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Pinyuan Chen - One of the best experts on this subject based on the ideXlab platform.
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anterior skull base tumor resection by transciliary supraorbital keyhole craniotomy a single institutional experience
World Neurosurgery, 2018Co-Authors: Koting Chen, Taiwei Erich Wu, Yincheng Huang, Yujen Lu, Chicheng Chuang, Pinyuan ChenAbstract:Background The prognosis and recurrence rate after resection of an anterior skull base lesion via transciliary supraorbital keyhole craniotomy depend on residual tumor volume. The extent to which pathology and size of tumor influence the resection rate using this approach is unknown. Methods Sixty-two patients underwent a total of 64 operations using the supraorbital keyhole approach in this retrospective study. Meningioma was the most common tumor, followed by pituitary adenoma and craniopharyngioma. Age, sex, tumor volume, operative duration, blood loss, and complication rates were evaluated. Pre- and postoperative residual tumor volumes were measured using OsiriX software (medical image viewer system) based on magnetic resonance imaging. A 15-mL cut value divided the subjects into large versus small Meningioma groups. Results The average resection rate for Meningiomas was 95.2% compared with 83.9% for craniopharyngiomas and 53.2% for pituitary adenomas. The major complication rate (primarily blindness and hemiplegia) was 4.48% in all tumors. No operative-related deaths occurred. There were no surgical revisions to traditional large craniotomies. No significant differences in age, sex, postoperative volumes, resection rates, or recurrence rates were noted between small and large Meningioma groups. However, longer operative times and hospital stays, and greater blood loss occurred in the large Meningioma group. Conclusions Transciliary keyhole craniotomy is a safe and effective approach for anterior skull base tumors, especially Meningiomas. Excellent resection results were achieved even in cases of large Meningiomas. Although longer operative times, longer hospital stays, and greater blood loss occurred in larger compared with smaller Meningioma cases, recurrence rates were similar.
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anterior skull base tumor resection by transciliary supraorbital keyhole craniotomy a single institutional experience
World Neurosurgery, 2018Co-Authors: Koting Chen, Taiwei Erich Wu, Yincheng Huang, Yujen Lu, Chicheng Chuang, Pinyuan ChenAbstract:Background The prognosis and recurrence rate after resection of an anterior skull base lesion via transciliary supraorbital keyhole craniotomy depend on residual tumor volume. The extent to which pathology and size of tumor influence the resection rate using this approach is unknown. Methods Sixty-two patients underwent a total of 64 operations using the supraorbital keyhole approach in this retrospective study. Meningioma was the most common tumor, followed by pituitary adenoma and craniopharyngioma. Age, sex, tumor volume, operative duration, blood loss, and complication rates were evaluated. Pre- and postoperative residual tumor volumes were measured using OsiriX software (medical image viewer system) based on magnetic resonance imaging. A 15-mL cut value divided the subjects into large versus small Meningioma groups. Results The average resection rate for Meningiomas was 95.2% compared with 83.9% for craniopharyngiomas and 53.2% for pituitary adenomas. The major complication rate (primarily blindness and hemiplegia) was 4.48% in all tumors. No operative-related deaths occurred. There were no surgical revisions to traditional large craniotomies. No significant differences in age, sex, postoperative volumes, resection rates, or recurrence rates were noted between small and large Meningioma groups. However, longer operative times and hospital stays, and greater blood loss occurred in the large Meningioma group. Conclusions Transciliary keyhole craniotomy is a safe and effective approach for anterior skull base tumors, especially Meningiomas. Excellent resection results were achieved even in cases of large Meningiomas. Although longer operative times, longer hospital stays, and greater blood loss occurred in larger compared with smaller Meningioma cases, recurrence rates were similar.
Guido Reifenberger - One of the best experts on this subject based on the ideXlab platform.
