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A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

ABSTRACT: A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

PROVIDER: PRJNA1015702 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26045487_1.fastq.gz	Fastqsanger.gz
	SRR26045487_2.fastq.gz	Fastqsanger.gz
	SRR26045488_1.fastq.gz	Fastqsanger.gz
	SRR26045488_2.fastq.gz	Fastqsanger.gz
	SRR26045489_1.fastq.gz	Fastqsanger.gz

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A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities

2023-09-12 | GSE242998 | GEO

A Compendium of Syngeneic, Transplantable Pediatric High-Grade Glioma Models Reveals Subtype-Specific Therapeutic Vulnerabilities.

Project description:Pediatric high-grade gliomas (pHGG) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomic locations, and tumor subtypes. We developed models representing 16 pHGG subtypes driven by different combinations of alterations targeted to specific brain regions. Tumors developed with varying latencies and cell lines derived from these models engrafted in syngeneic, immunocompetent mice with high penetrance. Targeted drug screening revealed unexpected selective vulnerabilities-H3.3G34R/PDGFRAC235Y to FGFR inhibition, H3.3K27M/PDGFRAWT to PDGFRA inhibition, and H3.3K27M/PDGFRAWT and H3.3K27M/PPM1DΔC/PIK3CAE545K to combined inhibition of MEK and PIK3CA. Moreover, H3.3K27M tumors with PIK3CA, NF1, and FGFR1 mutations were more invasive and harbored distinct additional phenotypes, such as exophytic spread, cranial nerve invasion, and spinal dissemination. Collectively, these models reveal that different partner alterations produce distinct effects on pHGG cellular composition, latency, invasiveness, and treatment sensitivity.SignificanceHistone-mutant pediatric gliomas are a highly heterogeneous tumor entity. Different histone mutations correlate with different ages of onset, survival outcomes, brain regions, and partner alterations. We have developed models of histone-mutant gliomas that reflect this anatomic and genetic heterogeneity and provide evidence of subtype-specific biology and therapeutic targeting. See related commentary by Lubanszky and Hawkins, p. 1516. This article is highlighted in the In This Issue feature, p. 1501.

| S-EPMC10326601 | biostudies-literature

Proteomics of Mouse Syngeneic Models

Project description:The cell line-derived xenografts and patient derived xenografts have limited use in cancer immunotherapy evaluation because an immune compromised host is required for xenotransplantation. Syngeneic mouse models are derived by transplanting established mouse cell lines or tumor tissues to strain matched mouse hosts, which are better suited to study the interplay between immune and tumor cells. We investigated the differences as well as similarities of a panel of ten mouse syngeneic models to features of human tumors by proteomics, which will provide valuable information to assist experimental biologists in model selection.

2019-12-03 | PXD011885 | Pride

Functional Genomics Identifies Metabolic Vulnerabilities in Pancreatic Cancer [CRISPR Screen]

Project description:Purpose: Modeling microenvironmental influences in cell culture has been challenging, and technical limitations have hampered the comprehensive study of tumor-specific metabolism in vivo. To systematically interrogate metabolic vulnerabilities in PDA, we employed parallel CRISPR-Cas9 genetic screens using both in vivo and in vitro model systems. Methods: A custom library of lentiviral vectors encoding ~18,000 sgRNAs targeting ~3,000 mouse metabolic genes and performed CRISPR-Cas9 screens using a C/57BL6 (B6) mouse pancreatic cancer cell line derived from a KrasG12D-driven autochthonous PDA model. After transduction and selection, parallel screens were performed by in vitro passage or tumor implantation subcutaneously into the flanks of syngeneic hosts. Genomic DNA was then harvaested in vitro after 7 passages (21 days in culture) and in vivo 21 days after implantation. Results: This work revealed striking overlap of in vivo metabolic dependencies with those in vitro, validating that standard 2D culture conditions are a reliable system for studying cancer metabolism. Moreover, we identified that intercellular nutrient sharing can mask cancer dependencies in pooled screening experiments, highlighting an important limitation of this approach to study tumor metabolism Conclusions:Our work demonstrates the power of genetic screening approaches to define the compendium of in vivo metabolic dependencies in PDA and highlights critical metabolic pathways that may have therapeutic utility.

2020-10-01 | GSE158789 | GEO

A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials [microarray]

Project description:A cell line was derived from a mammary carcinoma in the transgenic FVB/N-Tg(MMTV-ErbB2)NDL2-5Mul mouse. The line, referred to as “NDL(UCD)” is adapted to standard cell culture and can be transplanted into syngeneic FVB/N mouse. The line maintains stable phenotype over multiple in vitro passages and rounds of in vivo transplantation. The cell line exhibits high expression of ErbB2 and ErbB3 and signaling molecules downstream ErbB2. The line was previously shown to be reactive to anti-immune checkpoint therapy with responses conducive to immunotherapy studies. Here, using both histology/immunophenotyping and gene expression/microarray analysis, we show that the syngeneic transplant tumors elicit an immune reaction in the adjacent stroma, with additional tumor infiltrating lymphocytes. We also show that this immune activating effect is greater in the syngeneic transplants than in the tumors arising in the transgenic mouse. We further analyzed the PD-1 and PD-L-1 expression in the model and found strong PD-L1 expression in the tumors and in vitro. Three distinct transplantable syngenic mouse models of mammary carcinoma were compared to identify differentially expressed genes.

2019-03-06 | GSE112723 | GEO

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IBD HIBEC and HILEC transcriptome compendium

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Gene expression profiling primary mouse mammary tumours from five different transplantable models

Project description:To delineate gene expression levels in whole non-metastatic and metastatic transplantable primary mouse mammary tumour allografts Abstract to be provided from publication

2013-01-01 | GSE42272 | GEO

Gene expression profiling primary mouse mammary tumours from five different transplantable models

Project description:To delineate gene expression levels in whole non-metastatic and metastatic transplantable primary mouse mammary tumour allografts Abstract to be provided from publication Primary mouse mammary tumours were grown till 400-600mm3 in size. Five different tumour models were analysed in triplicate. Thus, 3 different tumours/mice were used per model for a total of 15 mice. Each sample was applied to a separate microarray. Total RNA was prepared from whole primary tumours using Trizol reagent. Each sample was applied to Affymetrix gene expression arrays Mouse Gene 1.0ST.

2013-01-01 | E-GEOD-42272 | biostudies-arrayexpress

Gene expression profiling of a transplantable model of preneoplastic progression in mice using p53-null mammary epithelial cells

Project description:We show that macrophages are recruited to ductal hyperplasias that have a high tumor-forming potential where they are differentiated and polarized toward a tumor-promoting phenotype. These studies suggest that therapeutic targeting of tumor-promoting macrophages may not only be an effective strategy to block tumor progression and metastasis, but may also have critical implications for breast cancer prevention. To investigate mechanisms that drive tumorigenesis in early breast cancer progression, we employed a transplantable model of preneoplastic progression. Transplantation of p53-null mammary epithelial cells into the cleared mammary fad pads of syngeneic wildtype mice led to the formation of several premalignant lines that histologically and genetically recapitulated the various subtypes of human breast cancer. Two of these lines, PN1a and PN1b, were derived from contralateral outgrowths from the same mouse, and tissue from these outgrowths was serially transplanted for over 10 generations to confirm stability. At 16 weeks post-transplantation, PN1a lesions develop a poorly differentiated, lobuloalveolar morphology with multifocal regions of atypical cells in solid nests, while PN1b lesions remain low grade, ductal hyperplasia.

2017-06-04 | GSE84828 | GEO

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