Radiological response in an incidental meningioma in a patient treated with chemotherapy combined with CP-751,871, an IGF-1R inhibitor

Collins, Ian M.; Beddy, Peter; O’Byrne, Kenneth J.

doi:10.3109/02841861003752408

Cited by 10 publications

(4 citation statements)

References 7 publications

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“…Previous studies suggest that the differential expression of IGF1R may be important in autocrine stimulation of brain tumor cell growth [25]. A recent study showed that inhibitors of IGF1R may have anti-tumoral effects in benign meningioma [26]. Our results by gene expression microarrays and real-time RT-PCR show that IGF1R is closely related to metabolic aggressiveness in histological benign meningioma but not in atypical meninhioma.…”

Section: Discussionsupporting

confidence: 51%

Gene Expression Profiles of Metabolic Aggressiveness and Tumor Recurrence in Benign Meningioma

et al. 2013

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Around 20% of meningiomas histologically benign may be clinically aggressive and recur. This strongly affects management of meningioma patients. There is a need to evaluate the potential aggressiveness of an individual meningioma. Additional criteria for better classification of meningiomas will improve clinical decisions as well as patient follow up strategy after surgery. The aim of this study was to determine the relationship between gene expression profiles and new metabolic subgroups of benign meningioma with potential clinical relevance. Forty benign and fourteen atypical meningioma tissue samples were included in the study. We obtained metabolic profiles by NMR and recurrence after surgery information for all of them. We measured gene expression by oligonucleotide microarray measurements on 19 of them. To our knowledge, this is the first time that distinct gene expression profiles are reported for benign meningioma molecular subgroups with clinical correlation. Our results show that metabolic aggressiveness in otherwise histological benign meningioma proceeds mostly through alterations in the expression of genes involved in the regulation of transcription, mainly the LMO3 gene. Genes involved in tumor metabolism, like IGF1R, are also differentially expressed in those meningioma subgroups with higher rates of membrane turnover, higher energy demand and increased resistance to apoptosis. These new subgroups of benign meningiomas exhibit different rates of recurrence. This work shows that benign meningioma with metabolic aggressiveness constitute a subgroup of potentially recurrent tumors in which alterations in genes regulating critical features of aggressiveness, like increased angiogenesis or cell invasion, are still no predominant. The determination of these gene expression biosignatures may allow the early detection of clinically aggressive tumors.

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Section: Discussionsupporting

confidence: 51%

Gene Expression Profiles of Metabolic Aggressiveness and Tumor Recurrence in Benign Meningioma

et al. 2013

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“…The latter genes are ALCAM, NRP1, IGF1R, CA1 , and ERCC4 . Of these, NRP1 and IGF1R do not have a clearly related role in meningioma yet, but evidence points toward the implication of the former in meningioma-associated neoangiogenesis (49) and for the blocking of the latter as therapeutic option (50). …”

Section: Resultsmentioning

confidence: 99%

An Integrative Analysis of Meningioma Tumors Reveals the Determinant Genes and Pathways of Malignant Transformation

Gómez¹,

Orgueira

2014

Front. Oncol.

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Meningiomas are frequent central nervous system neoplasms, which despite their predominant benignity, show sporadically malignant behavior. Type 2 neurofibromatosis and polymorphisms in several genes have been associated with meningioma risk and are probably involved in its pathogenesis. Although GWAS studies have found loci related to meningioma risk, little is known about the factors determining malignant transformation. Thus, this study is aimed to identify the genomic and transcriptomic factors influencing evolution from benignity toward aggressive phenotypes. By applying an integrative bioinformatics pipeline combining public information on a wealth of biological layers of complexity (from genetic polymorphisms to protein interactions), this study identified a module of co-expressed genes highly correlated with tumor stage and statistically linked to several genomic regions (module Quantitative Trait Loci, mQTLs). Ontology analysis of the transcription hub genes identified microtubule-associated cell-cycle processes as key drivers of such network. mQTLs and single nucleotide polymorphisms associated with meningioma stage were replicated in an alternative meningioma cohort, and integration of these results with up-to-date scientific literature and several databases retrieved a list of genes and pathways with a potentially important role in meningioma malignancy. As a result, cytoskeleton and cell–cell adhesion pathways, calcium-channels and glutamate receptors, as well as oxidoreductase and endoplasmic reticulum-associated degradation pathways were found to be the most important and redundant findings associated to meningioma progression. This study presents an integrated view of the pathways involved in meningioma malignant conversion and paves the way for the development of new research lines that will improve our understanding of meningioma biology.

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“… Hormones which are heavily involved in systemic glucose metabolism and glycolysis, such as the insulin-like growth factor (IGF), have already been shown to be a reliable marker of aggressive meningiomas [ 29 ]. Indeed, sporadic reports have already suggested that inhibition of the IGF receptor (IGF-1R) could have a role in future meningioma treatment [ 64 ]. Moreover, the expression of IGF-1R and its’ impact on cellular proliferation have been shown to be significantly influenced by glycaemia levels in other malignancies [ 65 , 66 ], indicating that a similar process could be possible in meningiomas as well.…”

Section: Discussionmentioning

confidence: 99%

Chronic hyperglycemia and intracranial meningiomas

Orešković,

Madero Pohlen,

Cvitković

et al. 2024

BMC Cancer

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Meningiomas are among the most common primary tumors of the central nervous system. Previous research into the meningioma histological appearance, genetic markers, transcriptome and epigenetic landscape has revealed that benign meningiomas significantly differ in their glucose metabolism compared to aggressive lesions. However, a correlation between the systemic glucose metabolism and the metabolism of the tumor hasn’t yet been found. We hypothesized that chronic levels of glycaemia (approximated with glycated hemoglobin (HbA1c)) are different in patients with aggressive and benign meningiomas. The study encompassed 71 patients with de novo intracranial meningiomas, operated on in three European hospitals, two in Croatia and one in Spain. Our results show that patients with WHO grade 2 meningiomas had significantly higher HbA1c values compared to patients with grade 1 lesions (P = 0.0290). We also found a significant number of patients (19/71; 26.7%) being hyperglycemic, harboring all the risks that such a condition entails. Finally, we found a significant correlation between our patients’ age and their preoperative HbA1c levels (P = 0.0008, ρ(rho) = 0.388), suggesting that older meningioma patients are at a higher risk of having their glycaemia severely dysregulated. These findings are especially important considering the current routine and wide-spread use of corticosteroids as anti-edematous treatment. Further research in this area could lead to better understanding of meningiomas and have immediate clinical impact.

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Radiological response in an incidental meningioma in a patient treated with chemotherapy combined with CP-751,871, an IGF-1R inhibitor

Cited by 10 publications

References 7 publications

Gene Expression Profiles of Metabolic Aggressiveness and Tumor Recurrence in Benign Meningioma

Gene Expression Profiles of Metabolic Aggressiveness and Tumor Recurrence in Benign Meningioma

An Integrative Analysis of Meningioma Tumors Reveals the Determinant Genes and Pathways of Malignant Transformation

Chronic hyperglycemia and intracranial meningiomas

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