Human Pancreatic Cancer-Associated Stellate Cells Remain Activated after in vivo Chemoradiation

Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extensive fibrotic reaction or desmoplasia and complex involvement of the surrounding tumor microenvironment. Pancreatic stellate cells are a key mediator of the pancreatic matrix and they promote progression and invasion of pancreatic c...

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Published inFrontiers in oncology Vol. 4; p. 102
Main Authors Cabrera, M Carla, Tilahun, Estifanos, Nakles, Rebecca, Diaz-Cruz, Edgar S, Charabaty, Aline, Suy, Simeng, Jackson, Patrick, Ley, Lisa, Slack, Rebecca, Jha, Reena, Collins, Sean P, Haddad, Nadim, Kallakury, Bhaskar V S, Schroeder, Timm, Pishvaian, Michael J, Furth, Priscilla A
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 01.01.2014
Subjects
Chemoradiotherapy
chemotherapy
gastrointestinal
Oncology
Pancreatic Cancer
Radiation
stellate cells
stellate cells
pancreatic cancer
gemcitabine
PDAC
radiation
chemotherapy
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Summary:Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extensive fibrotic reaction or desmoplasia and complex involvement of the surrounding tumor microenvironment. Pancreatic stellate cells are a key mediator of the pancreatic matrix and they promote progression and invasion of pancreatic cancer by increasing cell proliferation and offering protection against therapeutic interventions. Our study utilizes human tumor-derived pancreatic stellate cells (HTPSCs) isolated from fine needle aspirates of pancreatic cancer tissue from patients with locally advanced, unresectable pancreatic adenocarcinoma before and after treatment with full-dose gemcitabine plus concurrent hypo-fractionated stereotactic radiosurgery. We show that HTPSCs survive in vivo chemotherapy and radiotherapy treatment and display a more activated phenotype post-therapy. These data support the idea that stellate cells play an essential role in supporting and promoting pancreatic cancer and further research is needed to develop novel treatments targeting the pancreatic tumor microenvironment.
Bibliography:Reviewed by: Christopher James Bakkenist, University of Pittsburgh School of Medicine, USA; Joel S. Greenberger, University of Pittsburgh Medical Center-Shadyside, USA
This article was submitted to Radiation Oncology, a section of the journal Frontiers in Oncology.
Edited by: Joel S. Greenberger, University of Pittsburgh Medical Center Shadyside, USA
ISSN:2234-943X
2234-943X
DOI:10.3389/fonc.2014.00102