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Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 in combination with FGFR inhibitor BGJ398 vs. BLU6864 alone [BGJ398_24H + BLU6864_24H vs BLU6864_24H]

ABSTRACT: Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 in combination with FGFR inhibitor BGJ398 vs. BLU6864 alone [BGJ398_24H + BLU6864_24H vs BLU6864_24H]

PROVIDER: PRJNA818024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18390894_1.fastq.gz	Fastqsanger.gz
	SRR18390894_2.fastq.gz	Fastqsanger.gz
	SRR18390895_1.fastq.gz	Fastqsanger.gz
	SRR18390895_2.fastq.gz	Fastqsanger.gz
	SRR18390896_1.fastq.gz	Fastqsanger.gz

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Gene expression changes caused by treatment of TPC1 cells with RET, FGFR inhibitor

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Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 [BLU6864_6H vs DMSO]

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Gene expression profiling in TPC1 cell line treated with the RTK inhibitor RPI-1

Project description:We treated the papillary thyroid carcinoma-derived cell line TPC1 with the RTK inhibitor RPI-1 to obtain a thyroid carcinoma cell model. The RET tyrosine kinase is a target of the inhibitor. Gene expression changes were evaluated comparing cells treated with the inhibitor for 24 hours versus cells treated with DMSO for 24 hours. Biological triplicates for RPI-1 and DMSO treated cells were generated by independent treatments and total RNA extractions.

2014-06-30 | E-GEOD-49414 | biostudies-arrayexpress

microRNA expression profiling in TPC1 cell line treated with the RTK inhibitor RPI-1

Project description:We treated the papillary thyroid carcinoma-derived cell line TPC1 with the RTK inhibitor RPI-1 to obtain a thyroid carcinoma cell model. The RET tyrosine kinase is a target of the inhibitor. microRNA expression changes were evaluated comparing cells treated with the inhibitor fo 24 hours versus cells treated with DMSO for 24 hours. Biological triplicates for RPI-1 and DMSO treated cells were generated by independent treatments and total RNA extractions. One sample from each class did not pass quality control, and thus was discarded. The final dataset comprises two samples for each class.

2014-06-30 | E-GEOD-49401 | biostudies-arrayexpress

Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 from 6 to 24 hours [BLU6864_24H vs BLU6864_6H]

Project description:Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 from 6 to 24 hours [BLU6864_24H vs BLU6864_6H]

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Gene expression changes caused by treatment of TPC1 cells with FGFR inhibitor BGJ398 [BGJ398_6H and BGJ398_24H]

Project description:Gene expression changes caused by treatment of TPC1 cells with FGFR inhibitor BGJ398 [BGJ398_6H and BGJ398_24H]

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Microarray gene expression data from RET siRNA-mediated knockdown in CDK4/6 inhibitor breast cancer resistant cells

Project description:RET is overexpressed in breast cancer cell lines resistant to combined CDK4/6i and endocrine therapy. siRNA-mediated knockdown of RET was performed to identify main pathways altered upon RET-knockdown. We used microarrays to detail the global programme of gene expression following RET knockdown in 2 cell models resistant to combined CDK4/6 inhibitor palbociclib and fulvestrant (MPFR and TPFR). MPFR-ret and TPFR-ret were compared to MPFR-ctrl and TPFR-ctrl, respectively. The gene expression analysis revealed a significant number of genes altered in the knockdown (ret) vs. ctrl

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GDNF-RET signaling as a target in aromatase inhibitor resistant breast cancers

Project description:Understanding the complex molecular mechanisms underlying resistance to endocrine therapy is a major challenge in the treatment of estrogen receptor-positive (ER+) breast cancers. We have previously demonstrated that glial cell line-derived neurotrophic factor (GDNF) signaling via the receptor tyrosine kinase RET promotes estrogen independent activation of ER. Here we have addressed the relevance of GDNF-RET signaling in response to aromatase inhibitor treatment and explored the efficacy of using RET inhibitors in breast cancer models of aromatase inhibitor response and resistance. A GDNF-response gene set, identified from gene expression profiling, was demonstrated to be an independent prognostic marker of poor patient outcome and, importantly, to be predictive of poor response to aromatase inhibitor treatment and development of resistance. The relevance of these findings was validated first by demonstrating an association of RET protein expression in an independent cohort of aromatase inhibitor resistant patient samples. Second, in in vitro models, GDNF-mediated RET signaling was demonstrated to enhance the survival of aromatase inhibitor resistant cells and to increase resistance in aromatase inhibitor sensitive cells. These effects could be reversed by targeting GDNF/RET signaling with the RET selective inhibitor NVP-BBT594 thus identifying GDNF-RET signaling as a potential therapeutic target, particularly in breast cancers resistant to aromatase inhibitors.<br>MCF7 cells were E2-deprived by culturing in phenol red-free RPMI 1640 supplemented with 10% DCC for 3 days and then serum-starved overnight in the presence or absence of fulvestrant (ICI182,780) (100 nM). The following day, cells were treated with GDNF (20 ng/ml) for 0, 4, 8, 24 and 48 hours in the presence or absence of fulvestrant (ICI182,780) (100 nM).

2013-01-17 | E-MEXP-3662 | biostudies-arrayexpress

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