Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chemosensitive Relapse in Small Cell Lung Cancer Patient-Derived Xenografts

ABSTRACT:

Genetic and epigenetic analysis of patient-derived xenograft models of acquired chemoresistance in small cell lung cancer.

PROVIDER: phs001249 | dbGaP |

SECONDARY ACCESSION(S): PRJNA353969PRJNA353970

REPOSITORIES: dbGaP

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	GapExchange_phs001249.v1.p1.xml	Xml
	dbGaPEx2.1.5.xsd	Other
	Study_Report.phs001249.SmallCellLungCancer.v1.p1.MULTI.pdf	Pdf
	manifest_phs001249.SmallCellLungCancer.v1.p1.c1.HMB-PUB.pdf	Pdf
	datadict_v2.xsl	Other

Items per page:

1 - 5 of 13

Similar Datasets

Multi-omics profiling of non-small cell lung cancer patient-derived xenografts reveals proteome and phosphoproteome remodeling associated with patient outcome

Project description:131 patient-derived xenograft models were generated for non-small cell lung carcinoma and were profiled by analysis of gene copy number variation, whole exome sequence, methylome, transcriptome, proteome, and phospho(Tyr)-proteome. Proteome profiling resolved the known major histology subtypes and revealed 3 proteome subtypes (proteotypes) among adenocarcinoma and 2 in squamous cell carcinoma that were associated with distinct protein-phosphotyrosine signatures and patient survival. Proteomes of human tumor were discernible from murine stroma. Stromal proteomes were similar between histological subtypes, but two adenocarcinoma proteotypes had distinct stromal proteomes. Tumor and stromal proteotypes comprise signatures of targetable biological pathways suggesting that patient stratification by proteome profiling may be an actionable approach to precisely diagnose and treat cancer.

2021-11-24 | PXD016579 | Pride

Multi-omics profiling of non-small cell lung cancer patient-derived xenografts reveals proteome and phosphoproteome remodeling associated with patient outcome

Project description:131 patient-derived xenograft models were generated for non-small cell lung carcinoma and were profiled at the genome, transcriptome and proteome level by analysis of gene copy number variation, whole exome sequencing, DNA methylation, transcriptome, proteome and phospho(Tyr)-proteome. At the proteome level, the human tumor and murine stroma were discernible. Tumor proteome profiling resolved the known major histological subtypes and revealed 3 proteome subtypes (proteotypes) among adenocarcinoma and 2 in squamous cell carcinoma that were associated with distinct protein-phosphotyrosine signatures and patient survival. Stromal proteomes were similar between histological subtypes, but two adenocarcinoma proteotypes had distinct stromal proteomes. Proteotypes comprise tumor and stromal signatures of targetable biological pathways suggesting that patient stratification by proteome profiling may be an actionable approach to precisely diagnose and treat cancer.

2021-11-24 | PXD016674 | Pride

Acquired Cross-Resistance in Small Cell Lung Cancer Patient-Derived Xenografts

Project description:Acquired Cross-Resistance in Small Cell Lung Cancer Patient-Derived Xenografts

| PRJNA1049569 | ENA

Acquired Cross-Resistance in Small Cell Lung Cancer Patient-Derived Xenografts

Project description:Acquired Cross-Resistance in Small Cell Lung Cancer Patient-Derived Xenografts

| PRJNA1049570 | ENA

Integrative analysis of non-small cell lung cancer patient-derived xenografts identifies unique proteotypes associated with patient outcomes [HT12v4]

Project description:Non-small cell lung cancer (NSCLC) death rates exceed the next 3 prevalent cancers combined; however, most NSCLC tumors lack actionable mutations. Recent studies of NSCLC and other cancers revealed profound proteome remodelling with prognostic impact that is not fully predicted by DNA or RNA analyses. These revelations portend proteome-based cancer classification and treatment. This will require model systems that recapitulate tumor proteomes and phenotypes. A subset (~35%) of the most aggressive NSCLC can form a patient-derived xenograft (PDX). We generated 137 PDX models of aggressive NSCLC, which represent the histological, genome, transcriptome, and DNA methylation features and proteome remodelling of primary NSCLC. The models indicate 3 lung adenocarcinoma and 2 squamous cell carcinoma proteotypes that are associated with different patient outcomes, protein-phosphotyrosine profiles, candidate targets, and in adenocarcinoma, distinct stromal immune features. The PDX resource will foster proteome-directed stratification and development of new treatments for aggressive NSCLC.

