Retinoic Acid–Induced Pancreatic Stellate Cell Quiescence Reduces Paracrine Wnt–β-Catenin Signaling to Slow Tumor Progression

Froeling, Fieke E. M.; Feig, Christine; Chelala, Claude; Dobson, Richard; Mein, Charles E.; Tuveson, David A.; Clevers, Hans; Hart, Ian R.; Kocher, Hemant M.

doi:10.1053/j.gastro.2011.06.047

Cited by 328 publications

(332 citation statements)

References 38 publications

Supporting

Mentioning

316

Contrasting

Unclassified

Order By: Relevance

“…44,45 The inhibition or reversion of the PSC activation process, as well as induction of apoptosis in activated PSCs represent a promising new strategy for reducing fibrogenesis.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous characterization of pancreatic stellate cells and other pancreatic components within three-dimensional tissue environment during chronic pancreatitis

Hu¹,

2013

J. Biomed. Opt

View full text Add to dashboard Cite

“…44,45 The inhibition or reversion of the PSC activation process, as well as induction of apoptosis in activated PSCs represent a promising new strategy for reducing fibrogenesis.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous characterization of pancreatic stellate cells and other pancreatic components within three-dimensional tissue environment during chronic pancreatitis

Hu¹,

2013

J. Biomed. Opt

View full text Add to dashboard Cite

“…These mediators in turn lead to increased aggressiveness of surrounding cancer cells [61][62][63][64][65] . The importance of this crosstalk between PSC and pancreatic cancer cells is demonstrated by the fact, that restoration of PSC quiescence profoundly affects cancer cells in proximity [66] . Furthermore, we were able to show that an epithelial-stromal crosstalk mediated by the transcription factor ETV1 regulates stromal expansion, epithelial to mesenchymal transition and metastatic spread underscoring the importance of the stromal compartment in regulating epithelial plasticity [67] .…”

Section: Mechanisms Of Cellular Plasticitymentioning

confidence: 99%

Cellular Plasticity and Heterogeneity in Pancreatic Regeneration and Malignancy

2017

Can Cell Microenviron

View full text Add to dashboard Cite

Pancreatic regeneration in response to tissue injury is a complex process. Recent progress in the understanding of this process has underscored the need for cellular plasticity as a prerequisite in the course of regeneration. A number of different pancreatic cell types have been proposed as progenitors, stem cells or differentiated cells with a high degree of plasticity. Moreover, in the setting of an oncogenic mutation, similar mechanisms appear to drive pancreatic tumorigenesis. Here, we aim to summarize the recent advances in our understanding of cellular plasticity in the setting of regeneration and tumorigenesis.

show abstract

“…(21). In transgenic mice models, VDR activation reduced inflammatory markers and fibrosis, and increasing intratumoral gemcitabine level, Froeling et al showed that treatment with all-trans retinoic acid (ATRA) induced CAFs quiescence, leading to reduced cancer cell proliferation and invasion, and increased apoptosis via Wnt-β-catenin signaling (48).…”

Section: Cancer-associated Fibroblasts (Cafs)mentioning

confidence: 99%

Targeting stromal microenvironment in pancreatic ductal adenocarcinoma: controversies and promises

Mei¹,

Du²,

Wee³

2016

J. Gastrointest. Oncol.

View full text Add to dashboard Cite

Pancreatic cancer is a highly lethal disease. Conventional therapeutics targeting pancreas cancer cell compartment using cytotoxics improved patient survival but at the expense of significant toxicity.Microscopically, the tumor is characterized by thick desmoplastic stroma that surrounds islands of pancreatic cancer cells. The tumor microenvironment has been found to play important roles in carcinogenesis, the development of drug resistance, and mediating immunosuppression. The understanding the tumor-stromal interaction has led to the development of novel therapeutic approaches. Here, we review the strategies that are currently in (or, near to) clinical evaluation and the underlying preclinical rationales.

show abstract

Retinoic Acid–Induced Pancreatic Stellate Cell Quiescence Reduces Paracrine Wnt–β-Catenin Signaling to Slow Tumor Progression

Cited by 328 publications

References 38 publications

Simultaneous characterization of pancreatic stellate cells and other pancreatic components within three-dimensional tissue environment during chronic pancreatitis

Simultaneous characterization of pancreatic stellate cells and other pancreatic components within three-dimensional tissue environment during chronic pancreatitis

Cellular Plasticity and Heterogeneity in Pancreatic Regeneration and Malignancy

Targeting stromal microenvironment in pancreatic ductal adenocarcinoma: controversies and promises

Contact Info

Product

Resources

About