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[PMID]: 22494996 [Au] Autor: Manglik N; Sawicki J; Saad A; Fadare O; Soslow R; Liang SX [Ad] Dirección: Hofstra North Shore-LIJ School of Medicine, Lake Success, NY 11042, USA. [Ti] Título: Giant cell tumor of uterus resembling osseous giant cell tumor: case report and review of literature. [So] Fuente: Int J Surg Pathol;20(6):618-22, 2012 Dec. [Is] ISSN: 1940-2465 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Osteoclast-like giant cells (OLGCs) are multinucleated cells of histiocytic lineage and have been identified in a wide array of neoplasms. In the uterus, they have most frequently been reported in association with leiomyosarcomas. This article describes a case of an osteoclast-like giant cell-rich uterine tumor that was essentially indistinguishable at the morphologic and immunophenotypic levels, from typical giant cell tumor of bone. This is the first example of such a case that has been reported in the uterus to the authors' knowledge. [Mh] Términos MeSH primario: Neoplasias Óseas/diagnóstico Tumor Óseo de Células Gigantes/diagnóstico Tumores de Células Gigantes/diagnóstico Células Gigantes/patología Osteoclastos/patología Neoplasias Uterinas/diagnóstico [Mh] Términos MeSH secundario: Diagnóstico Diferencial Femenino Tumores de Células Gigantes/cirugía Tumores de Células Gigantes/ultrasonografía Hematómetra/diagnóstico Humanos Leiomioma/diagnóstico Mediana Edad Pólipos/diagnóstico Resultado del Tratamiento Neoplasias Uterinas/cirugía Neoplasias Uterinas/ultrasonografía [Pt] Tipo de publicación: CASE REPORTS; JOURNAL ARTICLE; REVIEW [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121122 [St] Status: MEDLINE [do] DOI: 10.1177/1066896912436554

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[PMID]: 22886559 [Au] Autor: Rajaraman P; Melin BS; Wang Z; McKean-Cowdin R; Michaud DS; Wang SS; Bondy M; Houlston R; Jenkins RB; Wrensch M; Yeager M; Ahlbom A; Albanes D; Andersson U; Freeman LE; Buring JE; Butler MA; Braganza M; Carreon T; Feychting M; Fleming SJ; Gapstur SM; Gaziano JM; Giles GG; Hallmans G; Henriksson R; Hoffman-Bolton J; Inskip PD; Johansen C; Kitahara CM; Lathrop M; Liu C; Le Marchand L; Linet MS; Lonn S; Peters U; Purdue MP; Rothman N; Ruder AM; Sanson M; Sesso HD; Severi G; Shu XO; Simon M; Stampfer M; Stevens VL; Visvanathan K; White E; Wolk A; Zeleniuch-Jacquotte A; Zheng W; Decker P; Enciso-Mora V; Fridley B; Gao YT; Kosel M; Lachance DH; Lau C; Rice T; Swerdlow A; Wiemels JL; Wiencke JK; Shete S; Xiang YB; Xiao Y; Hoover RN; Fraumeni JF; Chatterjee N; Hartge P; Chanock SJ [Ad] Dirección: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA. rajarama@mail.nih.gov [Ti] Título: Genome-wide association study of glioma and meta-analysis. [So] Fuente: Hum Genet;131(12):1877-88, 2012 Dec. [Is] ISSN: 1432-1203 [Cp] País de publicación: Germany [La] Idioma: eng [Ab] Resumen: Gliomas account for approximately 80 % of all primary malignant brain tumors and, despite improvements in clinical care over the last 20 years, remain among the most lethal tumors, underscoring the need for gaining new insights that could translate into clinical advances. Recent genome-wide association studies (GWAS) have identified seven new susceptibility regions. We conducted a new independent GWAS of glioma using 1,856 cases and 4,955 controls (from 14 cohort studies, 3 case-control studies, and 1 population-based case-only study) and found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to relatively more higher grade tumors being captured in the cohort studies. We further examined the 85 most promising single nucleotide polymorphism (SNP) markers identified in our study in three replication sets (5,015 cases and 11,601 controls), but no new markers reached genome-wide significance. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk. [Mh] Términos MeSH primario: Neoplasias Encefálicas/genética Glioma/genética [Mh] Términos MeSH secundario: Anciano Estudios de Casos y Controles Estudios de Cohortes Inhibidor p15 de las Quinasas Dependientes de la Ciclina/genética ADN Helicasas/genética Femenino Estudio de Asociación del Genoma Completo Glioblastoma/genética Humanos Masculino Mediana Edad Polimorfismo de Nucleótido Simple Telomerasa/genética [Pt] Tipo de publicación: JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL [Nm] Nombre de substancia: 0 (CDKN2B protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p15); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase); EC 3.6.1.- (DNA Helicases); EC 3.6.1.- (RTEL1 protein, human) [Em] Mes de ingreso: 1301 [Cu] Fecha actualización por clase: 130513 [Lr] Fecha última revisión: 130513 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121108 [St] Status: MEDLINE [do] DOI: 10.1007/s00439-012-1212-0

