In situ analysis of FGFR2 mRNA and comparison with FGFR2 gene copy number by dual-color in situ hybridization in a large cohort of gastric cancer patients

Kuboki, Yasutoshi; Schatz, Christoph A.; Koechert, Karl; Schubert, Sabine; Feng, Janine; Wittemer-Rump, Sabine; Ziegelbauer, Karl; Krahn, Thomas; Nagatsuma, Akiko Kawano; Ochiai, Atsushi

doi:10.1007/s10120-017-0758-x

Cited by 16 publications

(11 citation statements)

References 54 publications

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“…Gene amplification is a common cause for mRNA overexpression. In fact, a recent in situ analysis showed that FGFR2 mRNA is highly correlated with FGFR2 amplification in primary cases clinically, where a high expression level of FGFR2 is associated with poor survival rate of GC patients [76]. Recently, FGFR2 overexpression has been detected in a great portion of GC cases by immunohistochemistry staining, the high level FGFR2-IIIb isoform predicts poor overall survival in patients [19].…”

Section: Deregulation Of the Fgf-fgfr Signaling In Gastric Carcinomentioning

confidence: 99%

Targeting the Oncogenic FGF-FGFR Axis in Gastric Carcinogenesis

Zhang

Tang

Zhou

et al. 2019

Cells

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Gastric cancer (GC) is one of the most wide-spread malignancies in the world. The oncogenic role of signaling of fibroblast growing factors (FGFs) and their receptors (FGFRs) in gastric tumorigenesis has been gradually elucidated by recent studies. The expression pattern and clinical correlations of FGF and FGFR family members have been comprehensively delineated. Among them, FGF18 and FGFR2 demonstrate the most prominent driving role in gastric tumorigenesis with gene amplification or somatic mutations and serve as prognostic biomarkers. FGF-FGFR promotes tumor progression by crosstalking with multiple oncogenic pathways and this provides a rational therapeutic strategy by co-targeting the crosstalks to achieve synergistic effects. In this review, we comprehensively summarize the pathogenic mechanisms of FGF-FGFR signaling in gastric adenocarcinoma together with the current targeted strategies in aberrant FGF-FGFR activated GC cases.

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Section: Deregulation Of the Fgf-fgfr Signaling In Gastric Carcinomentioning

confidence: 99%

Targeting the Oncogenic FGF-FGFR Axis in Gastric Carcinogenesis

Zhang

Tang

Zhou

et al. 2019

Cells

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“…The amplified FGFR2 induces the activation of FGFR2 signaling. FGFR2 has been proposed as a target for targeted therapy of GC (Pearson et al, 2016;Kuboki et al, 2018;Kim et al, 2019). Yu et al (2018) revealed that overexpressed FGFR2 accelerated the production of cancer-initiating cells (CIC) and enhanced the resistance to lapatinib in HER2-positive GC cells.…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA ASNR Targeting miR-519e-5p Promotes Gastric Cancer Development by Regulating FGFR2

Chen

Yong

Tan

et al. 2021

Front. Cell Dev. Biol.

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Gastric cancer (GC), as a common gastrointestinal tumor, is an important cause of death from cancer all around the world. Long non-coding RNAs (lncRNAs), a novel class of transcripts, have attracted great attention of researchers. However, the mechanisms of the clinical significance of most lncRNAs in human cancer are mainly undocumented. This research desires to explore the clinical significance, biological function, and mechanism of Lnc_ASNR (apoptosis suppressing-non-coding RNA) in GC. Cell proliferation, cell cycle, cell migration, and invasion abilities were respectively determined by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT), flow cytometry, wound healing, and Transwell assay (Sigma-Aldrich, St. Louis, MO, United States). The association of Lnc_ASNR, miR-519e-5p, and fibroblast growth factor receptor 2 (FGFR2) was evaluated via luciferase reporter experiments. The tumor xenograft assay was conducted to confirm the results of cell experiments. High expressed Lnc_ASNR was detected in both GC cells and tissues using qRT-PCR. Downregulated Lnc_ASNR could reduce proliferation, migration, and invasion in GC cells, while upregulated Lnc_ASNR could promote the cell proliferation, migration, and invasion. Moreover, the effect of Lnc_ASNR on migration and invasion ability is closely related to epithelial-mesenchymal transition (EMT). The bioinformatics analysis, luciferase assay, and Western blot demonstrated that Lnc_ASNR inhibited miR-519e-5p expression but increased FGFR2 expression. Lnc_ASNR and FGFR2 were both targeted to miR-519e-5p, and they were negatively correlated with the expression of miR-519e-5p. All investigations indicated that Lnc_ASNR functioned as a ceRNA targeting miR-519e-5p and facilitated GC development by regulating the pathway of miR-519e-5p/FGFR2.

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“…Evaluation criteria for each immunohistochemical markers and RISH was described in Table S2. Evaluation criteria were referred from previous studies investigating each molecule [37][38][39][40].…”

Section: Evaluation Of Ihc and Rishmentioning

confidence: 99%

Dysregulation of PI3K/Akt/PTEN Pathway in Canine Mammary Tumor

Kim

Seung

Cho

et al. 2021

Animals

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The PI3K/Akt/PTEN axis is one of the most important signaling pathways in tumorigenesis. Recently, mutation of PIK3CA has been highlighted due to the similarities of mutational hotspots in both dogs and humans. PIK3CA H1047R (c.3140A > G) has been discovered as the most common mutational hot spot in canine mammary tumor in recent studies, while the feature of PIK3CA-mutated canine mammary tumor is obscure. Methods: A total of 83 mammary samples classified as normal (n = 13), adenoma (n = 25), low-grade carcinoma (n = 21), and high-grade carcinoma (n = 24) were included in this study. Genomic DNA from each sample was extracted, amplified by conventional PCR, and analyzed through Sanger sequencing. Analysis for the expression of PIK3CA, Akt, p-Akt, and PTEN was performed by immunohistochemistry, and of Akt2 by RNA in situ hybridization. Results: PIK3CA H1047R mutation was detected in 14.3% (10/70) of tumor samples. Dysregulation of p-Akt, Akt2, and PTEN was observed in mammary tumor samples, but only PTEN dysregulation was associated with PIK3CA H1047R mutation. Conclusions: The present study showed that dysregulation of components in the PI3K/Akt/PTEN pathway is a feature of canine mammary tumors, but this dysregulation is not directly correlated to the PIK3CA H1047R mutation except for PTEN expression.

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In situ analysis of FGFR2 mRNA and comparison with FGFR2 gene copy number by dual-color in situ hybridization in a large cohort of gastric cancer patients

Cited by 16 publications

References 54 publications

Targeting the Oncogenic FGF-FGFR Axis in Gastric Carcinogenesis

Targeting the Oncogenic FGF-FGFR Axis in Gastric Carcinogenesis

Long Non-coding RNA ASNR Targeting miR-519e-5p Promotes Gastric Cancer Development by Regulating FGFR2

Dysregulation of PI3K/Akt/PTEN Pathway in Canine Mammary Tumor

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