Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by in vivo screening of murine tumor derived xenografts

ABSTRACT: Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by in vivo screening of murine tumor derived xenografts

PROVIDER: PRJNA562170 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10021317.fastq.gz	Fastqsanger.gz
	SRR10021318.fastq.gz	Fastqsanger.gz
	SRR10021319.fastq.gz	Fastqsanger.gz
	SRR10021320.fastq.gz	Fastqsanger.gz
	SRR10021321.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by in vivo screening of murine tumor derived xenografts

Project description:Using a pooled shRNA library, we performed a focused screen of 81 shRNAs selected for involvement in response to chemotherapy in an ex vivo 3D primary tumor cell culture system. Our results establish Ankrd35, a previously uncharacterized ankyrin repeat domain protein, as an important mediator of chemoresistance in vivo.

2021-11-11 | GSE136317 | GEO

Identification of CMTM6 as a novel mediator of cisplatin resistance in oral squamous cell carcinoma

Project description:Identification of CMTM6 as a novel mediator of cisplatin resistance in oral squamous cell carcinoma

2020-01-07 | MSV000084761 | MassIVE

Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by ex vivo 3D screening of primary tumor spheroids

Project description:Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by ex vivo 3D screening of primary tumor spheroids

| PRJNA562169 | ENA

Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by ex vivo 3D screening of primary tumor spheroids

Project description:Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by ex vivo 3D screening of primary tumor spheroids

| PRJNA562272 | ENA

Gene expression profiling of xenografts generated by lung metastasis screening models

Project description:Gene expression profiling of xenografts generated by lung metastasis screening models

| PRJNA491643 | ENA

Ammonium tetrathiomolybdate treatment targets the copper transporter ATP7A in cisplatin-resistant breast cancer TM and cisplatin sensitize resistant breast cancer.

Project description:Chemotherapy resistance presents a major hurdle for cancer treatment. We proposed to identify the molecular changes through which breast cancer cells evolve resistance to conventional treatment, here cisplatin, so targeted therapy can be developed. Candidate approach RNAi screening was combined with cisplatin treatment in order to identify molecular pathways conferring survival advantages. The screening identified ATP7A, a copper transport ATPase responsible for the intercellular movement and sequestering of cisplatin, as a therapeutic target. Copper chelation with tetrathiomolybdate (TM) targets ATP7A. TM in combination with cisplatin sensitized drug-resistant breast cancer cells. Allograft and xenograft models in aythymic mice treated with TM/cisplatin combination therapy inhibited tumor growth and increased survival compared with monotreated mice. Examination of the molecular effects of TM on cisplatin efficacy in drug-resistant tumors revealed reduced levels of APT7A, reduced cisplatin sequestering by ATP7A and increased nuclear availability of cisplatin. Further, we showed that TM treatment combined with cisplatin reduced the half-life of ATP7A in human breast cancer cell lines. This finding offered the potential to combat drug platinum-resistant tumors and sensitize patients to conventional breast cancer treatments by identifying and targeting resistant tumors’ unique molecular adaptations.

2017-06-19 | GSE77515 | GEO

Apoptosis induced by Piroxicam/Cisplatin combined treatment is triggered by p21 in mesothelioma

2011-11-20 | GSE22445 | GEO

Identification of Ankrd35 as a mediator of cisplatin response in non-small cell lung cancer by ex vivo 3D screening of primary tumor spheroids

Project description:Using pooled shRNA libraries, we performed a focused screen of 515 genes selected for involvement in response to chemotherapy. The results of this screen confirmed Notch signaling is important for primary tumor cell survival and the importance of key DNA damage response regulators for platinum-induced damage, including Ercc1. Our results establish Ankrd35, a previously uncharacterized ankyrin repeat domain protein, as an important mediator of chemoresistance in ex vivo cultures.

2021-11-11 | GSE136316 | GEO

Cisplatin resistance screens in BRCA2-deficient cells

Project description:Cisplatin resistance screening in KB2P 2D cell lines

| PRJEB75036 | ENA

Apoptosis induced by Piroxicam/Cisplatin combined treatment is triggered by p21 in mesothelioma

Project description:Here we report that piroxicam/cisplatin combined treatment exerts an apoptotic effect on mesothelioma cells. Genome-wide transcriptome analyses lead us to identify p21 as the possible apoptosis mediator acting as downstream target of the piroxicam/cisplatin treatment. To analyze the potential therapeutic effect of the piroxicam/cisplatin treatment at molecular level, and to identify gene expression pattern modifications following the combined treatment, we performed a transcriptional profiling on HGU133A arrays, using cells treated with piroxicam, cisplatin or with piroxicam and cisplatin, choosing the time exposures in which apoptosis induction was absent or evident (8 and 24 hours). Biological duplicates or triplicates were generated for each prototypic situation and data were analyzed using the oneChannelGUI Bioconductor package (Sanges et al., 2007), comparing untreated cells with cells treated in single or combined treatment. After quality controls, the complexity of the data set was reduced removing the non-significant probe sets, resulting in a total of 4,247 out of the 22,283 probe sets present in the microarray. To assess differential expression, linked to piroxicam, cisplatin- and the combined treatment we used an empirical Bayes method together with a false discovery rate (FDR) correction of the P-value. Specifically genes were selected using a corrected p-value M-bM-^IM-$0.05 and |log2(fc)| M-bM-^IM-%1. We detect a total of 536 differentially expressed genes.

2011-11-20 | E-GEOD-22445 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data