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[PMID]: 23298839 [Au] Autor: Babic I; Mischel PS [Ad] Dirección: Ludwig Institute for Cancer Research, UCSD, La Jolla, California, USA. [Ti] Título: Multiple functions of a glioblastoma fusion oncogene. [So] Fuente: J Clin Invest;123(2):548-51, 2013 Feb 1. [Is] ISSN: 1558-8238 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: RNA sequencing facilitates the discovery of novel gene fusions in cancer. In this issue of the JCI, Parker et al. identify an FGFR3-TACC3 fusion oncogene in glioblastoma and demonstrate a novel mechanism of pathogenicity. A miR-99a binding site within the 3'-untranslated region (3'-UTR) of FGFR3 is lost, releasing FGFR3 signaling from miR-99a-dependent inhibition and greatly enhancing tumor progression relative to WT FGFR3. These results provide compelling insight into the pathogenicity of a novel fusion oncogene and suggest new therapeutic approaches for a subset of glioblastomas. [Mh] Términos MeSH primario: Neoplasias Encefálicas/genética Fusión Génica Glioblastoma/genética MicroARNs/genética Proteínas Asociadas a Microtúbulos/genética Receptor Tipo 3 de Factor de Crecimiento de Fibroblastos/genética [Mh] Términos MeSH secundario: Animales Humanos Masculino [Pt] Tipo de publicación: COMMENT; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (MIRN99 microRNA, human); 0 (MicroRNAs); 0 (Microtubule-Associated Proteins); 0 (TACC3 protein, human); EC 2.7.10.1 (FGFR3 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 3) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: AIM; IM [Da] Fecha de ingreso para procesamiento: 130419 [St] Status: MEDLINE

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[PMID]: 23298836 [Au] Autor: Parker BC; Annala MJ; Cogdell DE; Granberg KJ; Sun Y; Ji P; Li X; Gumin J; Zheng H; Hu L; Yli-Harja O; Haapasalo H; Visakorpi T; Liu X; Liu CG; Sawaya R; Fuller GN; Chen K; Lang FF; Nykter M; Zhang W [Ad] Dirección: Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA. [Ti] Título: The tumorigenic FGFR3-TACC3 gene fusion escapes miR-99a regulation in glioblastoma. [So] Fuente: J Clin Invest;123(2):855-65, 2013 Feb 1. [Is] ISSN: 1558-8238 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Fusion genes are chromosomal aberrations that are found in many cancers and can be used as prognostic markers and drug targets in clinical practice. Fusions can lead to production of oncogenic fusion proteins or to enhanced expression of oncogenes. Several recent studies have reported that some fusion genes can escape microRNA regulation via 3'-untranslated region (3'-UTR) deletion. We performed whole transcriptome sequencing to identify fusion genes in glioma and discovered FGFR3-TACC3 fusions in 4 of 48 glioblastoma samples from patients both of mixed European and of Asian descent, but not in any of 43 low-grade glioma samples tested. The fusion, caused by tandem duplication on 4p16.3, led to the loss of the 3'-UTR of FGFR3, blocking gene regulation of miR-99a and enhancing expression of the fusion gene. The fusion gene was mutually exclusive with EGFR, PDGFR, or MET amplification. Using cultured glioblastoma cells and a mouse xenograft model, we found that fusion protein expression promoted cell proliferation and tumor progression, while WT FGFR3 protein was not tumorigenic, even under forced overexpression. These results demonstrated that the FGFR3-TACC3 gene fusion is expressed in human cancer and generates an oncogenic protein that promotes tumorigenesis in glioblastoma. [Mh] Términos MeSH primario: Neoplasias Encefálicas/genética Fusión Génica Glioblastoma/genética MicroARNs/genética Proteínas Asociadas a Microtúbulos/genética Receptor Tipo 3 de Factor de Crecimiento de Fibroblastos/genética [Mh] Términos MeSH secundario: Regiones no Traducidas 3' Animales Secuencia de Bases Neoplasias Encefálicas/metabolismo Cromosomas Humanos Par 4/genética Regulación Neoplásica de la Expresión Génica Glioblastoma/metabolismo Glioma/genética Glioma/metabolismo Humanos Masculino Ratones Ratones Desnudos MicroARNs/metabolismo Proteínas Asociadas a Microtúbulos/metabolismo Datos de Secuencia Molecular Proteínas de Fusión Oncogénica/genética Proteínas de Fusión Oncogénica/metabolismo ARN Neoplásico/genética Receptor Tipo 3 de Factor de Crecimiento de Fibroblastos/metabolismo Secuencias Repetidas en Tándem Trasplante Heterólogo Células Tumorales Cultivadas [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (3' Untranslated Regions); 0 (MIRN99 microRNA, human); 0 (MicroRNAs); 0 (Microtubule-Associated Proteins); 0 (Oncogene Proteins, Fusion); 0 (RNA, Neoplasm); 0 (TACC3 protein, human); EC 2.7.10.1 (FGFR3 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 3) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: AIM; IM [Da] Fecha de ingreso para procesamiento: 130419 [St] Status: MEDLINE

