TNFα-producing Macrophages Determine Subtype Identity and Prognosis via AP1 Enhancer Reprogramming in Pancreatic Cancer
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ABSTRACT: Global mRNA expression profiling of patient derived pancreatic carcinoma xenograft models (N=4) were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Mice were treated daily with JQ1 (50 mg/kg, MedChem express/ Hycultec) to establish response characteristics.
Project description:Global mRNA expression profiling of patient derived pancreatic carcinoma xenograft Bo63 were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Two different sources of RNA were analyzed: 1.) Bo63 xenograft tumors grown on nude mice treated with vehicle only as control. 2.) Bo63 xenograft tumor grown on nude mice treated with JQ1 and SAHA (SAHA 25 mg/kg 1-0-0 and JQ1 50 mg/kg 0-0-1, treatment was imitated when tumor size reached 200 mm³ +/- 20 mm³.
Project description:Global mRNA expression profiling of patient derived pancreatic carcinoma xenograft Bo63 were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Two different sources of RNA were analyzed: 1.) Bo63 xenograft tumors grown on nude mice treated with vehicle only as control. 2.) Bo63 xenograft tumor grown on nude mice treated with JQ1 and SAHA (SAHA 25 mg/kg 1-0-0 and JQ1 50 mg/kg 0-0-1, treatment was imitated when tumor size reached 200 mm³ +/- 20 mm³. Two conditions (vehicle vs JQ1-SAHA treatment), each condition is represented by 3-4 biological replicates
Project description:Global mRNA expression profiling of patient derived colon cancer xenograft models (N=10) showing disease control under cetuximab treatment were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . All xenograft models were wildtype for KRAS, NRAS, BRAF and PIK3CA. All Mice were treated with cetuximab (Merck Serono) by intra peritoneal (i.p.) injection twice per week and dosed at 25mg/kg to establish response characteristics. Tumors were chronically treated to establish cetuximab secondary resistant tumors .
Project description:Global mRNA expression profiling of HCT116 cells overexpressing miR30a-5p were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Two different sources of RNA were analyzed: 1.) HCT116 colon cancer cells overexpressing human mir-30a-5p together with a sponge vector expressing binding sites for the antisense sequence of sh30a-5p vector construct to compete out possible miRNAs derived from the anti-guide strand of this vector. 2.) HCT116 colon cancer cells expressing control vector (pLKO.1-LV) and the sponge vector described above.
Project description:Global mRNA expression profiling of patient derived colon cancer xenograft models (N=13) were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . All xenograft models carried an activating. All Mice were either untreated (controls) or treated with treated with cetuximab (25 mg/kg, twice weekly, i.p., Merck) and trametinib (0.5 mg/kg, five subsequent days per week, p.o., Hycultec) to establish response characteristics. Tumors showing disease control under the combination treatment were chronically treated to establish cetuximab secondary resistant tumors which was successful for BoC2 and BoC56 .Primary resistant PDX tumors (BoC51, 109, 117, and 122) and secondary resistant tumors (BoC2 and BoC56) were harvested at the end of treatment (days 29 to 59). For BoC2 and 56, untreated control Tumors (K) were harvested once tumors reached approx. 1000mm3 in volume.
Project description:Global mRNA expression profiling of HCT116 cells overexpressing miR30a-5p were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Two different sources of RNA were analyzed: 1.) HCT116 colon cancer cells overexpressing human mir-30a-5p together with a sponge vector expressing binding sites for the antisense sequence of sh30a-5p vector construct to compete out possible miRNAs derived from the anti-guide strand of this vector. 2.) HCT116 colon cancer cells expressing control vector (pLKO.1-LV) and the sponge vector described above. Two conditions (sponge-LV vs sponge-sh30a-5p), each condition is represented by 3 biological replicates
Project description:According to our previous data, BRD4 controls the inflammatory cJUN transcription factor via enhancer interaction to promote a basal-like phenotype in pancreatic cancer. Therefore, in this study, we wanted to asses BRD4-mediated 3D chromatin interactions at a potential cJUN enhancer locus in pancreatic cancer. Hence, we performed i4C-seq in PANC1 cells in absencece and presence of the BET/BRD4 inhibitor JQ1 for this site.
Project description:4 replicates of either untreated controls or human skimmed milk treated cells for 12 hours were lysed to obtain total RNA. Untreated controls were labeled with Cy5 red dye, and human skimmed milk treatment were labeled with Cy3 green dye. 4 pairs of control-Cy5/treated-Cy3 labeled samples were hybridized to a 4*44k Agilent human array (G4845A, AMADID 026652 Human V2)
Project description:In pancreatic cancer, two distinct transcriptomic subtypes were identified with a high prognostic relevance: the classical and basal-like subtype. Therefore, in this study, we wanted to use an unbiased method to investigate the global chromatin accessibility in subtype-defined pancreatic cancer cell lines, as well as define the binding profile of the highly subtype-dependent JUN/AP1 transcription factors JUNB (classical) and cJUN (basal). Hence, we performed ATAC-seq in two classical and basal-like cells, as well as ChIP-seq for JUNB in classical CAPAN1 cells and for cJUN in basal-like PANC1 cells.