Cancer-associated stromal fibroblasts promote pancreatic tumor progression.

By R. Hwang, T. Moore, Thiruvengadam Arumugam, V. Ramachandran, Keith D. Amos, A. Rivera, B. Ji, Douglas B. Evans, C. Logsdon. Cancer Research, 2008

1,082 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/48cb64491432bc4eca3e8588e5beeb0ad7238d38

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Citations in the corpus

CANCER-ASSOCIATED FIBROBLAST EXOSOMES REGULATE SURVIVAL AND PROLIFERATION OF PANCREATIC CANCER CELLS (2016, neutral): “They were previously believed to serve merely a passive role in PDAC drug resistance, impeding drug delivery by physically blocking cytotoxic chemotherapeutics from reaching their target epithelial cells (6, 7).”
Fibroblast heterogeneity in the cancer wound (2014, background): “…has been shown to mediate chemotherapy resistance (Singh et al., 2010; Domanska et al., 2012), and furthermore, pancreatic stellate cells drive resistance to chemotherapyinduced apoptosis and radiation-induced apoptosis via a mechanism involving activation of the AKT pathway (Hwang et al., 2008).”
Recent progress in pancreatic cancer (2013, background): “In addition, much has been learned about the supportive tumor-stromal cell environment that is thought to not only influence the development of pancreatic cancer progression but which also supports mechanisms for resistance to effective treatment given its inherent protective properties.(208,209) Th”
Cancer-Associated Fibroblasts: Their Characteristics and Their Roles in Tumor Growth (2015, background): “These results demonstrate that CAFs affect the sensitivity of drugs by secretion of various factors [100].”
Stromal biology and therapy in pancreatic cancer (2010, background): “44 Interestingly, PSCs have emerged as pancreasspecific mesenchymal cells and important regulators of desmoplasia in pancreatic cancer.(36) 45 PSCs share many morphological and functional characteristics with hepatic stellate cells (HSCs) whose central role in liver fibrosis is well established.”
IL-1-induced JAK/STAT signaling is antagonized by TGF-β to shape CAF heterogeneity in pancreatic ductal adenocarcinoma. (2018, background): “The secretory phenotype of iCAFs suggest a role for this CAF subtype in promoting tumor progression, chemoresistance and other cancer-associated systemic effects, such as cachexia and immune suppression (6,9,11,21-24,38,45,46).”
Vitamin D Receptor-Mediated Stromal Reprogramming Suppresses Pancreatitis and Enhances Pancreatic Cancer Therapy (2014, positive): “CAFs enhance PDA growth in allograft models in part via paracrine activation of pro-survival pathways in tumor cells, and inhibition of tumor-stroma interactions limits tumor progression (Hwang et al., 2008; Ijichi et al., 2011; Vonlaufen et al., 2008).”
Epithelial to Mesenchymal Transition Contributes to Drug Resistance in Pancreatic Cancer (2009, background): “Furthermore, pancreatic cancer is exemplified by the presence of an extensive tumor-associated stroma, and recent studies have confirmed that stromal cells also contribute to drug resistance (47).”
The Pancreas Cancer Microenvironment (2012, background): “coinjection of PaSCs with tumor cells in orthotopic models of PDA increases tumor size and causes ahigher incidence of metastasis (25, 33).”
The brain tumor microenvironment (2011, background): “Stromal fibroblasts activated by their associated tumor cells have been identified by several reports to play a key role in the induction of angiogenesis and metastasis in melanoma (Gallagher et al., 2005; Goldstein et al., 2005) and pancreatic cancers (Hwang et al., 2008).”
Stromal elements act to restrain, rather than support, pancreatic ductal adenocarcinoma. (2014, background): “Such studies, which have mostly relied on cell transplantation or in vitro assays, have affirmed that the stroma plays a supportive role in of pancreatic cancer progression (Bailey et al., 2008; Feldmann et al., 2008a, 2008b; Hwang et al., 2008; Ikenaga et al., 2010; Lonardo et al., 2012; Xu et al.,”