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hypermethylation and transcriptional downregulation of the timp3 gene is associated with allelic loss on 22q12 3 and malignancy in Meningiomas
Brain Pathology, 2010Co-Authors: Dimitri Barski, Marietta Wolter, Guido Reifenberger, Markus J RiemenschneiderAbstract:The gene for the tissue inhibitor of metalloproteinase 3 (TIMP3) on 22q12.3 had been reported to be inactivated by promoter methylation in various types of cancers, with controversial findings in Meningiomas. We performed direct sodium bisulfite sequencing in a series of 50 Meningiomas, including 27 benign Meningiomas [World Health Organization (WHO) grade I], 11 atypical Meningiomas (WHO grade II) and 12 anaplastic Meningiomas (WHO grade III), and found hypermethylation of TIMP3 in 67% of anaplastic Meningiomas, but only 22% of atypical and 17% of benign Meningiomas. Moreover, TIMP3 methylation scores were significantly inversely correlated with TIMP3 mRNA expression levels (P = 0.0123), and treatment of the Meningioma cell line Ben-Men-1 with demethylating agents induced an increased TIMP3 mRNA expression. TIMP3 is located in the chromosomal band 22q12, the allelic loss of which occurs early in Meningioma tumorigenesis and preferentially targets the NF2 tumor suppressor gene. In our tumor panel, all Meningiomas with TIMP3 hypermethylation--except for a single case--exhibited allelic losses on 22q12.3. Thus, TIMP3 inactivation by methylation seems fairly exclusive to Meningiomas with allelic losses on 22q12 but--in contrast to NF2 mutation--appears to be involved in Meningioma progression as it is associated with a more aggressive, high-grade Meningioma phenotype.
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histological classification and molecular genetics of Meningiomas
Lancet Neurology, 2006Co-Authors: Markus J Riemenschneider, Arie Perry, Guido ReifenbergerAbstract:Meningiomas account for up to 30% of all primary intracranial tumours. They are histologically classified according to the World Health Organization (WHO) classification of tumours of the nervous system. Most Meningiomas are benign lesions of WHO grade I, whereas some Meningioma variants correspond with WHO grades II and III and are associated with a higher risk of recurrence and shorter survival times. Mutations in the NF2 gene and loss of chromosome 22q are the most common genetic alterations associated with the initiation of Meningiomas. With increase in tumour grade, additional progression-associated molecular aberrations can be found; however, most of the relevant genes are yet to be identified. High-throughput techniques of global genome and transcriptome analyses and new Meningioma models provide increasing insight into Meningioma biology and will help to identify common pathogenic pathways that may be targeted by new therapeutic approaches.
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integrative genomic analysis identifies ndrg2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive Meningioma
Cancer Research, 2005Co-Authors: Eriks A Lusis, Michael R Chicoine, Mark A Watson, David H Gutmann, Guido Reifenberger, Meghan Lyman, Peter Roerig, Arie PerryAbstract:Although Meningiomas are common central nervous system tumors, little is known about the genetic events responsible for malignant progression. In this study, we employed gene expression profiling to identify transcripts whose expression was lost in anaplastic (WHO grade III) versus benign (WHO grade I) Meningioma. Approximately 40% of genes down-regulated in anaplastic Meningioma were localized to chromosomes 1p and 14q. One specific gene located at 14q11.2, NDRG2, was consistently down-regulated in grade III Meningioma, a finding which we validated at both the transcript and protein levels in independent sets of clinically and pathologically diverse Meningiomas. Loss of NDRG2 expression was also seen in a subset of lower-grade Meningiomas, including atypical Meningiomas (WHO grade II) with clinically aggressive behavior. Furthermore, we found that the loss of NDRG2 expression was significantly associated with hypermethylation of the NDRG2 promoter. Collectively, these data identify NDRG2 as the first specific candidate tumor suppressor gene on chromosome 14q that is inactivated during Meningioma progression. In addition, these findings highlight the utility of combining genomic, epigenetic, and expression data to identify clinically significant tumor biomarkers, and suggest that NDRG2 expression will be a useful and functionally relevant biomarker to predict aggressive behavior in patients with Meningioma.
