1
|
Louis DN, Ohgaki H, Wiestler OD, Cavenee
WK, Burger PC, Jouvet A, Scheithauer BW and Kleihues P: The 2007
WHO classification of tumours of the central nervous system. Acta
Neuropathol. 114:97–109. 2007. View Article : Google Scholar : PubMed/NCBI
|
2
|
Stupp R, Hegi ME, Mason WP, van den Bent
MJ, Taphoorn MJ, Janzer RC, Ludwin SK, Allgeier A, Fisher B,
Belanger K, et al; European Organisation for Research and Treatment
of Cancer Brain Tumour and Radiation Oncology Groups; National
Cancer Institute of Canada Clinical Trials Group. Effects of
radiotherapy with concomitant and adjuvant temozolomide versus
radiotherapy alone on survival in glioblastoma in a randomised
phase III study: 5-year analysis of the EORTC-NCIC trial. Lancet
Oncol. 10:459–466. 2009. View Article : Google Scholar : PubMed/NCBI
|
3
|
Maugeri-Saccà M, Di Martino S and De Maria
R: Biological and clinical implications of cancer stem cells in
primary brain tumors. Front Oncol. 3:62013. View Article : Google Scholar : PubMed/NCBI
|
4
|
Cruceru ML, Neagu M, Demoulin JB and
Constantinescu SN: Therapy targets in glioblastoma and cancer stem
cells: Lessons from haematopoietic neoplasms. J Cell Mol Med.
17:1218–1235. 2013. View Article : Google Scholar : PubMed/NCBI
|
5
|
Lathia JD: Cancer stem cells: Moving past
the controversy. CNS Oncol. 2:465–467. 2013. View Article : Google Scholar
|
6
|
Hale JS, Sinyuk M, Rich JN and Lathia JD:
Decoding the cancer stem cell hypothesis in glioblastoma. CNS
Oncol. 2:319–330. 2013. View Article : Google Scholar
|
7
|
Beier D, Schulz JB and Beier CP:
Chemoresistance of glioblastoma cancer stem cells - much more
complex than expected. Mol Cancer. 10:1282011. View Article : Google Scholar :
|
8
|
Yan K, Yang K and Rich JN: The evolving
landscape of glioblastoma stem cells. Curr Opin Neurol. 26:701–707.
2013. View Article : Google Scholar : PubMed/NCBI
|
9
|
Molina JR, Hayashi Y, Stephens C and
Georgescu MM: Invasive glioblastoma cells acquire stemness and
increased Akt activation. Neoplasia. 12:453–463. 2010. View Article : Google Scholar : PubMed/NCBI
|
10
|
Cantley LC and Neel BG: New insights into
tumor suppression: PTEN suppresses tumor formation by restraining
the phosphoinositide 3-kinase/AKT pathway. Proc Natl Acad Sci USA.
96:4240–4245. 1999. View Article : Google Scholar : PubMed/NCBI
|
11
|
Kwiatkowska A, Kijewska M, Lipko M, Hibner
U and Kaminska B: Downregulation of Akt and FAK phosphorylation
reduces invasion of glioblastoma cells by impairment of MT1-MMP
shuttling to lamellipodia and downregulates MMPs expression.
Biochim Biophys Acta. 1813:655–667. 2011. View Article : Google Scholar : PubMed/NCBI
|
12
|
Nakada M, Nakada S, Demuth T, Tran NL,
Hoelzinger DB and Berens ME: Molecular targets of glioma invasion.
Cell Mol Life Sci. 64:458–478. 2007. View Article : Google Scholar : PubMed/NCBI
|
13
|
Cancer Genome Atlas Research Network.
Comprehensive genomic characterization defines human glioblastoma
genes and core pathways. Nature. 455:1061–1068. 2008. View Article : Google Scholar : PubMed/NCBI
|
14
|
Westhoff MA, Karpel-Massler G, Brühl O,
Enzenmüller S, La Ferla-Brühl K, Siegelin MD, Nonnenmacher L and
Debatin KM: A critical evaluation of PI3K inhibition in
Glioblastoma and Neuroblastoma therapy. Mol Cell Ther. 2:322014.
View Article : Google Scholar : PubMed/NCBI
|
15
|
Fan QW, Knight ZA, Goldenberg DD, Yu W,
Mostov KE, Stokoe D, Shokat KM and Weiss WA: A dual PI3 kinase/mTOR
inhibitor reveals emergent efficacy in glioma. Cancer Cell.
9:341–349. 2006. View Article : Google Scholar : PubMed/NCBI
|
16
|
Lefranc F, Brotchi J and Kiss R: Possible
future issues in the treatment of glioblastomas: Special emphasis
on cell migration and the resistance of migrating glioblastoma
cells to apoptosis. J Clin Oncol. 23:2411–2422. 2005. View Article : Google Scholar : PubMed/NCBI
|
17
|
Stegh AH, Chin L, Louis DN and DePinho RA:
What drives intense apoptosis resistance and propensity for
necrosis in glioblastoma? A role for Bcl2L12 as a multifunctional
cell death regulator. Cell Cycle. 7:2833–2839. 2008. View Article : Google Scholar : PubMed/NCBI
|
18
|
Utermark T, Rao T, Cheng H, Wang Q, Lee
SH, Wang ZC, Iglehart JD, Roberts TM, Muller WJ and Zhao JJ: The
p110α and p110β isoforms of PI3K play divergent roles in mammary
gland development and tumorigenesis. Genes Dev. 26:1573–1586. 2012.
