Immunocytochemical localization of fibroblast growth factor‐1 (FGF‐1) and FGF‐2 in oral squamous cell carcinoma (SCC)

Myoken, Yoshinari; Okamoto, Tomoyoshi; Jd, Sato; Takada, Kazuaki

doi:10.1111/j.1600-0714.1994.tb00443.x

Cited by 50 publications

(28 citation statements)

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“…Bansal et al (7) reported that the expression of FGF-1 is lower in breast cancer than in the normal human breast. Myoken et al (31) showed stronger expression of FGF-2 in oral squamous cell carcinomas than in normal tissue. Chow et al (14) demonstrated strong expression of FGF-1 and FGF-2 in normal liver cells, but weak expression of these factors in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of the fibroblast growth factor receptor-1 gene correlates with liver metastasis in colorectal cancer

Sato

Oshima²,

Yoshihara³

et al. 1994

Oncol Rep

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Abstract. Expression of the fibroblast growth factor (FGF)-1, FGF-2, fibroblast growth factor receptor (FGFR)-1, andFGFR-2 genes has been reported in various cancers and is associated with poor outcomes in patients with solid tumors. This study examined the relations between the relative expression of the FGF genes and clinicopathological factors, especially invasion and metastasis, in patients with colorectal cancer. We studied surgical specimens of cancer tissue and adjacent normal mucosa obtained from 202 patients with untreated colorectal carcinoma. The relative expression levels of FGF-1, FGF-2, FGFR-1, and FGFR-2 mRNA in cancer and in normal adjacent mucosa were measured by quantitative real-time, reverse-transcription polymerase chain reaction. The relative expression level of the FGFR-2 gene was higher in normal adjacent mucosa than in cancer, whereas the relative expression levels of the FGF-1, FGF-2, and FGFR-1 genes were similar. FGFR-1 gene expression levels were higher in the presence than in the absence of liver metastasis. An analysis of the relation between clinicopathological features and gene expression showed that overexpression of FGFR-1 correlated with liver metastasis. Our results suggested that overexpression of the FGFR-1 gene might lead to liver metastasis in colorectal cancer. Overexpression of the FGFR-1 gene may thus be a useful predictor of liver metastasis in patients with colorectal cancer. IntroductionFibroblast growth factors (FGFs) are a family of heparinbinding growth factors. FGFs promote angiogenesis by interacting with various endothelial cell-surface receptors, including tyrosine kinase receptors, heparin-sulfate proteoglycans, and integrins. The relation between angiogenesis and tumor growth is well established, and numerous inducers of angiogenesis have been identified (1). Gospodarowicz (2) discovered FGF-2 in 1974. This protein was found to strongly promote the proliferation of fibroblasts. Since then, 22 structurally-related members of the FGF family and 4 FGFhomologous factors have been identified. FGFs exert their biological activities by binding to high-affinity tyrosine kinase FGF receptors (FGFRs) on the surface of target cells. Angiogenic potential has been assessed for only a limited number of the 22 members of the FGF family in vitro and in vivo. Most experimental studies have focused on the prototypes FGF-1 and FGF-2 (3).FGFs exert their biologic activity by interacting with highaffinity FGFRs. Four members of the FGFR family (FGFR-1, FGFR-2, FGFR-3, and FGFR-4) are encoded by distinct genes, and their structural variability is increased by alternative splicing. FGFR-1 is expressed by endothelial cells in vivo and in vitro. Some cultured endothelial cells can express FGFR-2 (3,4).Expression levels of the FGF-1, FGF-2, FGFR-1, and FGFR-2 genes have been examined in various cancers, including breast cancer (5-8), brain tumors (9-12), hepatocellular carcinoma (13-15), cervical and esophageal cancers (16-20), and pancreatic cancer (21-23). Correlations between FGF...

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Section: Discussionmentioning

confidence: 99%

Overexpression of the fibroblast growth factor receptor-1 gene correlates with liver metastasis in colorectal cancer

Sato

Oshima²,

Yoshihara³

et al. 1994

Oncol Rep

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“…For example, high expression levels of FGF2, a well-characterized angiogenic factor, but also FGF1, FGFR1 and FGFR2, have been linked to the progression of HNSCC. [22][23][24] However, a role for FGFR4 in this type of tumor has not yet been determined.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the FGFR4 Arg388 allele in head and neck squamous cell carcinoma