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Alterations of the Tumor Suppressor Genes CDKN2A (p16INK4a), p14ARF, CDKN2B (p15INK4b), and CDKN2C (p18INK4c) in Atypical and Anaplastic Meningiomas
The American journal of pathology, 2001Co-Authors: Jan Boström, Birgit Meyer-puttlitz, Marietta Wolter, Britta Blaschke, Ruthild G. Weber, Peter Lichter, Koichi Ichimura, V. Peter Collins, Guido ReifenbergerAbstract:We investigated 67 meningothelial tumors (20 benign Meningiomas, 34 atypical Meningiomas, and 13 anaplastic Meningiomas) for losses of genetic information from chromosome arms 1p and 9p, as well as for deletion, mutation, and expression of the tumor suppressor genes CDKN2A (p16INKa/MTS1), p14ARF, CDKN2B (p15INK4b/MTS2) (all located at 9p21) and CDKN2C (1p32). Comparative genomic hybridization and microsatellite analysis showed losses on 1p in 11 anaplastic Meningiomas (85%), 23 atypical Meningiomas (68%), and 5 benign Meningiomas (25%). One atypical Meningioma with loss of heterozygosity on 1p carried a somatic CDKN2C mutation (c.202C>T: R68X). Losses on 9p were found in five anaplastic Meningiomas (38%), six atypical Meningiomas (18%), and one benign Meningioma (5%). Six anaplastic Meningiomas (46%) and one atypical Meningioma (3%) showed homozygous deletions of the CDKN2A, p14ARF, and CDKN2B genes. Two anaplastic Meningiomas carried somatic point mutations in CDKN2A (c.262G>T: E88X and c.262G>A: E88K) and p14ARF (c.305G>T: G102V and c.305G>A: G102E). One anaplastic Meningioma, three atypical Meningiomas, and one benign Meningioma without a demonstrated homozygous deletion or mutation of CDKN2A, p14ARF, or CDKN2B lacked detectable transcripts from at least one of these genes. Hypermethylation of CDKN2A, p14ARF, and CDKN2B could be demonstrated in one of these cases. Taken together, our results indicate that CDKN2C is rarely altered in Meningiomas. However, the majority of anaplastic Meningiomas either show homozygous deletions of CDKN2A, p14ARF, and CDKN2B, mutations in CDKN2A and p14ARF, or lack of expression of one or more of these genes. Thus, inactivation of the G1/S-phase cell-cycle checkpoint is an important aberration in anaplastic Meningiomas.
Ian F Dunn - One of the best experts on this subject based on the ideXlab platform.
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mismatch repair deficiency in high grade Meningioma a rare but recurrent event associated with dramatic immune activation and clinical response to pd 1 blockade
JCO precision oncology, 2018Co-Authors: Ian F Dunn, Mehdi Touat, Michael B Sisti, Patrick Y Wen, Renato Umeton, Adrian M Dubuc, Matthew D Ducar, Peter Canoll, Eric Allan SeversonAbstract:Meningiomas are the most common primary tumor of the central nervous system, with ~28,000 new diagnoses annually in the United States1. Currently, there are no approved systemic therapies for Meningiomas that recur following local treatment: chemotherapy and hormonal agents have demonstrated minimal benefit in numerous clinical trials2–4. Meningioma comprises a heterogeneous group of neoplasms driven by mutations in a wide array of tumor suppressor genes and oncogenes5–17. Characterization of these mutations has revealed opportunities for rational therapy18–20. For example, a durable therapeutic response has been reported for a metastatic AKT1(E17K)-mutant Meningioma treated with a pan-AKT inhibitor.21 Studies also suggest the potential for treating Meningioma with immune checkpoint modulators22–24: programmed death receptor 1 ligand (PD-L1) is expressed in a subset of Meningiomas and the tumor microenvironment is immunosuppressive22–28. Higher-grade Meningiomas also harbor mutations predicted to generate neoantigens, which may foster susceptibility to immunotherapies29. Based on these data, we initiated a phase II study of nivolumab, a humanized IgG4 PD-1 blocking monoclonal antibody, in patients with higher-grade Meningiomas that recurred following surgery and radiotherapy ({"type":"clinical-trial","attrs":{"text":"NCT02648997","term_id":"NCT02648997"}}NCT02648997). We report here a patient with an atypical Meningioma that was not controlled by repeated surgery and radiation but which was highly response to nivolumab.
