Recurrent FGFR1 amplification and high FGFR1 protein expression in oral squamous cell carcinoma (OSCC)

Freier, Kolja; Schwäenen, Carsten; Sticht, Carsten; Flechtenmacher, Christa; Mühling, Joachim; Hofele, Christof; Radlwimmer, Bernhard; Lichter, Peter; Joos, Stefan

doi:10.1016/j.oraloncology.2006.01.005

Cited by 148 publications

(138 citation statements)

References 24 publications

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“…To test this hypothesis, we examined a large number of primary and metastatic head and neck squamous cell carcinoma to determine the prevalence of FGFR1 amplification in these tumors. We found an overall FGFR1 amplification rate of 15% in primary head and neck squamous cell carcinoma, which is close to the frequency described previously by Weiss et al 14 for squamous cell lung cancer and also by Freier et al 19 for oral squamous cell carcinomas. Mirroring our findings in lung cancers, 14 acquisition of FGFR1 amplification in head and neck squamous cell carcinoma showed a dose-dependent association with exposure to chemical carcinogens (eg smoking and, in the case of head and neck squamous cell carcinoma, alcohol abuse).…”

Section: Discussionsupporting

confidence: 91%

“…Given the histomorphological and clinical similarities between head and neck squamous cell carcinoma and squamous cell lung cancer, we proposed that FGFR1 might be involved in the pathogenesis and aggressiveness of head and neck squamous cell carcinoma. Supporting this hypothesis, Freier et al 19 recently reported FGFR1 amplifications in 17% of oral squamous cell carcinomas in a limited number of patient samples. Furthermore, initial functional studies describe a potential role of FGFRs in head and neck squamous cell carcinoma.…”

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confidence: 83%

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Fibroblast growth factor receptor 1 amplification is a common event in squamous cell carcinoma of the head and neck

et al. 2013

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 83%

Fibroblast growth factor receptor 1 amplification is a common event in squamous cell carcinoma of the head and neck

et al. 2013

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“…19 Up-regulation of other known oncogenes, such as CCND1 and FGFR genes, was also frequently found in OSCC. 19,22,23 In this study, we demonstrate that a chromatin remodeling factor, RSF-1, may be involved in tumor progression, and may confer disease aggressiveness in OSCC. Moreover, RSF-1 knockdown experiments showed that RSF-1 expression was essential for tumor cell growth and survival in RSF-1-overexpressing OSCC cells.…”

Section: Discussionmentioning

confidence: 58%

Overexpression of a Chromatin Remodeling Factor, RSF-1/HBXAP, Correlates with Aggressive Oral Squamous Cell Carcinoma

Fang

Huang

et al. 2011

The American Journal of Pathology

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RSF-1, also known as hepatitis B X-antigen associated protein (HBXAP), is a subunit of an ISWI chromatin remodeling complex, remodeling and spacing factor (RSF). Recent studies have provided new evidence that chromatin remodeling participates in the pathogenesis of neoplastic diseases by altering cell cycle regulation and gene expression. In this report, we studied the biological roles of RSF-1 in oral squamous cell carcinoma (OSCC), a highly invasive neoplastic disease. Based on IHC and quantitative real-time PCR, we demonstrated that RSF-1 expression could be detected in the majority of OSCC cases, and the levels were significantly higher in OSCC cells than in their normal counterparts. Moreover, expression levels of RSF-1 significantly correlated with the presence of angiolymphatic invasion, abnormal mitoses, metastasis, tumor recurrence, and advanced stage disease at presentation. Univariate and multivariate analyses showed a significant association of RSF-1 overexpression and worse overall survival in OSCC patients. RSF-1 knockdown remarkably decreased cellular proliferation and induced apoptosis in OSCC cells with high RSF-1 expression levels, but not in those without. Taken together, our results suggest that RSF-1 up-regulation is associated with several clinicopathological features of disease aggressiveness in OSCC patients, and RSF-1 plays an important role in maintaining cellular growth and survival in OSCC.

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“…Recent studies have demonstrated focal FGFR1 amplification in non-small cell lung carcinoma cells in 3% of lung adenocarcinomas and 21% of squamous cell carcinomas [60,61]. FGFR1 amplifications have been observed also in oral squamous carcinomas [62] and are found at a low incidence in ovarian cancer [63], bladder cancer [58] and rhabodomyosarcoma [64]. As to FGFR2, approximately 10% of gastric cancers show FGFR2 amplification, which is associated with poor prognosis in diffuse-type cancers [65].…”

Section: Gene Overexpression and Amplificationmentioning

confidence: 99%

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

Giacomini

Chiodelli

Matarazzo

et al. 2016

Pharmacological Research

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a b s t r a c tFibroblast growth factors (FGFs) are a family of pleiotropic factors produced by stromal and parenchymal tumor cells. Even though FGFs have been firstly characterized as angiogenic factors, they exert autocrine and paracrine functions not only on endothelial cells but also on tumor cells and other stromal components. Thus, the FGF/FGF receptor (FGFR) pathway may represent a key player in tumor growth by regulating the complex cross-talk between stromal and tumor compartments.The ligand dependent or independent activation of the FGF/FGFR system by gene upregulation, oncogenic mutation or amplification occurs in a variety of human tumors and is implicated in various key steps of tumor growth and progression. In addition, FGF/FGFR activation has been described as a mechanism of tumor escape in response to antiangiogenic/anti-VEGF therapies.Experimental and clinical evidences provide a compelling biologic rationale for the development of anti-FGF/FGFR targeting agents in cancer therapy. However, the development of drugs specifically targeting the FGF/FGFR pathway proved to be difficult, also due to the high redundancy and pleiotropic effects of FGF and FGFR family members. On the other hand, the possibility to develop "two-compartment" targeting agents endowed with both antiangiogenic and antitumor activities remains promising.Here we will review the preclinical and clinical approaches and potential therapeutics currently available to block the FGF/FGFR system in human cancer.

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Recurrent FGFR1 amplification and high FGFR1 protein expression in oral squamous cell carcinoma (OSCC)

Cited by 148 publications

References 24 publications

Fibroblast growth factor receptor 1 amplification is a common event in squamous cell carcinoma of the head and neck

Fibroblast growth factor receptor 1 amplification is a common event in squamous cell carcinoma of the head and neck

Overexpression of a Chromatin Remodeling Factor, RSF-1/HBXAP, Correlates with Aggressive Oral Squamous Cell Carcinoma

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

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