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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="species">human</item><item key="factors"><item><item key="GSM767889 1"/></item><item><item key="GSM767890 1"/></item><item><item key="GSM767891 1"/></item><item><item key="GSM767892 1"/></item><item><item key="GSM767893 1"/></item><item><item key="GSM767894 1"/></item><item><item key="GSM767895 1"/></item><item><item key="GSM767896 1"/></item><item><item key="GSM767897 1"/></item><item><item key="GSM767898 1"/></item><item><item key="GSM767899 1"/></item><item><item key="GSM767900 1"/></item><item><item key="GSM767901 1"/></item><item><item key="GSM767902 1"/></item><item><item key="GSM767903 1"/></item><item><item key="GSM767904 1"/></item><item><item key="GSM767905 1"/></item><item><item key="GSM767906 1"/></item><item><item key="GSM767907 1"/></item><item><item key="GSM767908 1"/></item><item><item key="GSM767909 1"/></item><item><item key="GSM767910 1"/></item><item><item key="GSM767911 1"/></item><item><item key="GSM767912 1"/></item></item><item key="id">4183</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="platform">4</item><item key="summary_wrapped">Epigenetic changes accompany tumorigenesis and are required for tumor maintenance. Modulation of DNA methylation state, histone...</item><item key="geo_gse_id">E-GEOD-30985</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">0</item><item key="sample_count">24</item><item key="tags"><item>disease</item><item>histone</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_id_plat">E-GEOD-30985_A-AFFY-44</item><item key="slug">expression-profiling-of-dnmt1-inhibitors-in-hct116</item><item key="geo_gds_id"/><item key="name">Expression profiling of DNMT1 inhibitors in HCT116 cells</item><item key="created">Sep.16, 2014</item><item key="summary">Epigenetic changes accompany tumorigenesis and are required for tumor maintenance. Modulation of DNA methylation state, histone acetylation, and histone methylation, as well as reversal of disease-associated epigenetic state aberrations, can be disruptive to malignant disease progression. We produced lipophilic prodrugs of decitabine, which is a DNA methyltransferase inhibitor and is efficacious in treatment of myelodysplastic syndromes when dosed subcutaneously. Comparison of parent and prodrug activities in vitro and in vivo revealed comparable effects and unveiled several novel features of nucleoside analog molecular activity in vitro. HCT116 were treated for 72 hour with Decitabine, Azacytidine and various prodrugs in duplicates at different dose concentrations. Cells were also treated with DMSO as control (quadrpulets), RNA was extracted and samples were hybridized to Affymetrix Hu133plus 2.0 arrays.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-30985</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-30985/samples/</item></data></biogps>