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[PMID]: 23200177 [Au] Autor: Mercier L; Araujo D; Haegelen C; Del Maestro RF; Petrecca K; Collins DL [Ad] Dirección: McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Canada. [Ti] Título: Registering pre- and postresection 3-dimensional ultrasound for improved visualization of residual brain tumor. [So] Fuente: Ultrasound Med Biol;39(1):16-29, 2013 Jan. [Is] ISSN: 1879-291X [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: The goal of this study was to find a registration technique to improve the alignment of ultrasound images taken before and after brain tumor resection. Validation was performed on 16 tumor cases in 2 ways: (1) manually selected tags on pre- and postresection ultrasounds were used to compute the mean Euclidean distance between corresponding points in the 2 volumes before and after registration; and (2) the surgeon was asked to rank and rate the quality of the alignment before and after registration. The mean distance was 2.7 mm after a rigid registration and 1.7 mm after a nonlinear registration. Of 16 cases, the surgeon determined that initially only 2 were satisfactorily aligned; after the rigid registration, 5 were satisfactory, and after the nonlinear registration, 13 were satisfactory. According to both the distance and the ranking metrics, the nonlinear registration approach significantly improved the alignment of the ultrasound images. [Mh] Términos MeSH primario: Neoplasias Encefálicas/cirugía Neoplasias Encefálicas/ultrasonografía Glioblastoma/cirugía Glioblastoma/ultrasonografía Imagen Tridimensional Neoplasia Residual/ultrasonografía [Mh] Términos MeSH secundario: Femenino Humanos Masculino Mediana Edad [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121203 [St] Status: MEDLINE

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[PMID]: 22795538 [Au] Autor: Bexell D; Svensson A; Bengzon J [Ad] Dirección: Lund Stem Cell Center, BMC B10, Lund University, Lund, Sweden; Molecular Medicine, Center for Molecular Pathology, Lund University, Skåne University Hospital, Malmö, Sweden. daniel.bexell@med.lu.se [Ti] Título: Stem cell-based therapy for malignant glioma. [So] Fuente: Cancer Treat Rev;39(4):358-65, 2013 Jun. [Is] ISSN: 1532-1967 [Cp] País de publicación: Netherlands [La] Idioma: eng [Ab] Resumen: Stem cells have been extensively investigated as tumour-tropic vectors for gene delivery to solid tumours. In this review, we discuss the potential for using stem cells as cellular vector systems in gene therapy for malignant gliomas, with a focus on neural stem cells, and multipotent mesenchymal stromal cells. Tumour cell-derived substances and factors associated with tumour-induced inflammation and tumour neovascularisation can specifically attract stem cells to invasive gliomas. Injected stem cells engineered to produce anti-tumour substances have shown strong therapeutic effects in experimental glioma models. However, the potential caveats include the immunosuppressive functions of multipotent mesenchymal stromal cells, the contribution of stem cells to the pro-tumourigenic stroma, and the malignant transformation of implanted stem cells. In addition, it is not yet known which stem cell types and therapeutic genes will be most effective for the treatment of glioma patients. Here, we highlight the possibilities and problems for translating promising experimental findings in glioma models into the clinic. [Mh] Términos MeSH primario: Neoplasias Encefálicas/terapia Ingeniería Genética/métodos Terapia Genética/métodos Vectores Genéticos/fisiología Glioblastoma/terapia Células Madre/fisiología [Mh] Términos MeSH secundario: Neoplasias Encefálicas/genética Vectores Genéticos/metabolismo Glioblastoma/genética Humanos Células Madre/metabolismo [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130325 [St] Status: MEDLINE