View Article : Google Scholar : PubMed/NCBI
|
19
|
Knight ZA, Gonzalez B, Feldman ME, Zunder
ER, Goldenberg DD, Williams O, Loewith R, Stokoe D, Balla A, Toth
B, et al: A pharmacological map of the PI3-K family defines a role
for p110alpha in insulin signaling. Cell. 125:733–747. 2006.
View Article : Google Scholar : PubMed/NCBI
|
20
|
Chaussade C, Rewcastle GW, Kendall JD,
Denny WA, Cho K, Grønning LM, Chong ML, Anagnostou SH, Jackson SP,
Daniele N, et al: Evidence for functional redundancy of class IA
PI3K isoforms in insulin signalling. Biochem J. 404:449–458. 2007.
View Article : Google Scholar : PubMed/NCBI
|
21
|
Zhao JJ, Cheng H, Jia S, Wang L, Gjoerup
OV, Mikami A and Roberts TM: The p110alpha isoform of PI3K is
essential for proper growth factor signaling and oncogenic
transformation. Proc Natl Acad Sci USA. 103:16296–16300. 2006.
View Article : Google Scholar : PubMed/NCBI
|
22
|
Foukas LC, Claret M, Pearce W, Okkenhaug
K, Meek S, Peskett E, Sancho S, Smith AJ, Withers DJ and
Vanhaesebroeck B: Critical role for the p110alpha
phosphoinositide-3-OH kinase in growth and metabolic regulation.
Nature. 441:366–370. 2006. View Article : Google Scholar : PubMed/NCBI
|
23
|
Graupera M, Guillermet-Guibert J, Foukas
LC, Phng LK, Cain RJ, Salpekar A, Pearce W, Meek S, Millan J,
Cutillas PR, et al: Angiogenesis selectively requires the p110alpha
isoform of PI3K to control endothelial cell migration. Nature.
453:662–666. 2008. View Article : Google Scholar : PubMed/NCBI
|
24
|
Okkenhaug K, Turner M and Gold MR: PI3K
signaling in B cell and T cell biology. Front Immunol. 5:5572014.
View Article : Google Scholar : PubMed/NCBI
|
25
|
Schmit F, Utermark T, Zhang S, Wang Q, Von
T, Roberts TM and Zhao JJ: PI3K isoform dependence of
PTEN-deficient tumors can be altered by the genetic context. Proc
Natl Acad Sci USA. 111:6395–6400. 2014. View Article : Google Scholar : PubMed/NCBI
|
26
|
Thorpe LM, Yuzugullu H and Zhao JJ: PI3K
in cancer: Divergent roles of isoforms, modes of activation and
therapeutic targeting. Nat Rev Cancer. 15:7–24. 2015. View Article : Google Scholar :
|
27
|
Gallia GL, Rand V, Siu IM, Eberhart CG,
James CD, Marie SK, Oba-Shinjo SM, Carlotti CG, Caballero OL,
Simpson AJ, et al: PIK3CA gene mutations in pediatric and adult
glioblastoma multiforme. Mol Cancer Res. 4:709–714. 2006.
View Article : Google Scholar : PubMed/NCBI
|
28
|
Samuels Y, Wang Z, Bardelli A, Silliman N,
Ptak J, Szabo S, Yan H, Gazdar A, Powell SM, Riggins GJ, et al:
High frequency of mutations of the PIK3CA gene in human cancers.
Science. 304:5542004. View Article : Google Scholar : PubMed/NCBI
|
29
|
Mizoguchi M, Nutt CL, Mohapatra G and
Louis DN: Genetic alterations of phosphoinositide 3-kinase subunit
genes in human glioblastomas. Brain Pathol. 14:372–377. 2004.
View Article : Google Scholar : PubMed/NCBI
|
30
|
Hui AB, Lo KW, Yin XL, Poon WS and Ng HK:
Detection of multiple gene amplifications in glioblastoma
multiforme using array-based comparative genomic hybridization. Lab
Invest. 81:717–723. 2001. View Article : Google Scholar : PubMed/NCBI
|
31
|
Jia S, Roberts TM and Zhao JJ: Should
individual PI3 kinase isoforms be targeted in cancer? Curr Opin
Cell Biol. 21:199–208. 2009. View Article : Google Scholar : PubMed/NCBI
|
32
|
Fruman DA and Rommel C: PI3K and cancer:
Lessons, challenges and opportunities. Nat Rev Drug Discov.
