Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Carboplatin mutational signature

ABSTRACT: Carboplatin mutational signature in HepG2 and MCF10A

PROVIDER: PRJEB30310 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR3087512_1.fastq.gz	Fastqsanger.gz
	ERR3087512_2.fastq.gz	Fastqsanger.gz
	ERR3087513_1.fastq.gz	Fastqsanger.gz
	ERR3087513_2.fastq.gz	Fastqsanger.gz
	ERR3087514_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Doxorubicin mutational signature

Project description:Doxorubicin mutational signature in HepG2 and MCF10A

| PRJEB30311 | ENA

Oxaliplatin mutational signature

Project description:Oxaliplatin mutational signature in HepG2 and MCF10A

| PRJEB30309 | ENA

Mutational signature of AA1 in MCF10A and HepG2

Project description:Mutational signature of AA1 in MCF10A and HepG2

| PRJEB36497 | ENA

Mutational signature of aristolochic acid analogues in MCF10A and HepG2

Project description:Mutational signature of aristolochic acid analogues in MCF10A and HepG2

| PRJEB36499 | ENA

Duocarmycin mutational signature in HepG2 cells

Project description:Duocarmycin mutational signature in HepG2 cells

| PRJEB33544 | ENA

PA mutational signature in HCC

Project description:Mutational signature analysis reveals widespread contribution of pyrrolizidine alkaloid exposure to human liver cancer

| PRJEB39863 | ENA

Intragenomic variability and extended sequence patterns in the mutational signature of ultraviolet light

Project description:Mutational signatures can reveal properties of underlying mutational processes and are important when assessing signals of selection in cancer. Here we describe the sequence characteristics of mutations induced by ultraviolet (UV) light, a major mutagen in several human cancers, in terms of extended (longer than trinucleotide) patterns as well as variability of the signature across chromatin states. Promoter regions display a distinct UV signature with reduced TCG>TTG transitions, and genome-wide mapping of UVB-induced DNA photoproducts (pyrimidine dimers) showed that this may be explained by decreased damage formation at hypomethylated promoter CpG sites. Further, an extended signature model encompassing additional information from longer contextual patterns improves modeling of UV mutations, which may enhance discrimination between drivers and passenger events. Our study presents a refined picture of the UV signature and underscores that the characteristics of a single mutational process may vary across the genome.

2019-09-11 | GSE127966 | GEO

Transcription profiling of human epithelial ovarian cancer cell lines treated with Carboplatin reveals carboplatin induced gene expression changes in vitro are prognostic of survival - time series

Project description:We performed a time-course microarray experiment to define the transcriptional response to carboplatin in vitro, and to correlate this with clinical outcome in epithelial ovarian cancer (EOC). RNA was isolated from carboplatin and control-treated 36M2 ovarian cancer cells at several time points, followed by oligonucleotide microarray hybridization. Carboplatin induced changes in gene expression were assessed at the single gene as well as at the pathway level. Clinical validation was performed in publicly available microarray datasets using disease free and overall survival endpoints. Time-course and pathway analyses identified 317 genes and 40 pathways (designated time-course and pathway signatures) deregulated following carboplatin exposure. Both types of signatures were validated in two separate platinum-treated ovarian and NSCLC cell lines using published microarray data. Expression of time-course and pathway signature genes distinguished between patients with unfavorable and favorable survival in two independent ovarian cancer datasets. Among the pathways most highly induced by carboplatin in vitro, the NRF2, NF-kB, and cytokine and inflammatory response pathways were also found to be upregulated prior to chemotherapy exposure in poor prognosis tumors. Experiment Overall Design: we treated the 36M2 cell line with carboplatin 100Î¼M or vehicle-control for 24hrs and cells were harvested and processed for RNA isolation at 24, 30 and 36hrs after treatment.

2009-01-14 | E-GEOD-13525 | biostudies-arrayexpress

LC-MS/MS identification of differentially expressed proteins in carboplatin resistant Triple Negative Breast Cancer

Project description:Triple negative breast cancer (TNBC) is the subtype of breast cancer most lacking in efficient treatment options. Although many TNBCs show remarkable responses to carboplatin-based chemotherapy, they often develop resistance over time. With increasing use of carboplatin in clinics, there is a pressing need to understand mechanisms causing carboplatin resistance and identify the vulnerabilities of carboplatin-resistant tumors. We generated carboplatin-resistance models based on the TNBC cell line MDA-MB-468 and patient derived xenograft (PDX) models of TNBCs. By combining the results of mass spectrometry-based proteome profiling and a kinome RNA interference screen, we assessed the molecular changes and vulnerabilities of carboplatin-resistant TNBCs. Using pharmacological inhibition of the identified targets, we validated the dependencies of carboplatin-resistant cells in vitro and in PDX models. We found that carboplatin resistance in TNBC is accompanied by drastic proteome rewiring. Carboplatin-induced metabolism alterations and upregulation of anti-oxidative response keep low levels of DNA damage and support cell replication in the presence of carboplatin. Carboplatin-resistant cells also exhibited longer mitosis due to dysregulation of mitotic checkpoint. Whereas the components of the mitotic checkpoints, AURKA and BUB1, are essential for the viability of carboplatin-resistant cells, the checkpoint kinases CHEK1 and WEE1 are indispensable for survival of carboplatin-treated resistant cells. We confirmed that pharmacological inhibition of CHEK1 by prexasertib in the presence of carboplatin is well tolerated by mice and suppresses the growth of carboplatin-resistant TNBC xenografts. Abrogation of the mitotic checkpoint re-sensitizes carboplatin-resistant TNBCs to carboplatin. CHEK1 inhibition represents a potential strategy for the treatment of carboplatin-resistant TNBCs.

2021-07-07 | PXD021726 | Pride

Nitrosamine exposed HepG2 clones

Project description:Mutational signature of nitrosamines in HepG2

| PRJEB36272 | ENA