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[PMID]: 22722053 [Au] Autor: Laperriere N; Weller M; Stupp R; Perry JR; Brandes AA; Wick W; van den Bent MJ [Ad] Dirección: Department of Radiation Oncology, Princess Margaret Hospital/University Health Network, University of Toronto, Toronto, ON, Canada. norm.laperriere@rmp.uhn.on.ca [Ti] Título: Optimal management of elderly patients with glioblastoma. [So] Fuente: Cancer Treat Rev;39(4):350-7, 2013 Jun. [Is] ISSN: 1532-1967 [Cp] País de publicación: Netherlands [La] Idioma: eng [Ab] Resumen: Median age at diagnosis in patients with glioblastoma (GB) is slowly increasing with an aging population in Western countries, and was 64years in 2006. The number of patients age 65 and older with GB will double in 2030 compared with 2000. Survival in this older cohort of patients is significantly less than seen in younger patients. This may in part be related to more aggressive biology of tumor, reduced use of standard management approaches, increased toxicity of available therapies, and increased presence of comorbidities in this older patient population. Limited data do support the use of more extensive resection in these patients. Randomized data support the use of post-operative radiotherapy (RT) versus supportive care, but do not demonstrate a benefit for the use of the standard 6weeks course of RT over hypofractionated RT given over 3weeks. Preliminary data of randomized studies raise the possibility of temozolomide alone as an option for these patients. The use of 6weeks of RT with concurrent and adjuvant temozolomide has been associated with reasonably good survival in several uncontrolled small series of selected older patients; however, this better outcome may be related to the selection of better prognosis patients rather than the specific therapy utilized. The current National Cancer Institute of Canada (NCIC) and European Organization for Research and Treatment of Cancer (EORTC) CE.6/26062/22061 randomized study of short course RT with or without concurrent and adjuvant temozolomide will help determine the optimal therapy for this older cohort with currently available therapies. [Mh] Términos MeSH primario: Glioblastoma/terapia [Mh] Términos MeSH secundario: Factores de Edad Anciano Anciano de 80 o más Años Terapia Combinada Dacarbazina/análogos & derivados Dacarbazina/uso terapéutico Glioblastoma/patología Glioblastoma/radioterapia Glioblastoma/cirugía Humanos Mediana Edad Ensayos Clínicos Controlados Aleatorios como Asunto [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW [Nm] Nombre de substancia: 4342-03-4 (Dacarbazine); 85622-93-1 (temozolomide) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130325 [St] Status: MEDLINE

