Detection of<i>CCNE1/URI</i>(19q12) amplification by<i>in situ</i>hybridisation is common in high grade and type II endometrial cancer

Noske, Aurelia; Brandt, Simone; Valtcheva, Nadejda; Wagner, Ulrich; Zhong, Qing; Bellini, Elisa; Fink, Daniel; Obermann, Ellen C.; Moch, Holger; Wild, Peter J.

doi:10.18632/oncotarget.11605

Cited by 18 publications

(14 citation statements)

References 25 publications

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“…In accordance with the present study, amplification of CCNE1 was reported to be significantly associated with high grade EEC and non-endometrioid EC (35). More notably, the expression level of CCNE1 in poorly differentiated EAC cell line was detected as higher compared with in well-differentiated EAC cell line (1.6±0.19 vs. 1.4±0.33) (1).…”

Section: Discussionsupporting

confidence: 89%

Bioinformatics analysis of key differentially expressed genes in well and poorly differentiated endometrial carcinoma

et al. 2018

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Endometrial carcinoma (EC) is one of the most common gynecological malignancies. The malignant degree increases between grade (G)1 and G3, and EC of G3 usually presents a high recurrence rate and poor prognosis. Therefore, the present study aimed to examine the principal genes associated with the degree of differentiation in EC. The microarrays GSE17025, GSE24537 and GSE35784, representing data of Type I EC samples of G1 and G3, were downloaded from the Gene Expression Omnibus. The differentially expressed genes (DEGs) and differentially expressed micro (mi)RNAs (DEMs) were identified, followed by functional enrichment analyses and interaction network construction. In total, 83 upregulated and 130 downregulated DEGs with the same expression trends in two mRNA datasets were screened. The upregulated DEGs were primarily enriched in 'mitotic cell cycle process', 'cell cycle process' and 'mitotic cell cycle'; while the downregulated DEGs were enriched in 'cellular component assembly involved in morphogenesis', 'cell projection organization' and 'microtubule‑based movement'. From the protein‑protein interaction network, DNA topoisomerase IIα, kinesin family member 11, cyclin B1 and BUB1 mitotic checkpoint serine/threonine were identified as foremost hub genes. One module was extracted and involved in 'mitotic cell cycle process' and 'cell cycle process'. Based on the analysis of DEMs and the miRNA‑target regulatory network, miRNA‑9 may be the most important upregulated DEM, and the DEGs forkhead box P1 and cyclin E1 may serve vital roles in the differentiation of EC. In conclusion, principal genes were identified that may be determinants of the carcinogenesis of poorly differentiated EC, which may facilitate the examination of potential molecular mechanisms. These genes may additionally help identify candidate biomarkers and novel therapeutic targets for poorly differentiated EC.

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Section: Discussionsupporting

confidence: 89%

Bioinformatics analysis of key differentially expressed genes in well and poorly differentiated endometrial carcinoma

et al. 2018

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“…Tumors with poor DNA quality were excluded from the study. Genome-wide DNA copy-number alterations and allelic imbalances of 33 chRCC were determined using the Affymetrix OncoScan ® CNV Assay (Affymetrix/Thermo Fisher Scientific, Waltham, MA, USA) as previously described [33]. The demographic and clinicopathological characteristics for 33 Swiss chRCCs with clinical data are summarized in Table 1.…”

Section: Methodsmentioning

confidence: 99%

Classic Chromophobe Renal Cell Carcinoma Incur a Larger Number of Chromosomal Losses Than Seen in the Eosinophilic Subtype