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molecular typing of Meningiomas by desorption electrospray ionization mass spectrometry imaging for surgical decision making
International Journal of Mass Spectrometry, 2015Co-Authors: David Calligaris, Ian F Dunn, Daniel R Feldman, Isaiah Norton, Priscilla K Brastianos, Sandro Santagata, Nathalie Y R AgarAbstract:Meningiomas are the most frequent intracranial tumors. The majority is benign slow-growing tumors but they can be difficult to treat depending on their location and size. While Meningiomas are well delineated on magnetic resonance imaging by their uptake of contrast, surgical limitations still present themselves from not knowing the extent of invasion of the dura matter by Meningioma cells. The development of tools to characterize tumor tissue in real or near real time could prevent recurrence after tumor resection by allowing for more precise surgery, i.e. removal of tumor with preservation of healthy tissue. The development of ambient ionization mass spectrometry for molecular characterization of tissue and its implementation in the surgical decision-making workflow carry the potential to fulfill this need. Here, we present the characterization of Meningioma and dura mater by desorption electrospray ionization mass spectrometry to validate the technique for the molecular assessment of surgical margins and diagnosis of Meningioma from surgical tissue in real-time. Nine stereotactically resected surgical samples and three autopsy samples were analyzed by standard histopathology and mass spectrometry imaging. All samples indicated a strong correlation between results from both techniques. We then highlight the value of desorption electrospray ionization mass spectrometry for the molecular subtyping/subgrouping of Meningiomas from a series of forty genetically characterized specimens. The minimal sample preparation required for desorption electrospray ionization mass spectrometry offers a distinct advantage for applications relying on real-time information such as surgical decision-making. The technology here was tested to distinguish Meningioma from dura mater as an approach to precisely define surgical margins. In addition we classify Meningiomas into fibroblastic and meningothelial subtypes and more notably recognize Meningiomas with NF2 genetic aberrations.
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increased expression of the immune modulatory molecule pd l1 cd274 in anaplastic Meningioma
Oncotarget, 2015Co-Authors: Malak Abedalthagafi, Priscilla K Brastianos, Ayal A Aizer, Allison Mchenry, Heather Sun, Markanthony Bray, Omar Viramontes, Revaz Machaidze, David A Reardon, Ian F DunnAbstract:There are no effective medical treatments for WHO grade III (anaplastic) Meningioma. Patients with this high-grade malignancy have a median survival of less than two years. Therapeutics that modulate the mechanisms that inhibit local immune responses in the tumor microenvironment are showing significant and durable clinical responses in patients with treatment refractory high-grade tumors. We examined the immune infiltrate of 291 Meningiomas including WHO grade I-III Meningiomas using immunohistochemistry and we examined the expression of PD-L1 mRNA by RNAscope in situ hybridization and PD-L1 protein by immunohistochemistry. In Meningioma, the tumor infiltrating lymphocytes are predominantly T cells. In anaplastic Meningioma, there is a sharp decrease in the number of T cells, including the numbers of CD4+ and CD8+ T cells and cells expressing PD-1 and there is also an increase in the number of FOXP3 expressing immunoregulatory (Treg) cells. PD-L1 expression is increased in anaplastic Meningioma – both mRNA and protein. Using patient derived Meningioma cell, we confirm that PD-L1 is expressed in Meningioma cells themselves, and not solely in infiltrating immune cells. This work indicates that high-grade Meningioma harbor an immunosuppressive tumor microenviroment and that increased Treg cells and elevated PD-L1 may contribute to the aggressive phenotype of these tumors.
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Angiomatous Meningiomas have a distinct genetic profile with multiple chromosomal polysomies including polysomy of chromosome 5.
Oncotarget, 2014Co-Authors: Malak S. Abedalthagafi, Parker H. Merrill, Robert T. Jones, Marc L. Listewnik, Aaron R. Thorner, Rameen Beroukhim, Ian F Dunn, Shakti Ramkissoon, Brian M. AlexanderAbstract:// Malak S. Abedalthagafi 1 , Parker H. Merrill 1 , Wenya Linda Bi 2 , Robert T. Jones 1 , Marc L. Listewnik 3 , Shakti H. Ramkissoon 1 , Aaron R. Thorner 4,5 , Ian F. Dunn 2 , Rameen Beroukhim 4,6,9 , Brian M. Alexander 7 , Priscilla K. Brastianos 4,6,8 , Joshua M. Francis 4,6 , Rebecca D. Folkerth 1 , Keith L. Ligon 1,4 , Paul Van Hummelen 4,5 , Azra H. Ligon 3 and Sandro Santagata 1,9 1 Department of Pathology, Division of Neuropathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 2 Department of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 3 Clinical Cytogenetics Laboratory, Center for Advanced Molecular Diagnostics, Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 4 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA 5 Center for Cancer Genome Discovery, Dana-Farber Cancer Institute, Boston, MA, USA 6 Broad Institute of MIT and Harvard, Cambridge, MA, USA 7 Department of Radiation Oncology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 8 Department of Neuro-Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA 9 Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA Correspondence: Sandro Santagata, email: // Keywords : Meningioma, angiomatous, polysomy, aCGH, molecular diagnostics, Next Generation Sequencing Received : September 14, 