acquired value from p-nitrophenol formation rate.},
  language  = {en}
}
@article{GereckeScholtkaLoewensteinetal.2015,
  author    = {Gerecke, Christian and Scholtka, Bettina and Loewenstein, Yvonne and Fait, Isabel and Gottschalk, Uwe and Rogoll, Dorothee and Melcher, Ralph and Kleuser, Burkhard},
  title     = {Hypermethylation of ITGA4, TFPI2 and VIMENTIN promoters is increased in inflamed colon tissue: putative risk markers for colitis-associated cancer},
  series = {Journal of cancer research and clinical oncology : official organ of the Deutsche Krebsgesellschaft},
  volume    = {141},
  journal   = {Journal of cancer research and clinical oncology : official organ of the Deutsche Krebsgesellschaft},
  number    = {12},
  publisher = {Springer},
  address   = {New York},
  issn      = {0171-5216},
  doi       = {10.1007/s00432-015-1972-8},
  pages     = {2097 -- 2107},
  year      = {2015},
  abstract  = {Epigenetic silencing of tumor suppressor genes is involved in early transforming events and has a high impact on colorectal carcinogenesis. Likewise, colon cancers that derive from chronically inflamed bowel diseases frequently exhibit epigenetic changes. But there is little data about epigenetic aberrations causing colorectal cancer in chronically inflamed tissue. The aim of the present study was to evaluate the aberrant gain of methylation in the gene promoters of VIM, TFPI2 and ITGA4 as putative early markers in the development from inflamed tissue via precancerous lesions toward colorectal cancer. Initial screening of different cancer cell lines by using methylation-specific PCR revealed a putative colon cancer-specific methylation pattern. Additionally, a demethylation assay was performed to investigate the methylation-dependent gene silencing of ITGA4. The candidate markers were analyzed in colonic tissue specimens from patients with colorectal cancer (n = 15), adenomas (n = 76), serrated lesions (n = 13), chronic inflammation (n = 10) and normal mucosal samples (n = 9). A high methylation frequency of VIM (55.6 \%) was observed in normal colon tissue, whereas ITGA4 and TFPI2 were completely unmethylated in controls. A significant gain of methylation frequency with progression of disease as well as an age-dependent effect was detectable for TFPI2. ITGA4 methylation frequency was high in precancerous and cancerous tissues as well as in inflammatory bowel diseases (IBD). The already established methylation marker VIM does not permit a specific and sensitive discrimination of healthy and neoplastic tissue. The methylation markers ITGA4 and TFPI2 seem to be suitable risk markers for inflammation-associated colon cancer.},
  language  = {en}
}