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[PMID]: 23148444 [Au] Autor: Lin XY; Wang Y; Liu Y; Sun Y; Miao Y; Zhang Y; Yu JH; Wang EH [Ad] Dirección: Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, 110001, China. [Ti] Título: Pleomorphic lipoma lacking mature fat component in extensive myxoid stroma: a great diagnostic challenge. [So] Fuente: Diagn Pathol;7:155, 2012. [Is] ISSN: 1746-1596 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Pleomorphic lipoma is a relatively uncommon entity, and is considered as a variant of spindle cell lipoma. Histologically, spindle cell lipoma/pleomorphic lipoma consists of varying quantity of mature fat, bland spindle cells and ropey collagen. In addition, pleomorphic lipoma is characterized by multinucleate giant cells, which possess the "floret-like" nuclei and marked pleomorphism. So, in contrast to spindle cell lipoma, pleomorphic lipoma is more easily misdiagnosed as a malignant tumor. Herein, we report a peculiar case of pleomorphic lipoma occurring in axilla with entirely devoid of mature fat in a 71-year-old male. The histopathological findings demonstrated the tumor was made up of bland spindle cells admixed with scattered "floret-like" cells and irregular ropey collagen in an extensive myxoid stroma. Immunostaining showed that the tumor was positive for the Vimentin, Bcl-2 and CD34, and was negative for S-100, desmin, CD68, and α-SMA. Although no fat component was found in the whole section, the tumor was still diagnosed as a pelomprphic lipoma. To our knowledge, this is the third reported case of pelomprphic lipoma which entirely lacked lipomatous component. Because of the existence of atypical multinucleate giant cells and lack of mature fat, this tumor may be easily misdiagnosed nonlipomatous lesions, such as myxoid fibrosarcoma, giant cell fibroblastoma. So, it is necessary to pay careful attention to the histological spectrum of pleomorphic lipoma, including the tumor with devoid of fat, and it should be kept in mind that pelomprphic lipoma still can be diagnosed even if lacking lipomatous component. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1967123180611361. [Mh] Términos MeSH primario: Tejido Adiposo/patología Células Gigantes/patología Lipoma/patología Células del Estroma/patología [Mh] Términos MeSH secundario: Tejido Adiposo/química Anciano Biopsia Colágeno/análisis Diagnóstico Diferencial Humanos Inmunohistoquímica Lipoma/química Masculino Valor Predictivo de las Pruebas Células del Estroma/química Marcadores Biológicos de Tumor/análisis [Pt] Tipo de publicación: CASE REPORTS; JOURNAL ARTICLE [Nm] Nombre de substancia: 0 (Tumor Markers, Biological); 9007-34-5 (Collagen) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130301 [St] Status: MEDLINE [do] DOI: 10.1186/1746-1596-7-155

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[PMID]: 22975219 [Au] Autor: McDonald KL; Rapkins RW; Olivier J; Zhao L; Nozue K; Lu D; Tiwari S; Kuroiwa-Trzmielina J; Brewer J; Wheeler HR; Hitchins MP [Ad] Dirección: Prince of Wales Clinical School, University of NSW, Australia. k.mcdonald@unsw.edu.au [Ti] Título: The T genotype of the MGMT C>T (rs16906252) enhancer single-nucleotide polymorphism (SNP) is associated with promoter methylation and longer survival in glioblastoma patients. [So] Fuente: Eur J Cancer;49(2):360-8, 2013 Jan. [Is] ISSN: 1879-0852 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Clinical studies in patients with newly diagnosed glioblastoma treated with temozolomide have shown that the methylation status of the O(6)-methylguanine-DNA methyltransferase (MGMT) gene is both predictive and prognostic of outcome. Methylation of the promoter region of MGMT is the most clinically relevant measure of MGMT expression and its assessment has become integral in current and planned clinical trials in glioblastoma. Our study confirmed that MGMT methylation, assessed by pyrosequencing, is associated with a significant survival benefit in glioblastoma patients treated with temozolomide (either concurrently with radiotherapy or sequential treatment). More interestingly, our study demonstrated that a promoter variant, the c.-56C>T (rs16906252) single nucleotide polymorphism (SNP) located within a cis-acting enhancer element at the proximal end of MGMT, is associated with the presence of MGMT promoter methylation in de novo glioblastoma. Furthermore, we show that the overall survival of patients carrying both the SNP and MGMT methylation showed a strong survival benefit when compared to either molecular event on their own. Promoter reporter experiments in MGMT methylated glioblastoma cell lines showed the T allele conferred a ∼30% reduction in normalised MGMT promoter activity compared to the wild-type haplotype. This might account for the propensity of the T allele to undergo promoter methylation, and in turn, the improved survival observed in carriers of the T allele. An independent validation on larger cohorts is required to confirm the prognostic and predictive value of individuals carrying the T allele. [Mh] Términos MeSH primario: Neoplasias Encefálicas/genética Neoplasias Encefálicas/terapia Metilación de ADN Metilasas de Modificación del ADN/genética Enzimas Reparadoras del ADN/genética Glioblastoma/genética Glioblastoma/terapia Proteínas Supresoras de Tumor/genética [Mh] Términos MeSH secundario: Adulto Anciano Anciano de 80 o más Años Antineoplásicos Alquilantes/uso terapéutico Neoplasias Encefálicas/enzimología Estudios de Cohortes Terapia Combinada Dacarbazina/análogos & derivados Dacarbazina/uso terapéutico Femenino Genotipo Glioblastoma/enzimología Humanos Masculino Mediana Edad Polimorfismo de Nucleótido Simple Regiones Promotoras Genéticas Estudios Retrospectivos Análisis de Supervivencia Transfección Adulto Joven [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Antineoplastic Agents, Alkylating); 0 (Tumor Suppressor Proteins); 4342-03-4 (Dacarbazine); 85622-93-1 (temozolomide); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130109 [St] Status: MEDLINE

