20 results on '"López-Ginés, C"'
Search Results
2. Study of the activation of TLR receptors in neurospheres from glioblastoma cells in vitro
- Author
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Albert Bellver, D., primary, Gil-Benso, R., additional, Martínez, A., additional, San-Miguel, T., additional, Muñoz-Hidalgo, L., additional, Carratalá, A., additional, Gozalbo, D., additional, López-Ginés, C., additional, Cerdá-Nicolás, M., additional, Gil, M.L., additional, and Megías, J., additional
- Published
- 2018
- Full Text
- View/download PDF
3. Association between epidermal growth factor receptor amplification and ADP-ribosylation factor 1 methylation in human glioblastoma
- Author
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López-Ginés C, Navarro L, Muñoz-Hidalgo L, Buso E, Morales JM, Gil-Benso R, Gregori-Romero M, Megías J, Roldán P, Segura-Sabater R, Almerich-Silla JM, Monleón D, and Cerdá-Nicolás M
- Published
- 2017
4. Molecular Progression in Unusual Recurrent Non-Pediatric Intracranial Clear Cell Meningioma
- Author
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Domingo-Arrué, B., primary, Gil-Benso, Rosario, additional, Megías, J., additional, Navarro, L., additional, San-Miguel, T., additional, Muñoz-Hidalgo, L., additional, López-Ginés, C., additional, and Cerdá-Nicolás, M., additional
- Published
- 2017
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5. 44P - Study of the activation of TLR receptors in neurospheres from glioblastoma cells in vitro
- Author
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Albert Bellver, D., Gil-Benso, R., Martínez, A., San-Miguel, T., Muñoz-Hidalgo, L., Carratalá, A., Gozalbo, D., López-Ginés, C., Cerdá-Nicolás, M., Gil, M.L., and Megías, J.
- Published
- 2018
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6. Congenital hyperthyroidism with reciprocal translocation t(1;17)(q25;q21)
- Author
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Gregori-Romero, M., López-Ginés, C., Gil, R., and Pellín, A.
- Published
- 1989
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7. Reciprocal translocation t(1;18)(p32;q21) in a patient with some phenotypical anomalies
- Author
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Gil, R., López-Ginés, C., Gregori-Romero, M., Sánchez, M. D., and Pellin, A.
- Published
- 1987
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8. An azoospermic male with reciprocal translocation t(1;15)(q11;p11)
- Author
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López-Ginés, C., Gil, R., Gregori-Romero, M., and Pellin, A.
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- 1987
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9. An unusual translocation associated with recurrent spontaneous abortions
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Gregori-Romero, M., Gil, R., López-Ginés, C., and Pellín, A.
- Published
- 1989
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10. 44PStudy of the activation of TLR receptors in neurospheres from glioblastoma cells in vitro.
- Author
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Bellver, D Albert, Gil-Benso, R, Martínez, A, San-Miguel, T, Muñoz-Hidalgo, L, Carratalá, A, Gozalbo, D, López-Ginés, C, Cerdá-Nicolás, M, and Gil, M L
- Subjects
- *
CYTOLOGY , *CELLS , *BIOCHEMICAL engineering , *EXTRACELLULAR matrix - Published
- 2018
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11. Matched Paired Primary and Recurrent Meningiomas Points to Cell-Death Program Contributions to Genomic and Epigenomic Instability along Tumor Progression.
- Author
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San-Miguel T, Megías J, Monleón D, Navarro L, Muñoz-Hidalgo L, Montoliu C, Meri M, Roldán P, Cerdá-Nicolás M, and López-Ginés C
- Abstract
Meningioma (MN) is an important cause of disability, and predictive tools for estimating the risk of recurrence are still scarce. The need for objective and cost-effective techniques addressed to this purpose is well known. In this study, we present methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) as a friendly method for deepening the understanding of the mechanisms underlying meningioma progression. A large follow-up allowed us to obtain 50 samples, which included the primary tumor of 20 patients in which half of them are suffering one recurrence and the other half are suffering more than one. We histologically characterized the samples and performed MS-MLPA assays validated by FISH to assess their copy number alterations (CNA) and epigenetic status. Interestingly, we determined the increase in tumor instability with higher values of CNA during the progression accompanied by an increase in epigenetic damage. We also found a loss of HIC1 and the hypermethylation of CDKN2B and PTEN as independent prognostic markers. Comparison between grade 1 and higher primary MN's self-evolution pointed to a central role of GSTP1 in the first stages of the disease. Finally, a high rate of alterations in genes that are related to apoptosis and autophagy, such as DAPK1 , PARK2 , BCL2 , FHIT , or VHL , underlines an important influence on cell-death programs through different pathways.
