Gene expression profile for predicting survival of patients with meningioma

Chen, Feng; Xiang, Chun-Xiang; Zhou, Yi; Ao, Xiang-Sheng; Zhou, Daohong; Peng, Peng; Zhang, Haiquan; Liu, Handong; Huang, Xing

doi:10.3892/ijo.2014.2779

Cited by 12 publications

(10 citation statements)

References 27 publications

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“…Microarray gene expression analysis has identified potential biomarkers to distinguish benign meningiomas from those with higher risk of progression or recurrence. A 37-gene signature was identified to correlate well with overall survival, 74 and recently an 18-gene signature was found to correlate with progression-free survival after validation in an independent cohort. 75 These genes were found to be involved in pathways involving normal embryonic development, cell proliferation/invasion, and angiogenesis, among others.…”

Section: Transcriptomic Signatures In Meningiomamentioning

confidence: 99%

“…In addition to this, increased transglutaminase 2 (TGM2) expression has been described in higher-grade meningioma 76 and the deleted in colorectal cancer (DCC) gene, which encodes a transmembrane receptor for netrin-1 and has also been suggested to be a marker for risk of meningioma progression. 77 Most gene expression studies have been limited by their small sample size (10-50 tumors), with minimal overlap in the candidate genes identified between studies, 64,74,[76][77][78][79][80] and therefore further studies are needed to validate potential gene expression biomarkers.…”

Section: Transcriptomic Signatures In Meningiomamentioning

confidence: 99%

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Molecular and translational advances in meningiomas

et al. 2019

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Meningiomas are the most common primary intracranial neoplasm. The current World Health Organization (WHO) classification categorizes meningiomas based on histopathological features, but emerging molecular data demonstrate the importance of genomic and epigenomic factors in the clinical behavior of these tumors. Treatment options for symptomatic meningiomas are limited to surgical resection where possible and adjuvant radiation therapy for tumors with concerning histopathological features or recurrent disease. At present, alternative adjuvant treatment options are not available in part due to limited historical biological analysis and clinical trial investigation on meningiomas. With advances in molecular and genomic techniques in the last decade, we have witnessed a surge of interest in understanding the genomic and epigenomic landscape of meningiomas. The field is now at the stage to adopt this molecular knowledge to refine meningioma classification and introduce molecular algorithms that can guide prediction and therapeutics for this tumor type. Animal models that recapitulate meningiomas faithfully are in critical need to test new therapeutics to facilitate rapid-cycle translation to clinical trials. Here we review the most up-to-date knowledge of molecular alterations that provide insight into meningioma behavior and are ready for application to clinical trial investigation, and highlight the landscape of available preclinical models in meningiomas.

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Section: Transcriptomic Signatures In Meningiomamentioning

confidence: 99%

Section: Transcriptomic Signatures In Meningiomamentioning

confidence: 99%

Molecular and translational advances in meningiomas

et al. 2019

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“…The authors concluded that the development of recurrent meningiomas after gross total tumour resection is usually due to regrowth of the primary tumour and rarely to the emergence of an unrelated meningioma. A prognostic signature for meningioma prognosis was reported by Chen et al [ 27 ] who analysed genome wide expression profiles of 119 meningioma samples from two previously published DNA microarray studies [ 17 , 28 ] using the Cox proportional hazards regression models and found 37 genes to be specifically related to meningioma overall survival.…”

Section: Epidemiology and Histopathological Classificationmentioning

confidence: 99%

Molecular Genetics of Intracranial Meningiomas with Emphasis on Canonical Wnt Signalling

Pećina‐Šlaus

Kafka

Lechpammer

2016

Cancers

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Research over the last decade recognized the importance of novel molecular pathways in pathogenesis of intracranial meningiomas. In this review, we focus on human brain tumours meningiomas and the involvement of Wnt signalling pathway genes and proteins in this common brain tumour, describing their known functional effects. Meningiomas originate from the meningeal layers of the brain and the spinal cord. Most meningiomas have benign clinical behaviour and are classified as grade I by World Health Organization (WHO). However, up to 20% histologically classified as atypical (grade II) or anaplastic (grade III) are associated with higher recurrent rate and have overall less favourable clinical outcome. Recently, there is emerging evidence that multiple signalling pathways including Wnt pathway contribute to the formation and growth of meningiomas. In the review we present the synopsis on meningioma histopathology and genetics and discuss our research regarding Wnt in meningioma. Epithelial-to-mesenchymal transition, a process in which Wnt signalling plays an important role, is shortly discussed.

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“…Genomics microarray, a high-throughput platform, represents a great powerful technology to analyze gene expression comprehensively [ 22 , 23 ]. In combination with multiple bioinformatics analyses, microarray technology has been widely valued as a tool with great promise to obtain gene signals during tumor process, drug resistance, and verify prognostic biomarkers in cancers [ 24 – 26 ]. Detection and verification of vital targets of drug resistance by using microarray analysis is a novel research strategy and may in favor of uncovering the underlying mechanisms of drug resistance.…”

Section: Introductionmentioning

confidence: 99%

Identification of MMP1 as a potential gene conferring erlotinib resistance in non-small cell lung cancer based on bioinformatics analyses

Xiang

Zhang

et al. 2020

Hereditas

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Background: Non-small cell lung cancer (NSCLC) is the major type of lung cancer with high morbidity and poor prognosis. Erlotinib, an inhibitor of epidermal growth factor receptor (EGFR), has been clinically applied for NSCLC treatment. Nevertheless, the erlotinib acquired resistance of NSCLC occurs inevitably in recent years. Methods: Through analyzing two microarray datasets, erlotinib resistant NSCLC cells microarray (GSE80344) and NSCLC tissue microarray (GSE19188), the differentially expressed genes (DEGs) were screened via R language. DEGs were then functionally annotated by Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, which up-regulated more than 2-folds in both datasets were further functionally analyzed by Oncomine, GeneMANIA, R2, Coremine, and FunRich. Results: We found that matrix metalloproteinase 1 (MMP1) may confer the erlotinib therapeutic resistance in NSCL C. MMP1 highly expressed in erlotinib-resistant cells and NSCLC tissues, and it associated with poor overall survival. In addition, MMP1 may be associated with COPS5 and be involve in an increasing transcription factors HOXA9 and PBX1 in erlotinib resistance. Conclusions: Generally, these results demonstrated that MMP1 may play a crucial role in erlotinib resistance in NSCLC, and MMP1 could be a prognostic biomarker for erlotinib treatment.

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Gene expression profile for predicting survival of patients with meningioma

Cited by 12 publications

References 27 publications

Molecular and translational advances in meningiomas

Molecular and translational advances in meningiomas

Molecular Genetics of Intracranial Meningiomas with Emphasis on Canonical Wnt Signalling

Identification of MMP1 as a potential gene conferring erlotinib resistance in non-small cell lung cancer based on bioinformatics analyses

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