|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
High expression of cMyc and activation of the ERK1/2 pathway conferred resistance against alectinib in ALK expressing glioblastoma cells.
|
31776900 |
2020 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, identification of ALK-mediated molecular pathway(s) related to GBM carcinogenesis/ pathology and putative therapy resistance is of high priority and warrants further exploitation.
|
29336268 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we examined the functional role of the ALK gene in glioblastomas (GBMs).
|
28837676 |
2017 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
ALK overexpression can be identified in up to 70% of GBMs and does not correlate with underlying <i>alk</i> gene amplification.
|
27993946 |
2017 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Alterations more prevalent in the young GBM cohort compared to the older cohort (P < 0.05) were: overexpression of ALK, RRM1, TUBB3 and mutation of ATRX, BRAF, IDH1, and TP53.
|
27579614 |
2016 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We speculate that the pleiotrophin-ALK axis may be a promising target for the therapy of glioblastoma.
|
23686309 |
2014 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Various glioblastoma cell lines are analyzed for PTN and ALK expression.
|
19177199 |
2009 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition to those cancers for which a causative role for aberrant ALK activity is well validated, more circumstantial links implicate the full-length, normal ALK receptor in the genesis of other malignancies - including glioblastoma and breast cancer - via a mechanism of receptor activation involving autocrine and/or paracrine growth loops with the reported ALK ligands, pleiotrophin and midkine.
|
19275511 |
2009 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
While the cause-effect relationship between ALK fusions and malignancies such as ALCL and IMT is very well established, more circumstantial links implicate the involvement of the full-length, normal ALK receptor in the genesis of additional malignancies including glioblastoma, neuroblastoma, breast cancer, and others; in these instances, ALK is believed to foster tumorigenesis following activation by autocrine and/or paracrine growth loops involving the reported ALK ligands, pleiotrophin (PTN) and midkine (MK).
|
17694547 |
2008 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
ALK is also found expressed in neural crest-derived tumors such as human neuroblastomas or glioblastomas but its role is not fully elucidated.
|
17611412 |
2007 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In contrast to agonist monoclonal antibodies, both Pleiotrophin.15 and Pleiotrophin.18 failed to activate ALK in neuroblastoma and glioblastoma cells expressing this receptor.
|
17904822 |
2007 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
In contrast to agonist monoclonal antibodies, both Pleiotrophin.15 and Pleiotrophin.18 failed to activate ALK in neuroblastoma and glioblastoma cells expressing this receptor.
|
17904822 |
2007 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
However, the relevance of PTN expression itself is unknown especially since, besides PTN, at least one more growth factor, midkine (MK), signals through ALK and is expressed in glioblastoma.
|
15986444 |
2005 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The aberrant expression of full-length ALK receptor proteins has been reported in neuroblastomas and glioblastomas, while the occurrence of ALK fusion proteins in anaplastic large cell lymphoma (ALCL) has resulted in the identification of the new tumor entity, ALK-positive ALCL.
|
15583856 |
2004 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Cell lines established from solid tumors of ectodermal origin, including melanoma and breast carcinoma, exhibited widespread mRNA expression of the ALK receptor at a broad range (53/64), an association which was found to be strongest in cell lines derived from neuroblastoma (6/6), glioblastoma (8/8) as well as in cell lines established from Ewing sarcoma (4/4) and retinoblastomas (2/2).
|
12115586 |
2002 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
LHGDN |
These findings directly implicate ALK signaling as a rate-limiting factor in the growth of glioblastoma multiforme and suggest potential utility of therapeutic targeting of ALK.
|
11809760 |
2002 |