Literature DB >> 20694558

ASPM gene expression in medulloblastoma.

Tânia M Vulcani-Freitas1, Najsla Saba-Silva, Andréa Cappellano, Sérgio Cavalheiro, Sueli K N Marie, Sueli M Oba-Shinjo, Suzana M F Malheiros, Sílvia Regina Caminada de Toledo.   

Abstract

PURPOSE: Medulloblastomas are the most common malignant tumors of the central nervous system in childhood. The incidence is about 19-20% between children younger than 16 years old with peak incidence between 4 and 7 years. Despite its sensibility to no specific therapeutic means like chemotherapy and radiotherapy, the treatment is very aggressive and frequently results in regression, growth deficit, and endocrine dysfunction. From this point of view, new treatment approaches are needed such as molecular targeted therapies. Studies in glioblastoma demonstrated that ASPM gene was overexpressed when compared to normal brain and ASPM inhibition by siRNA-mediated inhibits tumor cell proliferation and neural stem cell proliferation, supporting ASPM gene as a potential molecular target in glioblastoma. The aim of this work was to evaluate ASPM expression in medulloblastoma fragment samples, and to compare the results with the patient clinical features.
METHODS: Analysis of gene expression was performed by quantitative PCR real time using SYBR Green system in tumor samples from 37 children. The t test was used to analyze the gene expression, and Mann-Whitney test was performed to analyze the relationship between gene expressions and clinical characteristics. Kaplan-Meier test evaluated curve survival.
RESULTS: All samples overexpressed ASPM gene more than 40-fold. However, we did not find any association between the overexpressed samples and the clinical parameters.
CONCLUSION: ASPM overexpression may modify the ability of stem cells to differentiate during the development of the central nervous system, contributing to the development of medulloblastoma, a tumor of embryonic origin from cerebellar progenitor cells.

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Year:  2010        PMID: 20694558     DOI: 10.1007/s00381-010-1252-5

Source DB:  PubMed          Journal:  Childs Nerv Syst        ISSN: 0256-7040            Impact factor:   1.475


  16 in total

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Authors:  Natalay Kouprina; Adam Pavlicek; N Keith Collins; Megumi Nakano; Vladimir N Noskov; Jun-Ichirou Ohzeki; Ganeshwaran H Mochida; John I Risinger; Paul Goldsmith; Michelle Gunsior; Greg Solomon; William Gersch; Jung-Hyun Kim; J Carl Barrett; Christopher A Walsh; Jerzy Jurka; Hiroshi Masumoto; Vladimir Larionov
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Authors:  B R Brinkley
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7.  Analysis of oncogenic signaling networks in glioblastoma identifies ASPM as a molecular target.

Authors:  S Horvath; B Zhang; M Carlson; K V Lu; S Zhu; R M Felciano; M F Laurance; W Zhao; S Qi; Z Chen; Y Lee; A C Scheck; L M Liau; H Wu; D H Geschwind; P G Febbo; H I Kornblum; T F Cloughesy; S F Nelson; P S Mischel
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Review 3.  A New Way to Treat Brain Tumors: Targeting Proteins Coded by Microcephaly Genes?: Brain tumors and microcephaly arise from opposing derangements regulating progenitor growth. Drivers of microcephaly could be attractive brain tumor targets.

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7.  Aberrant ASPM expression mediated by transcriptional regulation of FoxM1 promotes the progression of gliomas.

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9.  Aspm sustains postnatal cerebellar neurogenesis and medulloblastoma growth in mice.

Authors:  Scott E Williams; Idoia Garcia; Andrew J Crowther; Shiyi Li; Alyssa Stewart; Hedi Liu; Kendall J Lough; Sean O'Neill; Katherine Veleta; Esteban A Oyarzabal; Joseph R Merrill; Yen-Yu Ian Shih; Timothy R Gershon
Journal:  Development       Date:  2015-10-08       Impact factor: 6.868

10.  Elevated cyclin B2 expression in invasive breast carcinoma is associated with unfavorable clinical outcome.

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