2014 Accepted : September 24, 2014 Published : September 25, 2014 Abstract Meningiomas are a diverse group of tumors with a broad spectrum of histologic features. There are over 12 variants of Meningioma, whose genetic features are just beginning to be described. Angiomatous Meningioma is a World Health Organization (WHO) Meningioma variant with a predominance of blood vessels. They are uncommon and confirming the histopathologic classification can be challenging. Given a lack of biomarkers that define the angiomatous subtype and limited understanding of the genetic changes underlying its tumorigenesis, we compared the genomic characteristics of angiomatous Meningioma to more common Meningioma subtypes. While typical grade I Meningiomas demonstrate monosomy of chromosome 22 or lack copy number aberrations, 13 of 14 cases of angiomatous Meningioma demonstrated a distinct copy number profile – polysomies of at least one chromosome, but often of many, especially in chromosomes 5, 13, and 20. WHO grade II atypical Meningiomas with angiomatous features have both polysomies and genetic aberrations characteristic of other atypical Meningiomas. Sequencing of over 560 cancer-relevant genes in 16 cases of angiomatous Meningioma showed that these tumors lack common mutations found in other variants of Meningioma. Our study demonstrates that angiomatous Meningiomas have distinct genomic features that may be clinically useful for their diagnosis.
Koting Chen - One of the best experts on this subject based on the ideXlab platform.
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anterior skull base tumor resection by transciliary supraorbital keyhole craniotomy a single institutional experience
World Neurosurgery, 2018Co-Authors: Koting Chen, Taiwei Erich Wu, Yincheng Huang, Yujen Lu, Chicheng Chuang, Pinyuan ChenAbstract:Background The prognosis and recurrence rate after resection of an anterior skull base lesion via transciliary supraorbital keyhole craniotomy depend on residual tumor volume. The extent to which pathology and size of tumor influence the resection rate using this approach is unknown. Methods Sixty-two patients underwent a total of 64 operations using the supraorbital keyhole approach in this retrospective study. Meningioma was the most common tumor, followed by pituitary adenoma and craniopharyngioma. Age, sex, tumor volume, operative duration, blood loss, and complication rates were evaluated. Pre- and postoperative residual tumor volumes were measured using OsiriX software (medical image viewer system) based on magnetic resonance imaging. A 15-mL cut value divided the subjects into large versus small Meningioma groups. Results The average resection rate for Meningiomas was 95.2% compared with 83.9% for craniopharyngiomas and 53.2% for pituitary adenomas. The major complication rate (primarily blindness and hemiplegia) was 4.48% in all tumors. No operative-related deaths occurred. There were no surgical revisions to traditional large craniotomies. No significant differences in age, sex, postoperative volumes, resection rates, or recurrence rates were noted between small and large Meningioma groups. However, longer operative times and hospital stays, and greater blood loss occurred in the large Meningioma group. Conclusions Transciliary keyhole craniotomy is a safe and effective approach for anterior skull base tumors, especially Meningiomas. Excellent resection results were achieved even in cases of large Meningiomas. Although longer operative times, longer hospital stays, and greater blood loss occurred in larger compared with smaller Meningioma cases, recurrence rates were similar.
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anterior skull base tumor resection by transciliary supraorbital keyhole craniotomy a single institutional experience
World Neurosurgery, 2018Co-Authors: Koting Chen, Taiwei Erich Wu, Yincheng Huang, Yujen Lu, Chicheng Chuang, Pinyuan ChenAbstract:Background The prognosis and recurrence rate after resection of an anterior skull base lesion via transciliary supraorbital keyhole craniotomy depend on residual tumor volume. The extent to which pathology and size of tumor influence the resection rate using this approach is unknown. Methods Sixty-two patients underwent a total of 64 operations using the supraorbital keyhole approach in this retrospective study. Meningioma was the most common tumor, followed by pituitary adenoma and craniopharyngioma. Age, sex, tumor volume, operative duration, blood loss, and complication rates were evaluated. Pre- and postoperative residual tumor volumes were measured using OsiriX software (medical image viewer system) based on magnetic resonance imaging. A 15-mL cut value divided the subjects into large versus small Meningioma groups. Results The average resection rate for Meningiomas was 95.2% compared with 83.9% for craniopharyngiomas and 53.2% for pituitary adenomas. The major complication rate (primarily blindness and hemiplegia) was 4.48% in all tumors. No operative-related deaths occurred. There were no surgical revisions to traditional large craniotomies. No significant differences in age, sex, postoperative volumes, resection rates, or recurrence rates were noted between small and large Meningioma groups. However, longer operative times and hospital stays, and greater blood loss occurred in the large Meningioma group. Conclusions Transciliary keyhole craniotomy is a safe and effective approach for anterior skull base tumors, especially Meningiomas. Excellent resection results were achieved even in cases of large Meningiomas. Although longer operative times, longer hospital stays, and greater blood loss occurred in larger compared with smaller Meningioma cases, recurrence rates were similar.
