Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25796440
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25796440
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Cancer+Lett
2015 ; 362
(1
): 1-7
Nephropedia Template TP
Paw I
; Carpenter RC
; Watabe K
; Debinski W
; Lo HW
Cancer Lett
2015[Jun]; 362
(1
): 1-7
PMID25796440
show ga
Glioblastoma (GBM) is the most aggressive, deadliest, and most common brain
malignancy in adults. Despite the advances made in surgical techniques,
radiotherapy and chemotherapy, the median survival for GBM patients has remained
at a mere 14 months. GBM poses several unique challenges to currently available
treatments for the disease. For example, GBM cells have the propensity to
aggressively infiltrate/invade into the normal brain tissues and along the
vascular tracks, which prevents complete resection of all malignant cells and
limits the effect of localized radiotherapy while sparing normal tissue. Although
anti-angiogenic treatment exerts anti-edematic effect in GBM, unfortunately,
tumors progress with acquired increased invasiveness. Therefore, it is an
important task to gain a deeper understanding of the intrinsic and post-treatment
invasive phenotypes of GBM in hopes that the gained knowledge would lead to novel
GBM treatments that are more effective and less toxic. This review will give an
overview of some of the signaling pathways that have been shown to positively and
negatively regulate GBM invasion, including, the PI3K/Akt, Wnt, sonic
hedgehog-GLI1, and microRNAs. The review will also discuss several approaches to
cancer therapies potentially altering GBM invasiveness.
free
free
free
