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EGAS00001001614-sc-20160629 - samples

ABSTRACT: This study involves mutagenizing C32, a melanoma cell line, with ENU to identify those mutations which engender resistance to a targeted treatment.

PROVIDER: EGAD00001002234 | EGA |

REPOSITORIES: EGA

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Melanoma C32 ENU resistance to Combination Therapy

Project description:This study involves mutagenizing C32, a melanoma cell line, with ENU to identify those mutations which engender resistance to a targeted treatment.

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Project description:This study involves mutagenizing C32, a melanoma cell line, with ENU to identify those mutations which engender resistance to a targeted treatment.

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Melanoma C32 ENU Resistance to Single Agent Therapy

Project description:This study involves mutagenizing C32, a melanoma cell line, with ENU to identify those mutations which engender resistance to a targeted treatment.

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Project description:This study involves mutagenizing 11-18 with ENU to identify those mutations which engender resistance to targeted treatment. . This dataset contains all the data available for this study on 2019-06-10.

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Combination Therapies for Personalised Cancer Medicine in drug resistant EGFR mutant lung cancer

Project description:This study involves mutagenizing a range of different cell lines with ENU to identify those mutations which engender resistance to targeted treatment. In the last decade we have begun to move towards the use of targeted therapeutics in the clinic, often resulting in dramatic response rates in cancer patients. However, clinical experience has demonstrated time and time again that such responses are invariably followed by the development of drug resistance. Identification of the underlying mechanisms may enable us to reverse such resistance. Traditional methods of modelling this resistance in vitro can lead to a plethora of potential resistance mechanisms that can be difficult to decipher.

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Combination Therapies for Personalised Cancer Medicine in 11-18

Project description:This study involves mutagenizing 11-18 with ENU to identify those mutations which engender resistance to targeted treatment. In the last decade we have begun to move towards the use of targeted therapeutics in the clinic, often resulting in dramatic response rates in cancer patients. However, clinical experience has demonstrated time and time again that such responses are invariably followed by the development of drug resistance. Identification of the underlying mechanisms may enable us to reverse such resistance. Traditional methods of modelling this resistance in vitro can lead to a plethora of potential resistance mechanisms that can be difficult to decipher.

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Melanoma cell lines treated with dabrafenib ± trametinib

Project description:Rapid resistance to BRAF inhibitors in BRAFV600-mutant metastatic melanoma has produced an urgent need for new treatment options. BRAF inhibitor resistance commonly involves reactivation of mitogen-activated protein kinase (MAPK) signaling and yet inhibition of downstream kinases has not circumvented resistance, partly because MAPK is regulated via a complex network of feedback mechanisms that influence pathway rebound. To examine the transcriptome responses of melanoma cells to MAPK inhibition, a panel of 11 BRAFV600-mutant melanoma cell lines were treated with control (DMSO), 100nM dabrafenib alone (i.e BRAF inhibitor monotherapy) or 100nM dabrafenib + 10nM trametinib (i.e combination BRAF + MEK inhibition) for 24h.

2017-09-20 | GSE98314 | GEO

Time-series RNA-seq experiment performed on 10 melanoma cell lines treated with BRAF inhibitor vemurafenib.

Project description:BRAF targeted drug vemurafenib have shown very good clinical benefit in melanoma patient containing BRAF V600E mutation. However, resistance always occurs in patient. Early stage of the resistance development require the tumor cell adapted to the targeted drug. We are trying to study the kinetic of melanoma cell adaptation towards vemurafenib. 10 melanoma cell lines with BRAF mutation are treated with targeted therapy vemurafenib. RNA-seq samples are collected after drug treatment for different time (day3 and day21) to compare with DMSO-treated control samples for each cell line. Except innate resistant cell line M381, all other cell lines shows inhibition of proliferation. However, a small cluster of cell lines (M397, M229 and M263) shows some other unique transcriptomic change. For cell line M397, M229 and M263, we also collected the RNA-seq data for long-term (73day/90day) drug treatment condition where the cells developed resistance to vemurafenib treatment. Dedifferentiation is enriched in these unique transcriptomic change within these 3 cell lines. Similar cell state dedifferentiation phenomenon is also reported to cause resistance towards immunotherpay where the resistant de-differentiated melanoma cells are induced by TNF which is secreted by tumor-infiltrating T cells. We also treat our cultured melanoma cells with TNF and collected the treated sample for RNA-seq experiment.

2019-06-22 | E-MTAB-5493 | biostudies-arrayexpress

RNA-seq for MP, AML and MEFs from mice that carry a "knock-in" allele of the mutant splicing factor, U2af1(S34F), with or without homozygous deletion of the transcription factor, Runx1

Project description:We have generated mice that carry Cre-dependent "knock-in" alleles (MGS34F and IES34F) of U2af1(S34F), a mutation commonly encountered in human myelodysplastic syndromes and acute myeloid leukemia (AML). MEFs were generated from the progenies of these mice with those carrying a UBC-CreERT2 transgene, and were treated with 4-Hydroxytamoxifen (4OHT) to induce Cre-mediated recombination and subsequent U2af1(S34F) expression. Mice carrying the MGS34F allele were further crossed with those carrying a floxed Runx1 allele and Mx1-Cre. U2af1(S34F) expression and Runx1 deletion caused changes in gene expression and RNA splicing. Mice with a conditional "knock-in" U2af1(S34F) allele and conditional "knockout" alleles of Runx1 were mutagenized with low-dose N-Ethyl-N-Nitrosourea (ENU). Within 1.5 year, one of fourteen ENU-treated mice with U2af1(S34F) and Runx1 deletion developed AML, as did recipients of allografted splenic cells from two other such mice, but AML did not arise from cells with other genotypes or mice without ENU treatment.

2018-07-26 | GSE112174 | GEO

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