Book contents
- Frontmatter
- Contents
- List of contributors
- Foreword by Sidney Altman
- Foreword by Victor R. Ambros
- Introduction
- I Discovery of microRNAs in various organisms
- II MicroRNA functions and RNAi-mediated pathways
- III Computational biology of microRNAs
- IV Detection and quantitation of microRNAs
- V MicroRNAs in disease biology
- 22 Dysregulation of microRNAs in human malignancy
- 23 High throughput microRNAs profiling in cancers
- 24 Roles of microRNAs in cancer and development
- 25 miR-122 in mammalian liver
- 26 MiRNAs in glioblastoma
- 27 Role of microRNA pathway in Fragile X mental retardation
- 28 Insertion of miRNA125b-1 into immunoglobulin heavy chain gene locus mediated by V(D)J recombination in precursor B cell acute lymphoblastic leukemia
- 29 miRNAs in TPA-induced differentiation of HL-60 cells
- 30 MiRNAs in skeletal muscle differentiation
- 31 Identification and potential function of viral microRNAs
- 32 Lost in translation: regulation of HIV-1 by microRNAs and a key enzyme of RNA-directed RNA polymerase
- VI MicroRNAs in stem cell development
- Index
- Plate section
- References
26 - MiRNAs in glioblastoma
from V - MicroRNAs in disease biology
Published online by Cambridge University Press: 22 August 2009
- Frontmatter
- Contents
- List of contributors
- Foreword by Sidney Altman
- Foreword by Victor R. Ambros
- Introduction
- I Discovery of microRNAs in various organisms
- II MicroRNA functions and RNAi-mediated pathways
- III Computational biology of microRNAs
- IV Detection and quantitation of microRNAs
- V MicroRNAs in disease biology
- 22 Dysregulation of microRNAs in human malignancy
- 23 High throughput microRNAs profiling in cancers
- 24 Roles of microRNAs in cancer and development
- 25 miR-122 in mammalian liver
- 26 MiRNAs in glioblastoma
- 27 Role of microRNA pathway in Fragile X mental retardation
- 28 Insertion of miRNA125b-1 into immunoglobulin heavy chain gene locus mediated by V(D)J recombination in precursor B cell acute lymphoblastic leukemia
- 29 miRNAs in TPA-induced differentiation of HL-60 cells
- 30 MiRNAs in skeletal muscle differentiation
- 31 Identification and potential function of viral microRNAs
- 32 Lost in translation: regulation of HIV-1 by microRNAs and a key enzyme of RNA-directed RNA polymerase
- VI MicroRNAs in stem cell development
- Index
- Plate section
- References
Summary
Introduction
Glioblastoma multiforme: a lethal brain tumor still missing a thorough comprehension of molecular oncogenesis
Glioblastoma multiforme (GBM) is one of the most lethal forms of cancers and the most common brain tumor in adults, accounting for approximately 12%–15% of all intracranial neoplasms and 50%–60% of all astrocytic tumours (Zhu and Parada, 2002; Hulleman and Helin, 2005). In most European and North American countries, incidence is approximately 2–3 new cases per 100 000 people per year. Composed of poorly differentiated neoplastic astrocytes, glioblastomas are located preferentially in the subcortical white matter of the cerebral hemispheres, and either may develop from lower grade astrocytic tumors (secondary or progressive glioblastoma multiforme) or may arise very rapidly de novo (primary glioblastoma multiforme) (Wechsler-Reya and Scott, 2001). Despite progress in research on the molecular aspects of malignant gliomas, the prognosis of these brain tumors continues to be dismal, with a median survival time of 12 months from the time of diagnosis. Neither continuous improvements in surgery and radiation techniques, nor in chemotherapy, have been able to change glioblastoma patients' life expectancy over decades.
This highly malignant tumor is thought to arise from astrocytes or astrocyte precursors, but the heterogeneity of GBM tumor morphology and behavior (as indicated by the term “multiforme”) makes conclusions about its origin extremely difficult (Wechsler-Reya and Scott, 2001). Recently, several experimental observations have led to formulate the hypothesis that this type of malignancy might arise from the transformation of adult neural stem cells, normally present in the brain just in the main areas of distribution of brain tumors, and able to trigger gliomagenesis in response to oncogenic mutations (Singh et al., 2003; Singh et al., 2004; Galli et al., 2004; Tunici et al., 2004; Yuan et al., 2004; Sanai et al., 2005).
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- Information
- MicroRNAsFrom Basic Science to Disease Biology, pp. 350 - 362Publisher: Cambridge University PressPrint publication year: 2007