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[PMID]: 22929620 [Au] Autor: Mao RJ; Jiang ZM; Zhang HZ; Zhu XZ; Zhang QL [Ad] Dirección: Department of Pathology, Foshan Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Foshan, People's Republic of China. [Ti] Título: Clinical and pathological characteristics of giant cell angioblastoma: a case report. [So] Fuente: Diagn Pathol;7:113, 2012. [Is] ISSN: 1746-1596 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Giant cell angioblastoma (GCAB) is an extremely rare soft tissue tumor of early childhood and only five cases have been described to date. As such the clinical, pathological, and prognostic features are poorly defined. We prensent here a new case of GCAB in bone of a child aged 4-years old. The lesion was composed of dense and loose cell regions. The dense regions were characterized by nodular, linear, and plexiform aggregates of oval- to spindle-shaped tumor cells around small vascular channels and interspersed with large mononuclear cells and multinucleate giant cells. The loose cell areas were characterized by distributed fibroblasts and abundant myxoid matrix, which diminished with patient age. Infiltrative growth was observed in some areas. Oval-to-spindle cells showed positivity for Vimentin, CD31 and CD34 staining, and partial positivity for smooth muscle actin. Mononuclear cells and multinucleate giant cells showed Vimentin and CD68 positivity. Seventeen months after thorough curettage of the lesion, a local recurrence was found. Based upon the clinical, histological and immunohistochemical findings, infiltrate condition, and prognosis, we classified GCAB into two subtypes. Type I does not infiltrate surrounding tissues and has good prognosis. Type II infiltrates the surrounding tissues, relapses earlier, and has worse prognosis. This report augments the limited GCAB literature to promote our understanding and guide therapy of this rare disease. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/6699811297488137. [Mh] Términos MeSH primario: Neoplasias Femorales/patología Tumor Óseo de Células Gigantes/patología [Mh] Términos MeSH secundario: Preescolar Legrado Diagnóstico Diferencial Neoplasias Femorales/química Neoplasias Femorales/cirugía Tumor Óseo de Células Gigantes/química Tumor Óseo de Células Gigantes/cirugía Humanos Inmunohistoquímica Masculino Invasividad Neoplásica Recurrencia Local de Neoplasia Valor Predictivo de las Pruebas Factores de Tiempo Tomografía Computarizada por Rayos X Resultado del Tratamiento Marcadores Biológicos de Tumor/análisis [Pt] Tipo de publicación: CASE REPORTS; JOURNAL ARTICLE [Nm] Nombre de substancia: 0 (Tumor Markers, Biological) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130101 [St] Status: MEDLINE [do] DOI: 10.1186/1746-1596-7-113

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1			PalabrasDescriptor de asuntoDescriptor de asunto primarioLímitesAutorPalabras del títuloPalabras del resumenIdiomaPaís de publicaciónNombre de substanciaNombre personal como asuntoRevistaAsunto de RevistaISSNTipo de publicaciónIdentificador únicoMes de ingresoAño de publicaciónTexto completoActualización por claseCategoria DeCSCategoria DeCS explodidaCategoria CIE-10SubSetsPaís de AfiliaciónAfiliación
2	and or and not		PalabrasDescriptor de asuntoDescriptor de asunto primarioLímitesAutorPalabras del títuloPalabras del resumenIdiomaPaís de publicaciónNombre de substanciaNombre personal como asuntoRevistaAsunto de RevistaISSNTipo de publicaciónIdentificador únicoMes de ingresoAño de publicaciónTexto completoActualización por claseCategoria DeCSCategoria DeCS explodidaCategoria CIE-10SubSetsPaís de AfiliaciónAfiliación
3	and or and not		PalabrasDescriptor de asuntoDescriptor de asunto primarioLímitesAutorPalabras del títuloPalabras del resumenIdiomaPaís de publicaciónNombre de substanciaNombre personal como asuntoRevistaAsunto de RevistaISSNTipo de publicaciónIdentificador únicoMes de ingresoAño de publicaciónTexto completoActualización por claseCategoria DeCSCategoria DeCS explodidaCategoria CIE-10SubSetsPaís de AfiliaciónAfiliación

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