Microarray gene expression profiling in meningiomas: Differential expression according to grade or histopathological subtype

Fèvre-Montange,

doi:10.3892/ijo_00000457

Cited by 53 publications

(53 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Using a combination of gene expression microarrays and array comparative genomic hybridization, Carvalho et al [31] showed that 23 meningiomas of all three grades fell into two main molecular groups designated "low-proliferative" and "high-proliferative" meningiomas; CKS2 was highly expressed in grade III versus grade I meningiomas. Genes involved in proliferation pathways, including CKS2, were again found to be upregulated in a microarray study on 17 meningiomas [32]. Overall, these studies and our work point to CKS2 as a robust marker associated with meningioma recurrence and malignant transformation.…”

Section: Discussionmentioning

confidence: 52%

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Menghi¹,

Orzan²,

Eoli³

et al. 2011

The Oncologist

View full text Add to dashboard Cite

Meningiomas are the most frequent intracranial tumors. Surgery can be curative, but recurrences are possible. We performed gene expression analyses and loss of heterozygosity (LOH) studies looking for new markers predicting the recurrence risk. We analyzed expression profiles of 23 meningiomas (10 grade I, 10 grade II, and 3 grade III) and validated the data using quantitative polymerase chain reaction (qPCR). We performed LOH analysis on 40 meningiomas, investigating chromosomal regions on 1p, 9p, 10q, 14q, and 22q. We found 233 and 268 probe sets to be significantly down-and upregulated, respectively, in grade II or III meningiomas. Genes downregulated in high-grade meningiomas were overrepresented on chromosomes 1, 6, 9, 10, and 14. Based on functional enrichment analysis, we selected LIM domain and actin binding 1 (LIMA1), tissue inhibitor of metalloproteinases 3 (TIMP3), cyclin-dependent kinases regulatory subunit 2 (CKS2), leptin receptor (LEPR), and baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) for validation using qPCR and confirmed their differential expression in the two groups of tumors. We calculated ⌬Ct values of CKS2 and LEPR and found that their differential expression (C-L index) was significantly higher in grade I than in grade II or III meningiomas (p < .0001). Interestingly, the C-L index of nine grade I meningiomas from patients who relapsed in <5 years was significantly lower than in grade I meningiomas from patients who did not relapse. These findings indicate that the C-L index may be relevant to define the progression risk in meningioma patients, helping guide their clinical management. A prospective analysis on a larger number of cases is warranted.

show abstract

Section: Discussionmentioning

confidence: 52%

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Menghi¹,

Orzan²,

Eoli³

et al. 2011

The Oncologist

View full text Add to dashboard Cite

show abstract

“…Dysregulation of melanophilin was found in several types of tumors, e.g. lung cancer, meningiomas and breast cancer (Fevre-Montange, et al, 2009; Molina-Pinelo, et al, 2014; Pio, et al, 2010; Thakkar, et al, 2010). A very recent study found association of expression of MLPH (and some other genes) with nearby SNPs in prostate tissue (Penney, et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Putative Prostate Cancer Risk SNP in an Androgen Receptor‐Binding Site of the Melanophilin Gene Illustrates Enrichment of Risk SNPs in Androgen Receptor Target Sites

Narisu

Schlick

et al. 2015

Human Mutation

View full text Add to dashboard Cite

Genome-wide association studies have identified genomic loci, whose single nucleotide polymorphisms (SNPs) predispose to prostate cancer (PCa). However, the mechanisms of most of these variants are largely unknown. We integrated chromatin-IP coupled sequencing and microarray expression profiling in TMPRSS2-ERG gene rearrangement positive DUCaP cells with the GWAS PCa risk SNPs catalog to identify disease susceptibility SNPs localized within functional androgen receptor binding sites (ARBSs). Among the 48 GWAS index risk SNPs and 3,917 linked SNPs, 80 were found located in ARBSs. Of these, rs11891426:T>G in an intron of the melanophilin gene (MLPH), was within a novel putative auxiliary AR binding motif, which is enriched in the neighborhood of canonical androgen responsive elements. T→G exchange attenuated the transcriptional activity of the ARBS in an AR reporter gene assay. The expression of melanophilin in primary prostate tumors was significantly lower in those with the G compared to the T allele and correlated significantly with AR protein. Higher melanophilin level in prostate tissue of patients with a favourable PCa risk profile points out a tumor suppressive effect. These results unravel a hidden link between AR and a functional putative PCa risk SNP, whose allele alteration affects androgen regulation of its host gene MLPH.

show abstract

“…Although it may be the consequence of different haplotypes in the WT zebrafish population, the regulation of MHC I genes is found in a great number of cancers. arhgap28, the most overexpressed gene between the obese stimulated and healthy stimulated fish, is a signal transducer that is upregulated in grade II and III meningiomas (Fèvre-Montange et al 2009). Moreover, hepcidins and saa genes also exhibited different expression profiles following the stimulation of obese and healthy zebrafish.…”

Section: Differential Immune Response Against An Inflammatory Stimulumentioning

confidence: 99%

Liver immune responses to inflammatory stimuli in a diet-induced obesity model of zebrafish

Forn-Cuní¹,

Varela²,

Fernández-Rodrı́guez³

et al. 2014

Journal of Endocrinology

View full text Add to dashboard Cite

Obesity-and metabolic syndrome-related diseases are becoming important medical challenges for the western world. Non-alcoholic fatty liver disease (NAFLD) is a manifestation of these altered conditions in the liver, and inflammation appears to be a factor that is tightly connected to its evolution. In this study, we used a diet-induced obesity approach in zebrafish (Danio rerio) based on overfeeding to analyze liver transcriptomic modulation in the disease and to determine how obesity affects the immune response against an acute inflammatory stimulus such as lipopolysaccharide (LPS). Overfed zebrafish developed an obese phenotype, showed signs of liver steatosis, and its modulation profile resembled that observed in humans, with overexpression of tac4, col4a3, col4a5, lysyl oxidases, and genes involved in retinoid metabolism. In response to LPS, healthy fish exhibited a typical host defense reaction comparable to that which occurs in mammals, whereas there was no significant gene modulation when comparing expression in the liver of LPS-stimulated and non-stimulated obese zebrafish at the same statistical level. The stimulation of obese fish represents a double-hit to the already damaged liver and can help understand the evolution of the disease. Finally, a comparison of the differential gene activation between stimulated healthy and obese zebrafish revealed the expected difference in the metabolic state between healthy and diseased liver. The differentially modulated genes are currently being studied as putative new pathological markers in NAFLD-stimulated liver in humans.

show abstract

Microarray gene expression profiling in meningiomas: Differential expression according to grade or histopathological subtype

Cited by 53 publications

References 54 publications

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Putative Prostate Cancer Risk SNP in an Androgen Receptor‐Binding Site of the Melanophilin Gene Illustrates Enrichment of Risk SNPs in Androgen Receptor Target Sites

Liver immune responses to inflammatory stimuli in a diet-induced obesity model of zebrafish

Contact Info

Product

Resources

About