2021-11-23 | GSE166997 | GEO

Patient-derived xenograft models of non-small cell lung cancer for evaluating targeted drug sensitivity and resistance

Project description:Patient-derived xenograft models of non-small cell lung cancer for evaluating targeted drug sensitivity and resistance

| PRJNA534119 | ENA

Integrative analysis of non-small cell lung cancer patient-derived xenografts identifies unique proteotypes associated with patient outcomes [WG-DASL]

2021-11-23 | GSE166998 | GEO

Medulloblastoma Patient-Derived Xenograft Proteomics

Project description:Proteomic and phosphoproteomic characterization of 20 orthotopic patient-derived xenograft models of medulloblastoma

2022-09-01 | PXD035070 | Pride

Targeting FGFR overcomes EMT-mediated resistance in EGFR mutant non-small cell lung cancer

Project description:Acquired drug resistance to tyrosine kinase inhibitor (TKI) targeted therapies remains a major clinical challenge. In EGFR mutant non-small cell lung cancer (NSCLC), therapeutic failure of EGFR TKIs can result from both genetic and epigenetic mechanisms of acquired drug resistance. Histologic and gene expression changes consistent with an epithelial-to-mesenchymal transition (EMT) have been associated with resistance to EGFR TKIs in both experimental models and in patients, and may coincide with genetic mechanisms of resistance such as the EGFRT790M gatekeeper mutation. While therapeutic approaches targeting EGFRT790M have been developed, a strategy for overcoming EMT-related resistance remains unclear. We performed whole-genome CRISPR screening on patient-derived, mesenchymal EGFRT790M-positive cell lines and identified FGFR1 as a critical gene promoting resistance to third generation EGFR TKIs. The FGFR1-3 inhibitor, BGJ398 (infigratinib), resensitized resistant mesenchymal-like cell lines to EGFR inhibition in a synergistic manner. Combining EGFR + FGFR inhibitors also inhibited the in vitro survival and expansion of EGFR mutant drug tolerant cells with mesenchymal-like features prior to the development of drug resistance, and delayed the development of in vivo resistance in EGFR mutant NSCLC xenograft tumors. These results suggest that dual EGFR + FGFR blockade may be a promising clinical strategy for preventing and overcoming EMT-associated acquired drug resistance in EGFR mutant NSCLC.

2019-04-30 | GSE114647 | GEO

Effect of BET bromodomain inhibitor and/or mTOR inhibitor on transcriptome of small cell lung cancer patient-derived xenograft LX95 tumors

Project description:We report mTOR inhibitor (mTORi) is synergistic with BET inhibitor (BETi) in controlling tumor growth and inducing apoptosis in small cell lung cancer (SCLC) patient-derived xenograft (PDX) models. In this study, we studied impact of different treatment on whole-genome mRNA transcriptome in SCLC PDX tumors. Four different treatments (vehicle control, NHWD870 [BETi; 1.5mg/kg], everolimus [mTORi; 2mg/kg], and the combo [NHWD870 1mg/kg and everolimus 1.5mg/kg] were administered daily for one week in a small cell lung cancer PDX LX-95 model. Tumor cells were isolated from PDX tumors using a magnetic-activated cell sorting method to enrich human tumor cells and total RNA was extracted using the RNeasy Mini Kit (Qiagen). mRNA libraries were constructed and pair-ended sequenced using Illumina high-throughput sequencing technology. The length of sequence reads was 150 bp.The samples have 12 to 129 million pass filter reads with more than 90% of bases above the quality score of Q30. We found BET inhibitor increases expression of RPS6KA2, a gene that mediates crosstalk between MAPK and mTOR pathway.

2020-09-01 | GSE155923 | GEO