PDGF-C mediates the angiogenic and tumorigenic properties of fibroblasts associated with tumors refractory to anti-VEGF treatment.

By Yongping G. Crawford, I. Kasman, Lanlan Yu, Cuiling Zhong, Xiumin Wu, Z. Modrusan, J. Kaminker, N. Ferrara. Cancer Cell, 2009

618 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f540b8ab2e3e68f2c6455e5dae70efe1db009819

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Citations in the corpus

Regorafenib (BAY 73‐4506): A new oral multikinase inhibitor of angiogenic, stromal and oncogenic receptor tyrosine kinases with potent preclinical antitumor activity (2011, background): “Such responses include hypoxia-mediated induction of other proangiogenic factors, such as Ang1 and FGFs,(42,43) or upregulation of PDGF-C expression in tumor-associated fibroblasts.(44) Furthermore, TIE2-expressing monocytes (TEMs) appear to play an important role in tumor angiogenesis by secreting ”
Anti-angiogenic therapy for cancer: current progress, unresolved questions and future directions (2014, background): “Pre-clinical studies have identified numerous candidates including angiopoietins [129], Bv8; Bombina variagata peptide 8 [134], EGF; epidermal growth factor [135], the DeltaNotch pathway [136], FGF1 and FGF2; fibroblast growth factors 1 and 2 [137, 138], HGF; hepatocyte growth factor [139], IL-8; in”
Clonal Heterogeneity and Tumor Evolution: Past, Present, and the Future. (2017, positive): “Similar evidence in the field of anti-angiogenic therapies implicates the stroma in resistance to therapy through release of PDGF-C by cancer-associated fibroblasts (CAFs) (Crawford et al., 2009).”
Accessories to the crime: functions of cells recruited to the tumor microenvironment. (2012, neutral): “First, CAFs in different TMEs can produce a number of proangiogenic signaling proteins , including VEGF, FGF2 plus other FGFs, and IL-8/CXCL8 and PDGF-C; of note, PDGF-C may rescue angiogenesis in some anti-VEGF resistant tumors (Crawford et al., 2009).”
Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner. (2010, background): “Interestingly, CAFs can even mediate resistance to antiangiogenic therapy (Crawford et al., 2009).”
Targeting the tumour vasculature: insights from physiological angiogenesis (2010, background): “A recent report indicates that TAFs derived from tumours that are resistant to anti-VEGF drugs produced higher levels of pro-angiogenic factors (such as PDGFC, ANGPT2 and cyclooxygenase 2 (COX2)) than fibroblasts from tumours that respond to these agent”
Molecular mechanisms and clinical applications of angiogenesis (2011, background): “PDGF-CC, another family member released by cancer-associated fibroblasts in VEGF-inhibitor-resistant tumours, stimulates vessel growth and maturation, and attenuates the response to anti-VEGF treatmen”
Fibroblast heterogeneity in the cancer wound (2014, background): “Crawford et al. (2009) found that the expression of PDGF is up-regulated in CAFs from tumors that are resistant to anti-VEGF therapy and that a PDGF-neutralizing antibody impaired the observed anti-VEGF resistance, suggesting a crucial role for CAFs in mediating resistance to antiangiogenesis…”
Hallmarks of cancer: interactions with the tumor stroma. (2010, background): “Moreover, recent pre-clinical studies indicate that CAFs also mediate resistance to anti-angiogenic therapy and targeted therapy using tyrosine kinase inhibitors [39,40].”