Project description:To characterize sotorasib resistance in lung adenocarcinomas (LUAD), we implanted pieces derived from a patient-derived KRAS-G12C positive xenograft (PDX) lung tumor model in immunocompromised mice

2023-03-05 | GSE204753 | GEO

Mayo GBM Patient Derived Xenograft National Resource

Project description:Genome wide DNA methylation profiling of GBM xenografts. The Illumina EPIC 850k Human DNA methylation array used to obtain DNA methylation profiles across approximately 800,000 CpGs in GBM xenograft samples. Samples included xx GBM xenografts.

2019-06-26 | GSE132650 | GEO

ASCL1 defines differentiation-competent GBM cells and directs neoplastic cells towards neuronal fate

Project description:We identified a subgroup of patient-derived glioblastoma (GBM) cells that express high levels of the neurogenic transcription factor, ASCL1, which predicts response to pharmacological inhibition of the Notch signaling pathway. Treatment of ASCL1hi GBM cells with a Notch signaling inhibitor induced a change in cell fate from neoplastic to neuronal. Importantly, acquisition of the neuronal fate was accompanied by a reduction in tumorigenic potential. Loss of ASCL1 in GBM cells rendered cells no longer responsive to Notch signaling inhibition and we determined ASCL1 is required for the competency of GBM cells to undergo neuronal differentiation. Enforced ASCL1 expression directed GBM cells towards a neuronal cell fate reminiscent of terminal differentiation. RNA-seq analysis of GBM cells treated with the Notch signaling inhibitor reveals neuronal target gene activation is associated with increased stoichiometric levels of ASCL1, suggesting threshold levels of ASCL1 in GBM cells governs neuronal differentiation. We demonstrate that neoplastic cells which retain expression of key neurogenic programs can have their fates redirected towards terminal differentiation. Directed fate specification to neuronal cell types by exploiting latent neurogenic programs may be a strategy to treat a subset of GBM patients. Our findings therefore highlight the potential of differentiation therapy for a subset of molecularly defined GBMs.

2017-07-21 | GSE96088 | GEO

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

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

| PRJEB11482 | ENA

Proteomic Profiling of Breast Cancer Patient-Derived Xenograft

Project description:Mass spectrometry profiling of orthotopically transplanted breast cancer patient-derived xenograft (PDX) tumors prior to chemotherapy treatment.

2022-12-06 | PXD035857 | Pride

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.

2020-07-15 | GSE115637 | GEO

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