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3' UTR RNA-sequencing of osimertinib vs. untreated Patient Derived Xenograft (PDX) models derived from EGFR-mutant lung tumors

ABSTRACT: 3' UTR RNA-sequencing of osimertinib vs. untreated Patient Derived Xenograft (PDX) models derived from EGFR-mutant lung tumors

PROVIDER: PRJEB41847 | ENA |

REPOSITORIES: ENA

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3' UTR RNA-sequencing of osimertinib vs. untreated Patient Derived Xenograft (PDX) models derived from EGFR-mutant lung tumors

Project description:Patient derived xenografts (PDXs) of human EGFR-mutant lung cancer were propagated in mice and treated with osimertinib or control to investigate the transcriptional adaption resposne.

2021-07-19 | E-MTAB-9888 | biostudies-arrayexpress

3' UTR RNA-sequencing of human EGFR-mutant lung cancer cell lines under osimertinib treatment

Project description:Human EGFR-mutant lung cancer cells lines were investigated for their dynamic transcriptional response upon treatment with EGFR-inhibitor osimertinib in a time-series experiment

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3' UTR RNA-seq of CRISPR-edited human EGFR-mutant PC9 lung cancer cell lines after osimertinib treatment

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ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts [PDX RNA-seq]

Project description:The majority of EGFR mutant lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors (TKIs). However, most of these responses are partial with drug tolerant residual disease remaining even at the time of maximal response. This residual disease ultimately leads to relapses which eventually develop in most patients. To investigate the cellular and molecular properties of residual tumor cells in vivo, we leveraged patient-derived models of EGFR mutant lung cancer. Subcutaneous EGFR mutant PDXs were treated with the 3rd generation TKI osimertinib until maximal tumor regression. Residual tissue inevitably harbored tumor cells that were transcriptionally, but not mutationally, distinct from bulk pre-treatment tumor. Using single cell transcriptional profiling we found evidence of cells matching the profiles of drug-tolerant cells present in the pre-treatment tumor. In one of the PDXs analyzed, osimertinib treatment caused dramatic transcriptomic changes that featured upregulation of the neuroendocrine lineage transcription factor ASCL1. Mechanistically, we found that ASCL1 confers drug tolerance by initiating an epithelial-to-mesenchymal gene expression program in permissive cellular contexts. Our study reveals fundamental insights into the biology of drug tolerance, the plasticity of cells through TKI treatment and explains why specific phenotypes are only observed in certain tumors.

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Transcriptomic analysis of sotorasib-resistant patient-derived xenograft (PDX) lung tumor cells

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Expression data from 27 Asian gastric patient-derived xenograft (PDX) models

Project description:There is a strong need to develop patient-derived xenograft (PDX) tumor models for studying new treatment options for gastric cancer (GC). With low engraftment success, few collections of GC PDX have been reported and molecular basis of the model establishment remain largely unknown. Here we established n=27 PDX models from n=100 GC tumors and compared their characteristics to GC patient tumors based on the recent work done by ACRG and TCGA, to evaluate the representativeness and relevance of the collection for drug testing. We show that MSI, CIN and MSS/TP53- tumors were preferentially established as PDX, while MSS/EMT and EBV not and that PDX models retained histology and molecular subtypes of parental tumors. By using synapse database, we identified 48 druggable alterations that could be investigated with the collection. Counting alterations for these 48 genes in PDX compared to TCGA tumors revealed models frequently classified with heavily altered tumors but well preserved genomic alteration patterns specific of each GC subtype. The molecular analysis of n=8/27 tumors and corresponding PDX at passage P1, P2 and P3 revealed variations in somatic alteration content both at single nucleotide and chromosomal level in highly unstable MSI and CIN tumors, with changes occurring mainly at P1. In two cases, we show likely emergence of rare subclones carrying known oncogenic alterations in KRAS and PIK3CA. Significance. This study presents a resource of fully annotated GC PDX models for anticancer agent testing. We show that beside close resemblance of PDX with parental tumors, not all subtypes are established, and that the clonal selection plays a key role the establishment of certain tumors. This may have a bearing on translation of observations into the clinic and underline the need to frequently survey the molecular characteristics of the PDX models.

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3' UTR RNA-sequencing of human EGFR-mutant lung cancer cell lines under osimertinib treatment

Project description:3' UTR RNA-sequencing of human EGFR-mutant lung cancer cell lines under osimertinib treatment

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Whole transcriptome profiling of 79 patient derived xenograft (PDX) models

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2016-03-01 | E-MTAB-3980 | biostudies-arrayexpress

Patient-derived xenograft platform for metastatic melanoma: RNA sequencing of 4 melanoma PDX samples

Project description:The therapeutic landscape of melanoma is rapidly changing. While targeted inhibitors yield significant responses, their clinical benefit is often limited by the early onset of drug resistance. This motivates the pursuit to establish more durable clinical responses, by developing combinatorial therapies. But while potential new combinatorial targets steadily increase in numbers, they cannot possibly all be tested in patients. Similarly, while genetically engineered mouse melanoma models have great merit, they do not capture the enormous genetic diversity and heterogeneity typical in human melanoma. Furthermore, whereas in vitro studies have many advantages, they lack the presence of micro-environmental factors, which can have a profound impact on tumor progression and therapy response. This prompted us to develop an in vivo model for human melanoma that allows for studying the dynamics of tumor progression and drug response, with concurrent evaluation and optimization of new treatment regimens. Here, we present a collection of patient-derived xenografts (PDX), derived from BRAFV600E, NRASQ61 or BRAFWT/NRASWT melanoma metastases. The BRAFV600E PDX melanomas were acquired both prior to treatment with the BRAF inhibitor vemurafenib and after resistance had occurred, including six matched pairs. We find that PDX resemble their human donors’ melanomas regarding biomarkers, chromosomal aberrations, RNA expression profiles, mutational spectrum and targeted drug resistance patterns. Mutations, previously identified to cause resistance to BRAF inhibitors, are captured in PDX derived from resistant melanomThis melanoma PDX platform represents a comprehensive public resource to study both fundamental and translational aspects of melanoma progression and treatment in a physiologically relevant setting.

2016-05-27 | GSE73737 | GEO

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