Ohashi

Schraml

Angori

et al. 2019

Cancers

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Chromophobe renal cell carcinoma (chRCC) is a renal tumor subtype with a good prognosis, characterized by multiple chromosomal copy number variations (CNV). The World Health Organization (WHO) chRCC classification guidelines define a classic and an eosinophilic variant. Large cells with reticular cytoplasm and prominent cell membranes (pale cells) are characteristic for classic chRCC. Classic and eosinophilic variants were defined in 42 Swiss chRCCs, 119 Japanese chRCCs and in whole-slide digital images of 66 chRCCs from the Cancer Genome Atlas (TCGA) kidney chromophobe (KICH) dataset. 32 of 42 (76.2%) Swiss chRCCs, 90 of 119 (75.6%) Japanese chRCCs and 53 of 66 (80.3%) TCGA-KICH were classic chRCCs. There was no survival difference between eosinophilic and classic chRCC in all three cohorts. To identify a genotype/phenotype correlation, we performed a genome-wide CNV analysis using Affymetrix OncoScan® CNV Assay (Affymetrix/Thermo Fisher Scientific, Waltham, MA, USA) in 33 Swiss chRCCs. TCGA-KICH subtypes were compared with TCGA CNV data. In the combined Swiss and TCGA-KICH cohorts, losses of chromosome 1, 2, 6, 10, 13, and 17 were significantly more frequent in classic chRCC (p < 0.05, each), suggesting that classic chRCC are characterized by higher chromosomal instability. This molecular difference justifies the definition of two chRCC variants. Absence of pale cells could be used as main histological criterion to define the eosinophilic variant of chRCC.

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“…Aberrant increased CCNE1 indeed enhanced CDK2 conversely resulting in substrate phosphorylation of pRb, thus causing peculiar cell viability (Neganova et al, 2011). CCNE1 is found to be an oncogene in multiple cancer types, such as gastric cancer, colorectal cancer, prostate cancer, and NSCLC (Etemadmoghadam et al, 2010;Amininia et al, 2014;Pils et al, 2014;Kim et al, 2016;Noske et al, 2017). MiRNAs were considered as important regulators of CCNE1.…”

Section: Discussionmentioning

confidence: 99%

CircDENND2A Promotes Non-small Cell Lung Cancer Progression via Regulating MiR-34a/CCNE1 Signaling

et al. 2020

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The mechanism regulating non-small cell lung cancers (NSCLCs) is unclear. In this study, we aimed to determine the roles of DENN domain containing 2A (circDENND2A) in the progression of NSCLC. Circular RNAs (circRNAs) are composited by "head to tail" splicing of coding or non-coding RNAs (ncRNAs), whose crucial roles in human cancers had been revealed. CircDENND2A, a new circRNA, was revealed to induce cell proliferation and migration. Our data indicated that circDENND2A was a probable oncogene in human cancers. However, the roles of circDENND2A in NSCLC remained unknown. Here, we demonstrated that circDENND2A was down-regulated in NSCLC samples. Loss-of-function assays showed circDENND2A knockdown suppressed cell growth via inducing cell cycle arrest and apoptosis and inhibited cell migration and invasion. Bioinformatics analysis and competing endogenous RNA (ceRNA) network analysis revealed that circDENND2A was involved in regulating cell cycle and tumor protein p53 (TP53) signaling via miR-34a/CCNE1 (cyclin E1). Further validation showed that circDENND2A could directly bind to miR-34a, promoting CCNE1 expression in NSCLC. In addition, rescue assays demonstrated that restoration of CCNE1 significantly impaired the suppressive effects of circDENND2A silencing in terms of NSCLC growth, migration, and invasion. We thought this study indicated that circDENND2A/miR-34a/CCNE1 may be a potential therapeutic target for NSCLC.

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Detection ofCCNE1/URI(19q12) amplification byin situhybridisation is common in high grade and type II endometrial cancer

Cited by 18 publications

References 25 publications

Bioinformatics analysis of key differentially expressed genes in well and poorly differentiated endometrial carcinoma

Bioinformatics analysis of key differentially expressed genes in well and poorly differentiated endometrial carcinoma

Classic Chromophobe Renal Cell Carcinoma Incur a Larger Number of Chromosomal Losses Than Seen in the Eosinophilic Subtype

CircDENND2A Promotes Non-small Cell Lung Cancer Progression via Regulating MiR-34a/CCNE1 Signaling

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