Thomas Wurdinger - One of the best experts on this subject based on the ideXlab platform.
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downregulated microrna 200a in Meningiomas promotes tumor growth by reducing e cadherin and activating the wnt beta catenin signaling pathway
Molecular and Cellular Biology, 2009Co-Authors: Okay Saydam, Yiping Shen, Thomas Wurdinger, Ozlem Senol, Elvan Boke, Marianne James, Bakhos A Tannous, Anat Stemmerrachamimov, Ming YiAbstract:Meningiomas, one of the most common human brain tumors, are derived from arachnoidal cells associated with brain meninges, are usually benign, and are frequently associated with neurofibromatosis type 2. Here, we define a typical human Meningioma microRNA (miRNA) profile and characterize the effects of one downregulated miRNA, miR-200a, on tumor growth. Elevated levels of miR-200a inhibited Meningioma cell growth in culture and in a tumor model in vivo. Upregulation of miR-200a decreased the expression of transcription factors ZEB1 and SIP1, with consequent increased expression of E-cadherin, an adhesion protein associated with cell differentiation. Downregulation of miR-200a in Meningiomas and arachnoidal cells resulted in increased expression of β-catenin and cyclin D1 involved in cell proliferation. miR-200a was found to directly target β-catenin mRNA, thereby inhibiting its translation and blocking Wnt/β-catenin signaling, which is frequently involved in cancer. A direct correlation was found between the downregulation of miR-200a and the upregulation of β-catenin in human Meningioma samples. Thus, miR-200a appears to act as a multifunctional tumor suppressor miRNA in Meningiomas through effects on the E-cadherin and Wnt/β-catenin signaling pathways. This reveals a previously unrecognized signaling cascade involved in Meningioma tumor development and highlights a novel molecular interaction between miR-200a and Wnt signaling, thereby providing insights into novel therapies for Meningiomas.
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downregulated microrna 200a in Meningiomas promotes tumor growth by reducing e cadherin and activating the wnt β catenin signaling pathway
Molecular and Cellular Biology, 2009Co-Authors: Okay Saydam, Yiping Shen, Thomas Wurdinger, Ozlem Senol, Elvan Boke, Marianne James, Bakhos A Tannous, Anat Stemmerrachamimov, Robert M. StephensAbstract:Meningiomas, one of the most common human brain tumors, are derived from arachnoidal cells associated with brain meninges, are usually benign, and are frequently associated with neurofibromatosis type 2. Here, we define a typical human Meningioma microRNA (miRNA) profile and characterize the effects of one downregulated miRNA, miR-200a, on tumor growth. Elevated levels of miR-200a inhibited Meningioma cell growth in culture and in a tumor model in vivo. Upregulation of miR-200a decreased the expression of transcription factors ZEB1 and SIP1, with consequent increased expression of E-cadherin, an adhesion protein associated with cell differentiation. Downregulation of miR-200a in Meningiomas and arachnoidal cells resulted in increased expression of β-catenin and cyclin D1 involved in cell proliferation. miR-200a was found to directly target β-catenin mRNA, thereby inhibiting its translation and blocking Wnt/β-catenin signaling, which is frequently involved in cancer. A direct correlation was found between the downregulation of miR-200a and the upregulation of β-catenin in human Meningioma samples. Thus, miR-200a appears to act as a multifunctional tumor suppressor miRNA in Meningiomas through effects on the E-cadherin and Wnt/β-catenin signaling pathways. This reveals a previously unrecognized signaling cascade involved in Meningioma tumor development and highlights a novel molecular interaction between miR-200a and Wnt signaling, thereby providing insights into novel therapies for Meningiomas.