- Published
- 2022
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12. Desmoplastic infantile astrocytoma with atypical phenotype, PTEN homozygous deletion and BRAF V600E mutation.
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Megías J, San-Miguel T, Sánchez M, Navarro L, Monleón D, Calabuig-Fariñas S, Morales JM, Muñoz-Hidalgo L, Roldán P, Cerdá-Nicolás M, and López-Ginés C
- Subjects
- Homozygote, Humans, Mutation genetics, PTEN Phosphohydrolase genetics, Phenotype, Proto-Oncogene Proteins B-raf genetics, Sequence Deletion, Astrocytoma pathology, Brain Neoplasms pathology, Ganglioglioma genetics
- Abstract
Desmoplastic infantile astrocytoma (DIA) is rare, cystic and solid tumor of infants usually found in superficial cerebral hemispheres. Although DIA is usually benign, uncommon cases bearing malignant histological and aggressive clinical features have been described in the literature. We report a newborn patient who was diagnosed with a DIA and died postresection. Pathologic examination revealed that the main part of the tumor had benign features, but the internal region showed areas with a more aggressive appearance, with higher-proliferative cells, anaplastic GFAP positive cells with cellular polymorphism, necrosis foci, vascular hyperplasia with endothelial proliferation and microtrombosis. Genetic study, performed in both regions of the tumor, showed a BRAF V600E mutation and a homozygous deletion in PTEN, without changes in other relevant genes like EGFR, CDKN2A, TP53, NFKBIA, CDK4, MDM2 and PDGFRA. Although PTEN homozygous deletions are described in gliomas, the present case constitutes the first report of a PTEN mutation in a DIA, and this genetic feature may be related to the malignant behavior of a usually benign tumor. These genetic findings may point at the need of further and deeper genetic characterization of DIAs, in order to better understand the biology of this tumor and to obtain new prognostic approaches, a better clinical management and targeted therapies, especially in malignant cases of DIA., (© 2022. The Author(s).)
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- 2022
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13. Whole-exome sequencing, EGFR amplification and infiltration patterns in human glioblastoma.
- Author
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López-Ginés C, Muñoz-Hidalgo L, San-Miguel T, Megías J, Triviño JC, Calabuig S, Roldán P, Cerdá-Nicolás M, and Monleón D
- Abstract
Glioblastoma (GBM) is the most common malignant primary brain tumor in adults. This cancer shows rapid, highly infiltrative growth, that invades individually or in small groups the surrounding tissue. The aggressive tumor biology of GBM has devastating consequences with a median survival of 15 months. GBM often has Epidermal Growth Factor Receptor ( EGFR ) abnormalities. Despite recent advances in the study of GBM tumor biology, it is unclear whether mutations in GBM are related to EGFR amplification and relevant phenotypes like tumor infiltration. This study aimed to perform whole-exome sequencing analysis in 30 human GBM samples for identifying mutational portraits associated with EGFR amplification and infiltrative patterns. Our results show that EGFR -amplified tumors have overall higher mutation rates than EGFR-no-amplified. Six genes out of 2029 candidate genes show mutations associated with EGFR amplification status. Mutations in these genes for GBM are novel, not previously reported in GBM, and with little presence in the TCGA database. GPR179, USP48 , and BLK show mutation only in EGFR -amplified cases, and all the affected cases exhibit diffuse infiltrative patterns. On the other hand, mutations in ADGB, EHHADH , and PTPN13 , were present only in the EGFR -no-amplified group with a more diverse infiltrative phenotype. Overall, our work identified different mutational portraits of GBM related to well-established features like EGFR amplification and tumor infiltration., Competing Interests: Juan Carlos Triviño is an employee for Sistemas Genomicos SA. Daniel Monleón is a member of the editorial board of the American Journal of Cancer Research., (AJCR Copyright © 2021.)
