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Kidney Cancer PDOX Models

ABSTRACT: Kidney Cancer PDOX Models

PROVIDER: PRJNA662875 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12623253_1.fastq.gz	Fastqsanger.gz
	SRR12623253_2.fastq.gz	Fastqsanger.gz
	SRR12623254_1.fastq.gz	Fastqsanger.gz
	SRR12623254_2.fastq.gz	Fastqsanger.gz
	SRR12623255_1.fastq.gz	Fastqsanger.gz

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Kidney Cancer PDOX Models

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Molecular characterization of neuroendocrine prostate cancer organoids and PDOX by RNA-seq

Project description:We report the generation and characterization of tumor organoids and PDOX derived from needle biopsies of metastatic lesions from neuroendocrine prostate cancer patients.

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chromatin Remodeling in Patient-Derived Colorectal Cancer Models

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare the epigenomes of different patient-derived models of colorectal cancer (PDO, PDX and PDOX) to the original patient tumor. Methods: The Omni-ATAC protocol was utilized for ATAC library preparations. The nulcei were extracted from samples (PT, PDO, PDX and PDOX). For each sample set, three biological replicates were included. The libraries were sequenced using Illumina HiSeq 4000 PE 150bp. Results: Using an optimized data analysis workflow, we achieved high quality ATAC-seq library. Data were mapped to hg19 with over 90% mapping rate, and relative low mitochondria fraction (<30%). We used Diffbind to assess the chromatin accessibility enrichment in each model with a strict threshold of p <0.05 and |logFC|>1. Conclusions: Our study represents the first detailed analysis of CRC PDMC epigenome. CRC cells from all three models share chromatin alterations when compared to PT cells, representing a PT-PDMC epigenetic axis. Chromatin alterations in CRC cells are more similar betweeen PDOX and PDX than between PDOX and PDO, indicating that the growth environment of the model exerts strong influence on chraomtin adaptation in tumor cells.

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Generation and Integrated Analysis of Advanced Patient- derived Orthoxenograft Models (PDOX) for the Rational Assessment of Targeted Therapies in Endometrial Cancer

Project description:Clinical management of endometrial cancer (EC) is handicapped by the limited availability of second line treatments and bona fide molecular biomarkers to predict recurrence. These limitations have hampered the treatment of these patients, whose survival rates have not improved over the last four decades. The advent of coordinated studies such as the TCGA_UCEC have partially solved this issue, but the lack of proper experimental systems still represents a bottleneck that precludes translational studies from successful clinical testing in EC patients. Within this context, we present the first study reporting the generation of a collection of endometrioid EC patient-derived orthoxenograft (PDOX) mouse models that we believe can overcome these experimental constraints and pave the way towards state-of-the-art precision medicine in EC. We have characterized our collection of primary tumors and derived PDOXs through an integrative approach based on transcriptomics, mutational profiles and morphological analysis; and demonstrate that EC tumors engrafted in the mouse uterus retain the main molecular and morphological features from analogous tumor donors. Finally, we have harnessed the molecular properties of these tumors to assess the therapeutic potential of trastuzumab, a HER2 inhibitor with growing interest in EC, using patient-derived organotypic multicellular tumor spheroids and in vivo experiments.

2022-10-25 | GSE214657 | GEO

Generation and Integrated Analysis of Advanced Patient- derived Orthoxenograft Models (PDOX) for the Rational Assessment of Targeted Therapies in Endometrial Cancer

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Neuroendocrine prostate cancer models

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Patient-derived orthotopic xenograft models recapitulate the peritoneal dissemination of pancreatic cancer and delineate its transcriptional and regulatory programs [scATAC-seq]

Project description:BACKGROUND & AIMS: The mechanisms of peritoneal dissemination in pancreatic ductal adenocarcinoma (PDAC) remain unclear partly owing to the lack of patient-derived models that recapitulate this process. This study aimed to establish an orthotopic model of PDAC peritoneal dissemination and to uncover the transcriptional and regulatory programs underlying this process. METHODS: Organoids were established from primary pancreatic tumors and malignant effusions of patients with PDAC and orthotopically transplanted into the pancreas of immunodeficient mice to generate patient-derived orthotopic xenograft (PDOX) models. Subsequently, the organoids were rederived from pancreatic and peritoneal lesions of a representative model (PDOX12) and orthotopically reimplanted to assess the dissemination capacity. Single-nucleus RNA sequencing (snRNA-seq) and single-cell ATAC sequencing (scATAC-seq) were performed to analyze the tumors from these models. RESULTS: The organoids that were derived from malignant effusions reproducibly generated peritoneal metastases after orthotopic implantation. To dissect this process more precisely, we focused on one representative model (PDOX12) and rederived organoids from its pancreatic and peritoneal lesions. These organoids generated matched PDOX models that differed only in dissemination potential when reimplanted orthotopically. The results of snRNA-seq revealed a distinct subpopulation enriched in the high-dissemination model, which was characterized by the coordinated activation of genes involved in cytoskeletal dynamics, extracellular matrix remodeling, and plasticity-related signaling—suggesting a dissemination-primed state. Integration with scATAC-seq identified STAT3, SMAD3, and SOX2 as potential upstream regulators of this gene program. CONCLUSIONS: This study established PDOX models that isolate the peritoneal dissemination phenotype and reveal the transcriptional and regulatory programs driving this process.

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