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

Geou Yarh Liou; Peter Storz; Michael Leitges

doi:10.1080/23723556.2015.1035477

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

Geou Yarh Liou, Peter Storz, Michael Leitges

Cancer Biology

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

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-Kras^G12D-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 language	English (US)
Article number	e1035477
Journal	Molecular and Cellular Oncology
Volume	3
Issue number	1
DOIs	https://doi.org/10.1080/23723556.2015.1035477
State	Published - Jan 2 2016

Keywords

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

ASJC Scopus subject areas

Molecular Medicine
Cancer Research

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10.1080/23723556.2015.1035477

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

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.",

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AU - Leitges, Michael

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AB - 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.

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

Abstract

Keywords

ASJC Scopus subject areas

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