2018
DOI: 10.1016/j.urolonc.2018.05.020
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FGF-2 is a driving force for chromosomal instability and a stromal factor associated with adverse clinico-pathological features in prostate cancer

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Cited by 16 publications
(11 citation statements)
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References 27 publications
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“…It will be of interest to compare FGFR3-L and FGFR3-S in terms of dimer structure, receptor orientation, transmembrane separation, conformation sampling, and monomer versus dimer status in future studies. Dovitinib is a multi-target RTK SMI that has shown antitumor activity in preclinical and clinical models of solid tumors, including prostate cancer (41)(42)(43)(44). While dovitinib failed a critical phase III trial in metastatic renal cell carcinoma, recent efforts have been taken to identify and select potential responders (e.g., patients with driver FGFR alterations) in future clinical trials.…”
Section: Discussionmentioning
confidence: 99%
“…It will be of interest to compare FGFR3-L and FGFR3-S in terms of dimer structure, receptor orientation, transmembrane separation, conformation sampling, and monomer versus dimer status in future studies. Dovitinib is a multi-target RTK SMI that has shown antitumor activity in preclinical and clinical models of solid tumors, including prostate cancer (41)(42)(43)(44). While dovitinib failed a critical phase III trial in metastatic renal cell carcinoma, recent efforts have been taken to identify and select potential responders (e.g., patients with driver FGFR alterations) in future clinical trials.…”
Section: Discussionmentioning
confidence: 99%
“…Results of a recent study indicate that high FGF2 levels in osteoblasts (secondary to Tgfβ receptor 2 (Tgfβr2) loss) promote prostate cancer bone metastases in mice (Meng et al 2018). Prostate stromal cells express biologically relevant levels of FGF2, and therefore the increase in FGF2 in the bone microenvironment may promote prostate cancer cell growth by providing a prostate-like environment (Kwabi-Addo et al 2004, Pecqueux et al 2018. Together these studies suggest that loss of Tgfβr2 expression in osteoblasts enables FGF2-mediated crosstalk with prostate cancer cells and promotes bone metastasis (Meng et al 2018).…”
Section: R261 E Labanca Et Almentioning
confidence: 99%
“…The TME, the 'soil' of tumor growth, is composed of cancer cells and various interstitial cells, including the extracellular matrix, proteolytic enzymes, cytokines and chemokines, and interacts with tumors by altering the proteome and degradome (8)(9)(10). As a prominent member of the stroma and as the most stromal or interstitial cells in the TME, CAFs have their own gene expression profiles that are different from NFs, and interact with cancer cells via a variety of signals to affect the TME, tumorigenesis, development and therapeutic tolerance of cancer cells (11)(12)(13), which are also associated with the prognosis of various tumors by expressing FAP, FGF-2, IL-1β-IRAK4 and Podoplanin (15,16,(40)(41)(42)(43)(44). Notably, the presence of reactive stroma in the TME, particularly in CAFs, was revealed to affect the tumor treatment effectiveness and was associated with tumor drug resistance (17)(18)(19)(20).…”
Section: Univariate Analysis Multivariate Analysis ------------------mentioning
confidence: 99%