- Published
- 2021
14. The Status of EGFR Modulates the Effect of miRNA-200c on ZEB1 Expression and Cell Migration in Glioblastoma Cells.
- Author
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Muñoz-Hidalgo L, San-Miguel T, Megías J, Serna E, Calabuig-Fariñas S, Monleón D, Gil-Benso R, Cerdá-Nicolás M, and López-Ginés C
- Subjects
- Apoptosis, Biomarkers, Tumor genetics, Cell Movement, Cell Proliferation, ErbB Receptors genetics, Glioblastoma genetics, Glioblastoma metabolism, Humans, Mutation, Prognosis, Tumor Cells, Cultured, Zinc Finger E-box-Binding Homeobox 1 genetics, Biomarkers, Tumor metabolism, Gene Amplification, Gene Expression Regulation, Neoplastic, Glioblastoma pathology, MicroRNAs genetics, Zinc Finger E-box-Binding Homeobox 1 metabolism
- Abstract
Migration of glioblastoma cells into surrounding tissue is one of the main features that makes this tumor incurable. We evaluated whole-genome miRNA expression profiling associated with different EGFR amplification patterns in 30 cases of primary glioblastoma. From the 64 miRNAs that showed differential expression between tumors with a high level of EGFR amplification and tumors without EGFR amplification, 40% were related with cell migration, being miR-200c the most differentially expressed between these two groups. We investigated the effect of miR-200c on ZEB1 expression and cell migration in an in vitro transfection model with a miR-200c mimic, a miR-200c inhibitor and siRNA targeting EGFR in three short-term cultures with different levels of EGFR amplification obtained from resected glioblastomas. The cell culture with the highest EGFR amplification level presented the lowest miR-200c expression and the status of EGFR modulated the effect of miR-200c on ZEB1 expression. Silencing EGFR led to miR-200c upregulation and ZEB1 downregulation in transfected cultures, except in the presence of high levels of EGFR. Likewise, miR-200c upregulation decreased ZEB1 expression and inhibited cell migration, especially when EGFR was not amplified. Our results suggest that modulating miR-200c may serve as a novel therapeutic approach for glioblastoma depending on EGFR status.
- Published
- 2020
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15. Identification of New Genetic Clusters in Glioblastoma Multiforme: EGFR Status and ADD3 Losses Influence Prognosis.
- Author
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Navarro L, San-Miguel T, Megías J, Santonja N, Calabuig S, Muñoz-Hidalgo L, Roldán P, Cerdá-Nicolás M, and López-Ginés C
- Subjects
- Brain Neoplasms pathology, DNA Copy Number Variations genetics, ErbB Receptors metabolism, Female, Gene Amplification, Glioblastoma pathology, Humans, Male, Middle Aged, Prognosis, Signal Transduction genetics, Survival Analysis, Brain Neoplasms genetics, Calmodulin-Binding Proteins metabolism, Glioblastoma genetics, Multigene Family
- Abstract
Glioblastoma multiforme (GB) is one of the most aggressive tumors. Despite continuous efforts to improve its clinical management, there is still no strategy to avoid a rapid and fatal outcome. EGFR amplification is the most characteristic alteration of these tumors. Although effective therapy against it has not yet been found in GB, it may be central to classifying patients. We investigated somatic-copy number alterations (SCNA) by multiplex ligation-dependent probe amplification in a series of 137 GB, together with the detection of EGFR vIII and FISH analysis for EGFR amplification. Publicly available data from 604 patients were used as a validation cohort. We found statistical associations between EGFR amplification and/or EGFR vIII, and SCNA in CDKN2A, MSH6, MTAP and ADD3 . Interestingly, we found that both EGFR vIII and losses on ADD3 were independent markers of bad prognosis ( p = 0.028 and 0.014, respectively). Finally, we got an unsupervised hierarchical classification that differentiated three clusters of patients based on their genetic alterations. It offered a landscape of EGFR co-alterations that may improve the comprehension of the mechanisms underlying GB aggressiveness. Our findings can help in defining different genetic profiles, which is necessary to develop new and different approaches in the management of our patients.
- Published
- 2020
- Full Text
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16. Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.
- Author
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Muñoz-Hidalgo L, San-Miguel T, Megías J, Monleón D, Navarro L, Roldán P, Cerdá-Nicolás M, and López-Ginés C
- Subjects
- Adult, Aged, Biomarkers, Tumor, Biopsy, Disease Progression, ErbB Receptors genetics, ErbB Receptors metabolism, Female, Glioblastoma pathology, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Male, Middle Aged, Mutation, Prognosis, Survival Analysis, Young Adult, DNA Copy Number Variations, Gene Amplification, Glioblastoma genetics, Glioblastoma mortality
- Abstract
Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of aggressiveness. Interestingly, accumulation of CNAs, as a measure of tumor mutational burden, was frequent and significantly associated to shortened survival. EGFR-amplified GBMs displayed both a higher number of concrete CNAs and a higher global tumor mutational burden than their no EGFR-amplified counterparts. In addition to genetic changes previously described in GBM, we found PARK2 and LARGE1 CNAs associated to EGFR amplification. The set of genes analyzed allowed us to explore relevant signaling pathways on GBM. Both PARK2 and LARGE1 are related to receptor tyrosine kinase/PI3K/PTEN/AKT/mTOR-signaling pathway. Finally, we found an association between the molecular pathways altered, EGFR amplification and a poor outcome. Our results underline the potential interest of categorizing GBM according to their EGFR amplification level and the usefulness of assessing the tumor mutational burden. These approaches would open new knowledge possibilities related to GBM biology and therapy., (Copyright © 2019 Neoplasia Press, Inc. Published by Elsevier Inc. All rights reserved.)
