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

Oxaliplatin mutational signature

Project description:Oxaliplatin mutational signature in HepG2 and MCF10A

| PRJEB30309 | ENA

Doxorubicin mutational signature

Project description:Doxorubicin mutational signature in HepG2 and MCF10A

| PRJEB30311 | 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

Carboplatin-resistance-related DNA damage repair prognostic gene signature and its association with immune infiltration in breast cancer

Project description:Breast cancer is among the most prevalent malignant tumors globally, with carboplatin serving as a standard treatment option. However, resistance often compromises its efficacy. DNA damage repair (DDR) pathways are crucial in determining responses to treatment and are also associated with immune infiltration. This study aimed to identify the DDR genes involved in carboplatin resistance and to elucidate their effects on prognosis, immune infiltration, and drug sensitivity in breast cancer patients. We constructed the 3D-culture model of the MDA-MB-231 cell line, both resistant and sensitive to carboplatin, and identified a set of DDR genes. By integrating data from a public database, we established a prognostic signature comprising thirteen DDR genes. Our analysis indicated that this model is associated with immune infiltration patterns in breast cancer patients, particularly concerning CD8+ T cells and NK cells. Additionally, it demonstrated a significant correlation with sensitivity to other DDR-related drugs, suggesting its potential as a biomarker for treatment efficacy. Compared to the control group, TONSL-knockdown cell lines exhibited a diminished response to DNA-damaging agents, marked by a notable increase in DNA damage levels and enhanced drug sensitivity. Furthermore, single-cell analysis revealed elevated TONSL expression in dendritic and epithelial cells, particularly in triple-negative breast cancers.

2025-02-19 | GSE280942 | GEO

Colibactin DNA damage signature indicates mutational impact in colorectal cancer

Project description:Colibactin DNA damage signature indicates mutational impact in colorectal cancer

| PRJNA607699 | ENA