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A new mouse model of pancreatic cancer: PTEN gets its Akt together

Anirban Maitra1, Ralph H Hruban

  • 1The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.

Cancer Cell
|September 20, 2005
PubMed

Insights

Loss of PTEN (phosphatase and tensin homolog deleted on chromosome 10) in mice causes pancreatic metaplasia and a potential origin for pancreatic cancer. This study explores the PI3-K/Akt pathway

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • PTEN (phosphatase and tensin homolog deleted on chromosome 10) acts as a tumor suppressor by inhibiting the PI3-K/Akt pathway.
  • Loss-of-function PTEN mutations are implicated in various human solid cancers.
  • The role of PTEN in pancreatic ductal metaplasia and neoplasia requires further in vivo investigation.

Purpose of the Study:

  • To develop and characterize a murine model of conditional Pten inactivation in the pancreas.
  • To investigate the cellular origin and phenotype of Pten-deficient pancreatic metaplasia.
  • To establish a platform for studying PI3-K/Akt signaling in pancreatic cancer development.

Main Methods:

  • Conditional Pten gene inactivation in pancreatic cells of mice.
  • Histological and phenotypic analysis of pancreatic tissue.
  • In vivo modeling of pancreatic neoplasia.

Main Results:

  • Conditional Pten inactivation induced a significant metaplastic ductal phenotype.
  • Loss of differentiated acinar cells was observed.
  • Metaplastic "neoductules" originated from centroacinar cells.
  • A low frequency of invasive pancreatic adenocarcinomas developed.

Conclusions:

  • Conditional Pten loss in the pancreas drives metaplasia and provides a model for studying pancreatic cancer.
  • Centroacinar cells are a potential cell of origin for Pten-driven pancreatic neoplasia.
  • This model is valuable for exploring the PI3-K/Akt pathway's role in pancreatic cancer.

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