Project description:RNA Sequencing of claudin-low triple negative breast cancer cells T11 treated with FPP-1746-Omomyc, Omomyc, FPP-1746 and vehicle control (PBS) to determine differentially regulated genes induced by FPP-1746-Omomyc
Project description:Analysis of Kras-driven lung adenocarcinoma of mice intranasally treated with 2.37 mg/kg Omomyc or vehicle (10 mM sodium acetate pH 6.5) for three days. KRasLSL-G12D/+ mice were treated with Omomyc by intranasal administration sixteen weeks after Adeno-Cre infection. Mice (n=2 for vehicle treated and n=3 for Omomyc treated group) were euthanized three days post-treatment and lung tumors were excised and frozen at -80ºC until processing.
Project description:The following CGH experiments were conducted on six sectors (S1-S6) from a single primary ductal carcinoma tumor (T11) using the Sector-Ploidy-Profiling (SPP) Approach. SPP involves macro-dissecting the tumor, flow-sorting nuclei by differences in total genomic DNA content and profiling the genome of the tumor subpopulations.
Project description:Skin melanomas are highly aggressive and metastatic. Omomyc is the best MYC inhibitor currently available. We analysed the effect of Omomyc expression in a transgenic and inducible (upon Doxycycline addition) manner in spontaneous lymph node metastases from SkMel147 (mutated in NRAS) melanoma cells in vivo. We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 2.
Project description:Skin melanomas are highly aggressive and metastatic. Omomyc is the best MYC inhibitor currently available. We analysed the effect of Omomyc expression in a transgenic and inducible (upon Doxycycline addition) manner in melanoma cells in vivo in two different melanoma cell lines: A375 (mutated in BRAF), SkMel147 (mutated in NRAS). We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 7.
Project description:Skin melanomas are highly aggressive and metastatic. Omomyc is the best MYC inhibitor currently available. We analysed the effect of Omomyc expression in a transgenic and inducible (upon Doxycycline addition) manner in melanoma cells in vivo in two different melanoma cell lines: A375 (mutated in BRAF), SkMel147 (mutated in NRAS). We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 7.
Project description:Myc is a multifaceted bHLHZip transcription factor deregulated in the majority of human cancers. How to target Myc for cancer therapy is unclear, given its involvement in a variety of key functions in healthy cells. We used microarrays to capture the cellular transcriptional response to Omomyc – a Myc interfering molecule acting at the level of protein protein interactions that demonstrated a remarkable therapeutic efficacy in transgenic mouse cancer models. We found that Omomyc differently affects Myc induced gene repression and activation, channelling the Myc interactome activity to repression. To determine whether Omomyc causes widespread changes of the cell transcriptome, we analysed the transcriptional response to serum stimulation of Rat1 fibroblasts stably infected with an Omomer – Omomyc fused to the tamoxifen inducible oestrogen receptor ERTM – producing retrovirus (Rat1_Omomer) as compared to Rat1 cells infected with a control virus (Rat1_Control). Endogenous c-Myc is known to be sharply induced by serum and is critical for cell cycle re-entry. Cells were grown, serum-starved for 48 h in presence of tamoxifen (4-OHT) and stimulated by addition of fresh serum. Total RNA was collected from Rat1_Control and Rat1-Omomer cells at the time of serum re-addition (T0) and 90' thereafter (T90'), in the presence of tamoxifen.