alexa Malignant Progression of Glioblastoma | OMICS International
ISSN: 2157-7013
Journal of Cell Science & Therapy

Like us on:

Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

Malignant Progression of Glioblastoma

Yasuo Iwadate*

Department of Neurological Surgery Chiba University Graduate School of Medicine, Chiba, Japan

*Corresponding Author:
Yasuo Iwadate
Department of Neurological Surgery
Graduate School of Medicine, Chiba University
1-8-1, Inohana, Chuo-ku, 260-2870 Chiba, Japan
Tel: 81-43-226-2158
Fax: 81-43-226-2159
E-mail: [email protected]

Received Date: September 03, 2014; Accepted Date: September 26, 2014; Published Date: September 29, 2014

Citation: Iwadate Y (2014) Malignant Progression of Glioblastoma. J Cell Sci Ther 5:182. doi: 10.4172/2157-7013.1000182

Copyright: © 2014 Iwadate Y. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Cell Science & Therapy

Abstract

Glioblastoma (GBM) is the most devastating type of human cancers with a median survival time ranging from 12-18 months following maximal therapies [1]. Glioma is classified into four malignancy grades according to histological features; the low-grade tumors including WHO Grade I (localized gliomas) and WHO Grade II (diffuse astrocytoma or oligodendrogliomas), and the high-grade tumors including WHO Grades III (anaplastic gliomas) and WHO Grade IV (GBM).

Commentary

Glioblastoma (GBM) is the most devastating type of human cancers with a median survival time ranging from 12-18 months following maximal therapies [1]. Glioma is classified into four malignancy grades according to histological features; the low-grade tumors including WHO Grade I (localized gliomas) and WHO Grade II (diffuse astrocytoma or oligodendrogliomas), and the high-grade tumors including WHO Grades III (anaplastic gliomas) and WHO Grade IV (GBM). The concept of malignant progression is usually applied to secondary GBM which is originally a grade II or grade III glioma and is diagnosed as GBM at the time of recurrence. Most of this tumor carries IDH1 mutation, in contrast to primary GBM without carrying isocitrate dehydrogenase-1 (IDH1) mutation which is the majority of GBM [2]. Although GBM is considered to be a final stage of tumorigenesis collecting many types of genetic alterations in the oncogenes and tumor suppressor genes, large variations of survival time exist within the same category of GBM. Recently, the Cancer Genome Atlas (TCGA) showed that GBM can be categorized into four subclasses based on molecular genetic properties, which is partially relevant to patient survival [3]. The proneural subtype is associated with a good prognosis, and neural, classic, and mesenchymal subtypes are identified [3]. The mesenchymal subtype is characterized by neo-angiogenesis and highly-invasive nature, leading to poor prognosis [3,4]. Non-mesenchymal subtypes usually acquire the gene expression pattern of mesenchymal subtype at recurrence after chemotherapy and radiotherapy [4]. One of the most striking features of mesenchymal subtype is the expression of stem cell markers [3,4]. Actually, glioma cells that express stem cell markers are highly invasive and resistant to radiotherapy and chemotherapy in vitro and in the clinical setting [5]. The heterogeneous survival periods of GBM patients may reflect the acquisition of mesenchymal features or stem cell properties on the course of disease progression.

Such a phenotypic change in cancer tissue may be caused by various stimuli from cancer microenvironment. Differentiated cells can change their phenotype under the influences of repair-associated or pathological stresses. One phenomenon that facilitates such dynamic reprogramming of the cellular state is epithelial-mesenchymal transition (EMT) [6]. EMT is a biological process that induces a polarized epithelial cell to undergo multiple biochemical changes into mesenchymal phenotype including enhanced migratory capacity and elevated resistance to genotoxic insults. EMT is also known as an important inducer of cancer stem cells. The shift toward mesenchymal phenotype of GBM after various therapies at recurrence suggests the contribution of EMT activated in hypoxic microenvironments and tissue repair processes [7]. Since GBM usually contains large areas of necrosis, many GBM of mesenchymal subtype would have progressed from other subtypes in the natural course of the disease. The stem cell phenotype may be induced by EMT-related transcription factor network through epigenetic regulations, which contributes to the poor prognosis of GBM. The “malignant progression of GBM” can be a main target of future therapies for GBM.

References

Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Relevant Topics

Recommended Conferences

Article Usage

  • Total views: 12018
  • [From(publication date):
    October-2014 - Jul 16, 2018]
  • Breakdown by view type
  • HTML page views : 8237
  • PDF downloads : 3781
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2018-19
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri & Aquaculture Journals

Dr. Krish

[email protected]

+1-702-714-7001Extn: 9040

Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001Extn: 9040

Clinical Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

Food & Nutrition Journals

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

General Science

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics & Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Materials Science Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Nursing & Health Care Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

Ann Jose

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001Extn: 9042

 
© 2008- 2018 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
Leave Your Message 24x7