Streit

Bange²,

Fichtner

et al. 2004

Intl Journal of Cancer

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After decades of rigorous investigations of chemotherapeutic cancer therapies, many cancers, including those of the head and neck, remain beyond our clinical ability to control them. From 3% to 5% of all patients initially cured of early-stage head and neck cancer will develop second primary tumors or local recurrences. 1 This phenomenon has been explained by the concept of field cancerization, which argues that certain risk factors such as alcohol and tobacco change the lining of the upper aerodigestive tract into a so-called condemned mucosa. In such a scenario, alcohol may represent the key risk factor for neoplastic transformation in the oral cavity, the oro-and hypopharynx. [2][3][4] An increasing amount of evidence suggests that alcohol intake and smoking play a synergistic role in the neoplastic progress.One of the most important achievements of molecular oncology has been the demonstration that cancer represents a genetic disease that begins with genetic damages in the genome of one cell in the form of point mutations, DNA rearrangement and gene amplification leading to the distortion of the expression and biochemical function of respective gene products. Growth factor receptors of the class I subfamily, which include the epidermal growth factor receptor (EGFR/HER1) and the related proteins HER2, HER3 and HER4, have shown that amplification or overexpression of those receptors, especially well documented for HER2 in patients with breast and ovarian cancers, plays an important role in carcinogenesis and tumor progression. [5][6][7][8] Multivariate survival analysis showed that HER2 amplification or overexpression is more predictive of clinical outcome than all other known prognosticators with the exception of positive lymph nodes. 9,10 These findings have validated the HER2 receptor as a target for therapeutic intervention. Moreover, recent clinical investigations have confirmed the benefit of antagonistic HER2 antibody therapy in breast cancer using herceptin. 11 Minute genetic changes such as point mutations have been found to cause constitutive activation of the HER2/neu kinase activity and to induce neoplastic disorders. 12 Similarly, the 2 amino acid substitutions Gly380Arg and Ala391Glu in the transmembrane domain of fibroblast growth factor receptor 3 (FGFR3) have been shown to be responsible for 2 forms of human dwarfism, namely, achondroplasia and morbus crouzon. [13][14][15] Other mutations in the FGFR3 gene have been associated with bladder and cervix cancer. 16 The FGFR signaling system is composed of 4 receptor tyrosine kinases (RTKs) and more than 20 known ligands and has been implicated in the regulation of a multitude of both physiologic and pathophysiologic processes, including migration, wound healing, angiogenesis and cancer. 17 More recently, we have identified a single nucleotide polymorphism (SNP) in codon 388 of the FGFR4 gene, which plays a pivotal role in the progression of breast cancer. This SNP is present at a significantly higher rate in breast cancer patients with early relap...

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“…Studies on Hox gene expression in chick embryos show that FGF modified the expressions of Hoxa2, b6-9, c6-9 and d9 (26)(27)(28)(29). The expression levels of FGF-1 nad FGF-2 are higher in SCC than in normal oral mucosa (30), and high affinity receptors for FGFs, FGFR2 and FGFR3, are highly expressed in dysplasia and SCC compared to those in normal mucosa (31). We showed here that the expression levels of HOXC6 were significantly higher in Sample code Histology T pN Location #11 C11 SCC 1 0 Tongue #14 C14 SCC 1 0 Tongue #20 C20 SCC 1 0 Tongue #25 C25 SCC 1 0 Tongue #1 C1 SCC 2 0 Tongue #3 C3 SCC 2 0 Tongue #5 C5 SCC 2 0 Tongue #10 C10 …”

Section: Discussionmentioning

confidence: 99%

Aberrant Expression of HOX Genes in Oral Dysplasia and Squamous Cell Carcinoma Tissues

et al. 2006

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Human HOX genes consist of 39 genes and encode transcription factors that function as master developmental regulators. We hypothesized that the misexpression of HOX genes was associated with carcinogenesis and malignant progression. The expression levels of 39 HOX genes in 31 human oral squamous cell carcinoma (SCC), 11 dysplasia and 10 normal mucosa tissues were quantified by the real-time RT-PCR method. The expression levels of 18 HOX genes in the SCC tissues were significantly higher than those in the normal mucosa tissues. The dysplasia tissues showed higher expression of HOXA2, A3, B3 and D10 than normal mucosa tissues whereas they showed lower expression of HOXA1, B7, B9 and C8 than SCC. The SCC with lymph node metastasis showed high expression of HOXC6 compared to the SCC without it.These results suggest that misexpressions of particular HOX genes are implicated in the development of oral dysplasia and SCC.2

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Immunocytochemical localization of fibroblast growth factor‐1 (FGF‐1) and FGF‐2 in oral squamous cell carcinoma (SCC)

Cited by 50 publications

References 28 publications

Overexpression of the fibroblast growth factor receptor-1 gene correlates with liver metastasis in colorectal cancer

Overexpression of the fibroblast growth factor receptor-1 gene correlates with liver metastasis in colorectal cancer

Involvement of the FGFR4 Arg388 allele in head and neck squamous cell carcinoma

Aberrant Expression of HOX Genes in Oral Dysplasia and Squamous Cell Carcinoma Tissues

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