Project description:The present study was designed to identify genes induced by irradiation in the 4T1 breast cancer model mimicking aggressive local relapse after radiotherapy. For this purpose, we obtained the transcriptomes of 4T1 tumors grown in either preirradiated (IRR+4T1) or non-irradiated (4T1) mammary tissue.
Project description:Investigation of whole genome gene expression level changes in mouse 4T1 mammary tumors expressing Cebpb shRNA, compared to 4T1 tumors expressing control shRNA. Analysis of mouse 4T1 mammary tumors expressing Cebpb shRNA compared to control shRNA are further described in Johansson & Berg et al 2012.
Project description:Investigation of whole genome gene expression level changes in mouse 4T1 mammary tumors expressing Cebpb shRNA, compared to 4T1 tumors expressing control shRNA. Analysis of mouse 4T1 mammary tumors expressing Cebpb shRNA compared to control shRNA are further described in Johansson & Berg et al 2012. A 10 chip study using total RNA recovered from five separate 4T1 tumors expressing Cebpb shRNA and five separate 4T1 tumors expressing control shRNA. All tumors were surgically removed after subcutaneous implantation in syngeneic BALB/c mice two weeks earlier. Each chip measures the expression level of 44,170 genes from Mus Musculus with fourteen 24-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.
Project description:4T1 mouse mammary carcinoma cells have an autocrine FGFR active loop leading to constitutive activation of downstream signaling pathways. We found that FGFR inhibitors have a strong effect on 4T1 tumors in-vivo. We used microarray to understand the contribution of FGFR signaling to the tumor formation upon TKI258 treatment. 4T1 cells were injected in the 4th mammary gland of Balb/C mice. After 7 days, daily treatment with TKI258 or water was performed for 14 days. At the end of the experiment, the RNA were extracted from three individual tumors per condition and hybridized on Affimetrix microarrays.
Project description:4T1 mouse mammary carcinoma cells have an autocrine FGFR active loop leading to constitutive activation of downstream signaling pathways. We found that FGFR inhibitors have a strong effect on the proliferation and survival of these cells. We used microarray to understand the contribution of FGFR signaling to the tumorigenic phenotype of the 4T1 cells. 4T1 cells were grown in tissue culture and treated with TKI258 or DMSO as vehicle control for 16 hours. The RNA were extracted from three individual dishes per condition and hybridized on Affimetrix microarrays.
Project description:We have previously described a sub-clones of the 4T1 mammary carcinoma cell line that are proficient for vasculogenic mimciry (VM), namely 4T1-E and 4T1-T. In vitro assays suggest that not all cells within these lines a VM-competent. To explore subsets of cells within tumors derived from these cells that may display VM properties we utilized single cell RNA-Seq of 4T1-T mammary fat-pad tumors.
