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Single cell analysis of an engineered organoid based model of pancreatic cancer identifies hypoxia as a contributing factor in the determination of transcriptional subtypes

ABSTRACT: Single cell analysis of an engineered organoid based model of pancreatic cancer identifies hypoxia as a contributing factor in the determination of transcriptional subtypes

PROVIDER: PRJNA1167332 | ENA |

REPOSITORIES: ENA

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Single cell analysis of an engineered organoid based model of pancreatic cancer identifies hypoxia as a contributing factor in the determination of transcriptional subtypes

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Analysis of an engineered organoid model of pancreatic cancer identifies hypoxia as a contributing factor in determining transcriptional subtypes.

Project description: Not available

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An engineered ovarian somatic organoid model exhibits age-dependent changes in cellular organization and function

Project description:Ovarian somatic cells are essential for tissue function, but there are no ex vivo models which maintain the cellular heterogeneity, in addition to the cell-cell and cell-matrix interactions of this compartment. We engineered a novel ovarian somatic organoid model in which a stroma-enriched fraction of primary mouse ovarian somatic cells was cultured in scaffold-free agarose micromolds. We sought to use this ovarian somatic organoid model to investigate mechanisms of ovarian aging and performed single cell RNA sequencing using primary ovarian somatic cells isolated from reproductively young and old mice, as well as organoids generated from young and old mice at days 1 and 6 of culture to assess age-dependent changes to cellular composition.

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Project description:Lung cancer is the leading cause of cancer-related death worldwide. Lung adenocarcinoma (LUAD), the most common histological subtype, accounts for 40% of all cases. While existing genetically engineered mouse models (GEMMs) recapitulate the histological progression and transcriptional evolution of human LUAD, they are time-consuming and technically demanding. In contrast, cell line transplant models are fast and flexible, but these models fail to capture the full spectrum of disease progression. Organoid technologies provide a means to create next-generation cancer models that integrate the most advantageous features of autochthonous and transplant-based systems. However, robust and faithful LUAD organoid platforms are currently lacking. Here, we describe optimized conditions to continuously expand murine alveolar type 2 cells (AT2), a prominent cell-of-origin for LUAD, in organoid culture. These organoids display canonical features of AT2 cells, including marker gene expression, the presence of lamellar bodies, and an ability to differentiate into the AT1 lineage. We used this system to develop flexible and versatile immunocompetent organoid-based models of KRAS, BRAF, and ALK-mutant LUAD. Notably, organoid-based tumors display extensive burden and complete penetrance, and are histopathologically indistinguishable from their autochthonous counterparts. Altogether, this organoid platform is a powerful, versatile new model system to study LUAD.

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RNA-sequencing of genetically engineered intestinal organoid lines modeling colorectal cancer (CRC) progression

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Prospective derivation of a 'Living Organoid Biobank' of colorectal cancer patients

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