A bright future for protein kinase D1 as a drug target to prevent or treat pancreatic cancer

Geou Yarh Liou, Peter Storz, Michael Leitges

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Pancreatic ductal adenocarcinoma originates from acinar cells that undergo acinar-to-ductal metaplasia (ADM). ADM is initiated in response to growth factors, inflammation, and oncogene activation and leads to a de-differentiated, duct-like phenotype. Our recent publication demonstrated a transforming growth factor α-KrasG12D-protein kinase D1-Notch1 signaling axis driving the induction of ADM and further progression to pancreatic intraepithelial neoplasia. This suggests that protein kinase D1 might be an early marker for tumor development and a potential target for drug development.

Original languageEnglish (US)
Article numbere1035477
JournalMolecular and Cellular Oncology
Volume3
Issue number1
DOIs
StatePublished - Jan 2 2016

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Metaplasia
Pancreatic Neoplasms
Protein Kinases
Acinar Cell Carcinoma
Pharmaceutical Preparations
Transforming Growth Factors
Tumor Biomarkers
Oncogenes
Intercellular Signaling Peptides and Proteins
Inflammation
Phenotype
Neoplasms

Keywords

  • Acinar-to-ductal metaplasia
  • mechanisms of oncogenesis and tumor progression
  • mouse model
  • oncogenic Kras
  • pancreatic cancer
  • protein kinase D1

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Medicine

Cite this

A bright future for protein kinase D1 as a drug target to prevent or treat pancreatic cancer. / Liou, Geou Yarh; Storz, Peter; Leitges, Michael.

In: Molecular and Cellular Oncology, Vol. 3, No. 1, e1035477, 02.01.2016.

Research output: Contribution to journalArticle

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