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Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs [lenti]

ABSTRACT: Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs [lenti]

PROVIDER: PRJNA691528 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13416213_1.fastq.gz	Fastqsanger.gz
	SRR13416213_2.fastq.gz	Fastqsanger.gz
	SRR13416214_1.fastq.gz	Fastqsanger.gz
	SRR13416214_2.fastq.gz	Fastqsanger.gz
	SRR13416215_1.fastq.gz	Fastqsanger.gz

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Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs [lenti]

Project description:Identifying resistance mutations in a drug target provides crucial information. Lentiviral transduction creates multiple types of mutations due to the error-prone nature of the HIV-1 reverse transcriptase (RT) and we show this property can be leveraged to identify mutations that confer resistance to targeted anti-cancer drugs, a technique we term “LentiMutate”. First, we improved LentiMutate by making the lentiviral RT more error-prone. Next, we applied this technique to two anti-cancer drugs, imatinib and AMG 510. We find novel deletions in BCR-ABL that confer resistance to BCR-ABL inhibitors and point mutations in the AMG 510 binding pocket or oncogenic non-G12C mutations, in KRAS-G12C or wild-type KRAS, respectively, that confer resistance to AMG 510. LentiMutate may prove highly valuable to clinical and preclinical cancer drug development

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Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs [umi]

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Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs

Project description:Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs

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Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs [umi]

Project description:Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs [umi]

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Lentiviral-based mutagenesis to identify mutations that confer resistance to anti-cancer drugs

Project description:This SuperSeries is composed of the SubSeries listed below.

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Lentiviral-driven discovery of cancer drug resistance mutations

Project description:Identifying resistance mutations in a drug target provides crucial information. Lentiviral transduction creates multiple types of mutations due to the error-prone nature of the HIV-1 reverse transcriptase (RT). We optimized and leveraged this property to identify drug resistance mutations, a technique we term LentiMutate. After validating this technique by identifying clinically relevant EGFR resistance mutations, we applied this technique to two additional anti-cancer drugs, imatinib and AMG 510. We find novel deletions in BCR-ABL1 that confer resistance to BCR-ABL1 inhibitors and point mutations in the AMG 510 binding pocket or oncogenic non-G12C mutations, in KRAS-G12C or wild-type KRAS, respectively, that confer resistance to AMG 510. LentiMutate may prove highly valuable to clinical and preclinical cancer drug development.

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Lentiviral vector-based insertional mutagenesis identifies new clinically relevant cancer genes involved in the pathogenesis of hepatocellular carcinoma

Project description:We devised a novel insertional mutagenesis approach based on lentiviral vectors to induce hepatocellular carcinoma in three mouse models and identified four novel cancer initiating genes. Two genes are the well characterized Braf and Sos1, while the other two are Fign, encoding an AAA ATPase whose functions are poorly understood, and the complex Dlk1-Dio3 imprinted region which has been recently implicated in cancer and stemness. Activation of Fign or Braf and upregulation of the Dlk1-Dio3 imprinted region are functionally interconnected and may altogether control cell transformation, stemness and energy metabolism. Moreover, all the genes identified play a relevant role in human hepatocarcinogenesis as their expression levels and/or transcriptional signatures induced by their deregulation predict a different clinical outcome in hepatocellular carcinoma patients. These series consists of mRNA expression microarray data (The GeneChip® Mouse Gene 1.0 ST Array, Affymetrix) from 8 non-tumoral liver and 21 hepatocellular carcinoma induced by insertional mutagenesis. LV.ET.LTR was administered to newborn mice with 3 different genetic backgrounds. Hepatocellular carcinomas were induced in all the mouse models. Vector integrations were retrieved form each single liver mass. From 21 liver masses, RNA was collected to perform whole transcriptome analysis.

2012-12-20 | E-GEOD-31409 | biostudies-arrayexpress

Lentiviral vector-based insertional mutagenesis identifies new clinically relevant cancer genes involved in the pathogenesis of hepatocellular carcinoma

2012-12-20 | GSE31409 | GEO

Lentiviral vector-based insertional mutagenesis identifies new clinically relevant candidate cancer genes involved in the pathogenesis of hepatocellular carcinoma

Project description:We devised a novel insertional mutagenesis approach based on lentiviral vectors to induce hepatocellular carcinoma in three mouse models and identified four novel cancer initiating genes. Two genes are the well characterized Braf and Sos1, while the other two are Fign, encoding an AAA ATPase whose functions are poorly understood, and the paternally expressed gene Rtl1 within the complex Dlk1-Dio3 imprinted region recently involved in stemness. Interestingly, Fign and Braf regulate the expression of the maternal genes of the Dlk1-Dio3 imprinted region, suggesting that both maternally and paternally expressed genes of this region play a role in hepatocarcinogenesis. Moreover, all the genes identified are upregulated and/or amplified/deleted in human hepatocellular carcinoma and play a relevant role in human hepatocarcinogenesis, as their expression levels and/or transcriptional signatures induced by their deregulation predict a different clinical outcome in hepatocellular carcinoma patients. Primary human hepatocytes were transduced with SINLV.ET.trBRAF, SINLV.PGK.GFP or mock treated. RNA was collected at 5 different timepoints post-transduction: 24h, 36h, 48h, 72h, 144h (6d). Each experimental point was done in triplicate (A,B,C)

2015-02-19 | E-GEOD-35986 | biostudies-arrayexpress

Lentiviral vector-based insertional mutagenesis identifies new clinically relevant candidate cancer genes involved in the pathogenesis of hepatocellular carcinoma

Project description:We devised a novel insertional mutagenesis approach based on lentiviral vectors to induce hepatocellular carcinoma in three mouse models and identified four novel cancer initiating genes. Two genes are the well characterized Braf and Sos1, while the other two are Fign, encoding an AAA ATPase whose functions are poorly understood, and the paternally expressed gene Rtl1 within the complex Dlk1-Dio3 imprinted region recently involved in stemness. Interestingly, Fign and Braf regulate the expression of the maternal genes of the Dlk1-Dio3 imprinted region, suggesting that both maternally and paternally expressed genes of this region play a role in hepatocarcinogenesis. Moreover, all the genes identified are upregulated and/or amplified/deleted in human hepatocellular carcinoma and play a relevant role in human hepatocarcinogenesis, as their expression levels and/or transcriptional signatures induced by their deregulation predict a different clinical outcome in hepatocellular carcinoma patients.

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