- Published
- 2020
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17. Characterization of the new human pleomorphic undifferentiated sarcoma TP53-null cell line mfh-val2.
- Author
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Gil-Benso R, Megías J, San-Miguel T, Pinto S, Callaghan RC, López-Ginés C, and Cerdá-Nicolás M
- Abstract
Pleomorphic undifferentiated sarcoma (PUS), also called malignant fibrous histiocytoma, is a soft tissue sarcoma which occurs predominantly in the extremities. Its origin is a poorly defined mesenchymal cell, which derives to histiocytic and fibroblastic cells. The patient, a 58 year-old man, presented a lesion located in the forearm composed by spindle cells and multinucleated giant cells, which expressed vimentin and adopted a histological pattern formed by irregular-swirling fascicles. Cells were cultured in vitro and a new cell line was established. We characterized this new cell line by histological analyses, cytogenetics (using G-bands and spectral karyotype technique) and cytometric analyses. Cells were grown in culture for more than 100 passages. They had elongated or polygonal morphology. The cells presented a saturation rate of 70,980 cells/cm
2 , a plating efficiency of 21.5% and a mitotic index of 21 mitoses per field. The cell line was tumorigenic in nude mice. The ploidy study using flow cytometry revealed an aneuploid peak with a DNA index of 1.43. A side population was detected, demonstrating the presence of stem and progenitor cells. Cytogenetics showed a hypotriploid range with many clonal unbalanced rearrangements. Loss of p53 gene was evidenced by MLPA. We describe, for the first time, the characterization of a new human PUS TP53-null cell line called mfh-val2. Mfh-val2 presents a wide number of applications as a TP53-null cell line and a great interest in order to characterize genetic alterations influencing the oncogenesis or progression of PUS and to advance in the biological investigation of this tumor.- Published
- 2017
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18. Expression of the Chemokine Receptors CXCR3, CXCR4, CXCR7 and Their Ligands in Rhabdomyosarcoma.
- Author
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San-Miguel T, Pinto S, Navarro L, Callaghan RC, Monteagudo C, López-Ginés C, Cerdá-Nicolás M, and Gil-Benso R
- Subjects
- Adolescent, Child, Child, Preschool, Female, Humans, Infant, Male, Receptors, CXCR genetics, Receptors, CXCR3 genetics, Receptors, CXCR4 genetics, Rhabdomyosarcoma genetics
- Abstract
Rhabdomyosarcomas (RMS) are soft tissue malignant tumors of childhood and adolescents. The mechanisms underlying their aggressiveness are still poorly understood. Chemokines are chemotactic proteins involved in pathological processes that have been intensely studied in several types of cancers because of their influence in migration, angiogenesis, or metastases. We analyzed the expression of the chemokine receptors CXCR3, CXCR4 and CXCR7 and their ligands CXCL9, CXCL10, CXCL11 and CXCL12, in 15 RMS samples derived from nine patients. Expression was measured in tumors and primary cultures of RMS by Real-Time Polymerase Chain Reaction, immunostaining and flow cytometry. Our results show that these receptors are widely expressed in RMS. A significant difference between CXCL12/CXCR4, CXCL12/CXCR7, CXCL11/CXCR7 expression ratios was found in alveolar versus embryonal RMS and similarly between CXCL12/CXCR4 and CXCL11/CXCR3 ratios in primary versus recurrent tumors. These findings suggest a possible association between the interrelation of chemokine/chemokine-receptor and an aggressive biological behavior in RMS.
- Published
- 2015
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19. Arterial and venous endothelia display differential functional fractalkine (CX3CL1) expression by angiotensin-II.
