Related Experiment Video

Updated: Jan 23, 2026

Isolation and Characterization of Patient-derived Pancreatic Ductal Adenocarcinoma Organoid Models
08:43

Isolation and Characterization of Patient-derived Pancreatic Ductal Adenocarcinoma Organoid Models

Published on: January 14, 2020

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Pancreatic Ductal Organoids React Kras Dependent to the Removal of Tumor Suppressive Roadblocks

Lukas Perkhofer1, Melanie Engler1, Johann Gout1

  • 1Department of Internal Medicine I, University Hospital Ulm, Albert Einstein Allee 23, 89081 Ulm, Germany.

Stem Cells International
|June 26, 2019
PubMed

Insights

Mouse pancreatic organoids were genetically modified to model pancreatic ductal adenocarcinoma (PDAC). PTEN and RNF43 deficiency enhanced KRAS-driven proliferation, offering new avenues for PDAC research.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) presents a significant challenge in oncology due to high mortality and increasing incidence.
  • PDAC development is a stepwise process involving precursor lesions and accumulating mutations, leading to genetic heterogeneity.
  • Modeling specific mutations and their functional impact in PDAC remains a challenge.

Purpose of the Study:

  • To establish and utilize genetically modified mouse pancreatic organoids for studying PDAC development.
  • To investigate the effects of specific genetic alterations, such as PTEN and RNF43 deficiency, in the context of oncogenic KRAS.
  • To explore the potential of organoids in recapitulating in vitro the in vivo characteristics relevant to PDAC.

Main Methods:

  • Isolation, culture, and genetic modification of ductal mouse organoids.
  • Introduction of key effectors implicated in the IPMN-PDAC sequence.
  • Assessment of cellular proliferation and self-renewal capacities.

Main Results:

  • Successfully established and developed tools for genetically modifying mouse pancreatic ductal organoids.
  • Demonstrated that PTEN and RNF43 deficiency significantly increases proliferative and self-renewal capacities.
  • Observed these effects in the context of oncogenic KRAS G12D mutation.

Conclusions:

  • Genetically modified mouse pancreatic organoids are a valuable tool for PDAC research.
  • PTEN and RNF43 deficiencies, alongside KRAS G12D, play crucial roles in promoting PDAC progression.
  • This study provides a foundation for future research focusing on ductal organoids in PDAC.

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