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• W2944934418 abstract "Pancreatic ductal adenocarcinoma (PDAC) is still the Achilles heel in modern oncology, with an increasing incidence accompanied by a persisting high mortality. The developmental process of PDAC is thought to be stepwise via precursor lesions and sequential accumulation of mutations. Thereby, current sequencing studies recapitulate this genetic heterogeneity in PDAC and show besides a handful of driver mutations (KRAS, TP53) a plethora of passenger mutations that allow to define subtypes. However, modeling the mutations of interest and their effects is still challenging. Interestingly, organoids have the potential to recapitulate in vitro , the in vivo characteristics of the tissue they originate from. Here, we could establish and develop tools allowing us to isolate, culture, and genetically modify ductal mouse organoids. Transferred to known effectors in the IPMN-PDAC sequence, we could reveal significantly increased proliferative and self-renewal capacities for PTEN and RNF43 deficiency in the context of oncogenic KRAS G12D in mouse pancreatic organoids. Overall, we were able to obtain promising data centering ductal organoids in the focus of future PDAC research." @default.
• W2944934418 created "2019-05-29" @default.
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• W2944934418 date "2019-05-19" @default.
• W2944934418 modified "2023-09-23" @default.
• W2944934418 title "Pancreatic Ductal Organoids React Kras Dependent to the Removal of Tumor Suppressive Roadblocks" @default.
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• W2944934418 doi "https://doi.org/10.1155/2019/2079742" @default.
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