- Author
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Rius C, Piqueras L, González-Navarro H, Albertos F, Company C, López-Ginés C, Ludwig A, Blanes JI, Morcillo EJ, and Sanz MJ
- Subjects
- Angiotensin II Type 1 Receptor Blockers pharmacology, Animals, Apolipoproteins E genetics, Apolipoproteins E metabolism, Arteries drug effects, Arterioles drug effects, Arterioles metabolism, Atherosclerosis genetics, Atherosclerosis metabolism, Atherosclerosis pathology, Atherosclerosis prevention & control, CX3C Chemokine Receptor 1, Cell Adhesion, Cells, Cultured, Chemokine CX3CL1 genetics, Disease Models, Animal, Endothelial Cells drug effects, Extracellular Signal-Regulated MAP Kinases metabolism, Female, Human Umbilical Vein Endothelial Cells metabolism, Humans, Interferon-gamma metabolism, Leukocyte Rolling, Leukocytes metabolism, Losartan pharmacology, Male, Membrane Glycoproteins genetics, Membrane Glycoproteins metabolism, Membrane Proteins genetics, Membrane Proteins metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, NADPH Oxidase 2, NADPH Oxidase 4, NADPH Oxidase 5, NADPH Oxidases genetics, NADPH Oxidases metabolism, NF-kappa B metabolism, RNA Interference, Receptors, Chemokine genetics, Receptors, Chemokine metabolism, Signal Transduction, Time Factors, Transfection, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, Veins drug effects, Venules drug effects, Venules metabolism, p38 Mitogen-Activated Protein Kinases metabolism, Angiotensin II metabolism, Arteries metabolism, Chemokine CX3CL1 metabolism, Endothelial Cells metabolism, Veins metabolism
- Abstract
Objective: Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX(3)CL1) was explored., Methods and Results: Enhanced CX(3)CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX(3)CL1 receptor (CX(3)CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX(3)CL1 expression, yet neutralization of CX(3)CL1 activity only significantly inhibited Ang-II-induced mononuclear cell-human umbilical arterial endothelial cell interactions (73%) but not with human umbilical venous endothelial cells. The use of small interfering RNA revealed the involvement of tumor necrosis factor-α in Ang-II-induced CX(3)CL1 upregulation and mononuclear cell arrest. Nox5 knockdown with small interfering RNA or pharmacological inhibition of extracellular signal-regulated kinases1/2, p38 mitogen-activated protein kinase, and nuclear factor-κB also abolished these responses. Finally, when human umbilical arterial endothelial cells were costimulated with Ang-II, tumor necrosis factor-α, and interferon-γ, CX(3)CL1 expression and mononuclear cell adhesiveness were more pronounced than when each stimulus was provided alone., Conclusions: These results suggest that Ang-II induces functional CX(3)CL1 expression in arterial but not in venous endothelia. Thus, targeting endothelial CX(3)CL1-mononuclear leukocyte CX(3)CR1 interactions may constitute a new therapeutic strategy in the treatment of Ang-II-associated cardiovascular diseases.
- Published
- 2013
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20. Metabolic aggressiveness in benign meningiomas with chromosomal instabilities.
- Author
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Monleón D, Morales JM, Gonzalez-Segura A, Gonzalez-Darder JM, Gil-Benso R, Cerdá-Nicolás M, and López-Ginés C
- Subjects
- Cytogenetic Analysis, Humans, In Situ Hybridization, Fluorescence, Magnetic Resonance Spectroscopy, Meningeal Neoplasms metabolism, Meningeal Neoplasms pathology, Meningioma metabolism, Meningioma pathology, Neoplasm Staging, Tumor Cells, Cultured, Chromosomal Instability, Chromosome Aberrations, Meningeal Neoplasms genetics, Meningioma genetics, Metabolome genetics
- Abstract
Meningiomas are often considered benign tumors curable by surgery, but most recurrent meningiomas correspond to histologic benign tumors. Because alterations in chromosome 14 among others have suggested clinical aggressiveness and recurrence, determining both the molecular phenotype and the genetic profile may help distinguish tumors with aggressive metabolism. The aim of this study was to achieve higher specificity in the detection of meningioma subgroups by measuring chromosomal instabilities by fluorescence in situ hybridization and cytogenetics and metabolic phenotypes by high-resolution magic angle spinning spectroscopy. We studied 46 meningioma biopsies with these methodologies. Of these, 34 were of WHO grade 1 and 12 were of WHO grade 2. Genetic analysis showed a subgroup of histologic benign meningioma with chromosomal instabilities. The metabolic phenotype of this subgroup indicated an aggressive metabolism resembling that observed for atypical meningioma. According to the metabolic profiles, these tumors had increased energy demand, higher hypoxic conditions, increased membrane turnover and cell proliferation, and possibly increased resistance to apoptosis. Taken together, our results identify distinct metabolic phenotypes for otherwise benign meningiomas based on cytogenetic studies and global metabolic profiles of intact tumors. Measuring the metabolic phenotype of meningioma intact biopsies at the same time as histopathologic analysis may allow the early detection of clinically aggressive tumors., (©2010 AACR.)
- Published
- 2010
- Full Text
- View/download PDF
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