Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1113303 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29078700_1.fastq.gz | Fastqsanger.gz | |||
| SRR29078701_1.fastq.gz | Fastqsanger.gz | |||
| SRR29078702_1.fastq.gz | Fastqsanger.gz | |||
| SRR29078703_1.fastq.gz | Fastqsanger.gz | |||
| SRR29078704_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Nanopore targeted sequencing to identify tuberculosis drug resistance
| PRJNA1196171 | ENA
Project description:The emergence of drug resistance among tuberculosis (TB) patients is often associated with their non-compliance to the length of the chemotherapy, which can reach up to 2 years for the treatment of multi-drug-resistant (MDR) TB. Drugs that would kill TB faster and would not lead to the development of drug resistance could shorten chemotherapy significantly. In Escherichia coli, the common mechanism of cell death by bactericidal antibiotics is the generation of highly reactive hydroxyl radicals via the Fenton reaction. Since ascorbic acid (vitamin C) is known to drive the Fenton reaction, we tested whether the Fenton reaction could lead to a bactericidal event in Mycobacterium tuberculosis by treating M. tuberculosis cultures with vitamin C. Here, we report that the addition of vitamin C to drug-susceptible, MDR and extensively drug-resistant (XDR) M. tuberculosis strains results in sterilization of the cultures in vitro. We show that the sterilizing effect of vitamin C on M. tuberculosis was dependent on the production of high ferrous ion levels and reactive oxygen species. Although, this potent sterilizing activity of vitamin C against M. tuberculosis in vitro was not observed in mice, we believe this activity needs further investigation. Comparison of vitamin C treated Mycobacterium tuberculosis transcriptome relative to untreated; Three biological replicates, second is a dye flip
2013-05-24 | E-GEOD-42293 | biostudies-arrayexpress
Project description:Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation.
2020-10-22 | GSE159394 | GEO
Project description:Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation.
2020-10-22 | GSE159391 | GEO
Project description:Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation.
2020-10-22 | GSE159331 | GEO
Project description:Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation.
2020-10-22 | GSE159324 | GEO
Project description:Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation.
2020-10-22 | GSE159317 | GEO
Project description:Jamshidi2007 - Genome-scale metabolic network
of Mycobacterium tuberculosis (iNJ661)
This model is described in the article:
Investigating the metabolic
capabilities of Mycobacterium tuberculosis H37Rv using the in
silico strain iNJ661 and proposing alternative drug
targets.
Jamshidi N, Palsson BØ.
BMC Syst Biol 2007; 1: 26
Abstract:
BACKGROUND: Mycobacterium tuberculosis continues to be a
major pathogen in the third world, killing almost 2 million
people a year by the most recent estimates. Even in
industrialized countries, the emergence of multi-drug resistant
(MDR) strains of tuberculosis hails the need to develop
additional medications for treatment. Many of the drugs used
for treatment of tuberculosis target metabolic enzymes.
Genome-scale models can be used for analysis, discovery, and as
hypothesis generating tools, which will hopefully assist the
rational drug development process. These models need to be able
to assimilate data from large datasets and analyze them.
RESULTS: We completed a bottom up reconstruction of the
metabolic network of Mycobacterium tuberculosis H37Rv. This
functional in silico bacterium, iNJ661, contains 661 genes and
939 reactions and can produce many of the complex compounds
characteristic to tuberculosis, such as mycolic acids and
mycocerosates. We grew this bacterium in silico on various
media, analyzed the model in the context of multiple
high-throughput data sets, and finally we analyzed the network
in an 'unbiased' manner by calculating the Hard Coupled
Reaction (HCR) sets, groups of reactions that are forced to
operate in unison due to mass conservation and connectivity
constraints. CONCLUSION: Although we observed growth rates
comparable to experimental observations (doubling times ranging
from about 12 to 24 hours) in different media, comparisons of
gene essentiality with experimental data were less encouraging
(generally about 55%). The reasons for the often conflicting
results were multi-fold, including gene expression variability
under different conditions and lack of complete biological
knowledge. Some of the inconsistencies between in vitro and in
silico or in vivo and in silico results highlight specific loci
that are worth further experimental investigations. Finally, by
considering the HCR sets in the context of known drug targets
for tuberculosis treatment we proposed new alternative, but
equivalent drug targets.
This model is hosted on
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and identified by:
MODEL1507180001.
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2024-10-15 | MODEL1507180001 | BioModels
Project description:The emergence of drug resistance among tuberculosis (TB) patients is often associated with their non-compliance to the length of the chemotherapy, which can reach up to 2 years for the treatment of multi-drug-resistant (MDR) TB. Drugs that would kill TB faster and would not lead to the development of drug resistance could shorten chemotherapy significantly. In Escherichia coli, the common mechanism of cell death by bactericidal antibiotics is the generation of highly reactive hydroxyl radicals via the Fenton reaction. Since ascorbic acid (vitamin C) is known to drive the Fenton reaction, we tested whether the Fenton reaction could lead to a bactericidal event in Mycobacterium tuberculosis by treating M. tuberculosis cultures with vitamin C. Here, we report that the addition of vitamin C to drug-susceptible, MDR and extensively drug-resistant (XDR) M. tuberculosis strains results in sterilization of the cultures in vitro. We show that the sterilizing effect of vitamin C on M. tuberculosis was dependent on the production of high ferrous ion levels and reactive oxygen species. Although, this potent sterilizing activity of vitamin C against M. tuberculosis in vitro was not observed in mice, we believe this activity needs further investigation.
2013-05-24 | GSE42293 | GEO