13:140–156. 2014. View Article : Google Scholar : PubMed/NCBI
|
33
|
Filbin MG, Dabral SK, Pazyra-Murphy MF,
Ramkissoon S, Kung AL, Pak E, Chung J, Theisen MA, Sun Y,
Franchetti Y, et al: Coordinate activation of Shh and PI3K
signaling in PTEN-deficient glioblastoma: New therapeutic
opportunities. Nat Med. 19:1518–1523. 2013. View Article : Google Scholar : PubMed/NCBI
|
34
|
Jhanwar-Uniyal M, Albert L, McKenna E,
Karsy M, Rajdev P, Braun A and Murali R: Deciphering the signaling
pathways of cancer stem cells of glioblastoma multiforme: Role of
Akt/mTOR and MAPK pathways. Adv Enzyme Regul. 51:164–170. 2011.
View Article : Google Scholar
|
35
|
Paul-Samojedny M, Pudełko A, Suchanek-Raif
R, Kowalczyk M, Fila-Daniłow A, Borkowska P and Kowalski J:
Knockdown of the AKT3 (PKBγ), PI3KCA, and VEGFR2 genes by RNA
interference suppresses glioblastoma multiforme T98G cells
invasiveness in vitro. Tumour Biol. 36:3263–3277. 2015. View Article : Google Scholar
|
36
|
Höland K, Boller D, Hagel C, Dolski S,
Treszl A, Pardo OE, Cwiek P, Salm F, Leni Z, Shepherd PR, et al:
Targeting class IA PI3K isoforms selectively impairs cell growth,
survival, and migration in glioblastoma. PLoS One. 9:e941322014.
View Article : Google Scholar : PubMed/NCBI
|
37
|
Broadley KW, Hunn MK, Farrand KJ, Price
KM, Grasso C, Miller RJ, Hermans IF and McConnell MJ: Side
population is not necessary or sufficient for a cancer stem cell
phenotype in glioblastoma multiforme. Stem Cells. 29:452–461. 2011.
View Article : Google Scholar : PubMed/NCBI
|
38
|
Jamieson S, Flanagan JU, Kolekar S,
Buchanan C, Kendall JD, Lee WJ, Rewcastle GW, Denny WA, Singh R,
Dickson J, et al: A drug targeting only p110α can block
phosphoinositide 3-kinase signalling and tumour growth in certain
cell types. Biochem J. 438:53–62. 2011. View Article : Google Scholar : PubMed/NCBI
|
39
|
Jackson SP, Schoenwaelder SM, Goncalves I,
Nesbitt WS, Yap CL, Wright CE, Kenche V, Anderson KE, Dopheide SM,
Yuan Y, et al: PI 3-kinase p110beta: A new target for
antithrombotic therapy. Nat Med. 11:507–514. 2005. View Article : Google Scholar : PubMed/NCBI
|
40
|
Sadhu C, Masinovsky B, Dick K, Sowell CG
and Staunton DE: Essential role of phosphoinositide 3-kinase delta
in neutrophil directional movement. J Immunol. 170:2647–2654. 2003.
View Article : Google Scholar : PubMed/NCBI
|
41
|
Maira SM, Stauffer F, Brueggen J, Furet P,
Schnell C, Fritsch C, Brachmann S, Chène P, De Pover A, Schoemaker
K, et al: Identification and characterization of NVP-BEZ235, a new
orally available dual phosphatidylinositol 3-kinase/mammalian
target of rapamycin inhibitor with potent in vivo antitumor
activity. Mol Cancer Ther. 7:1851–1863. 2008. View Article : Google Scholar : PubMed/NCBI
|
42
|
Berridge MV, Herst PM and Tan AS:
Tetrazolium dyes as tools in cell biology: New insights into their
cellular reduction. Biotechnol Annu Rev. 11:127–152. 2005.
View Article : Google Scholar : PubMed/NCBI
|
43
|
Berridge MV and Tan AS: Characterization
of the cellular reduction of
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT):
Subcellular localization, substrate dependence, and involvement of
mitochondrial electron transport in MTT reduction. Arch Biochem
Biophys. 303:474–482. 1993. View Article : Google Scholar : PubMed/NCBI
|
44
|
Fan QW, Cheng CK, Nicolaides TP, Hackett
CS, Knight ZA, Shokat KM and Weiss WA: A dual
phosphoinositide-3-kinase alpha/mTOR inhibitor cooperates with
blockade of epidermal growth factor receptor in PTEN-mutant glioma.
Cancer Res. 67:7960–7965. 2007. View Article : Google Scholar : PubMed/NCBI
|
45
|
He K, Xu T, Xu Y, Ring A, Kahn M and
Goldkorn A: Cancer cells acquire a drug resistant, highly
tumorigenic, cancer stem-like phenotype through modulation of the
PI3K/Akt/β-catenin/CBP pathway. Int J Cancer. 134:43–54. 2014.
View Article : Google Scholar
|
46
|
Matsubara S, Ding Q, Miyazaki Y, Kuwahata
T, Tsukasa K and Takao S: mTOR plays critical roles in pancreatic
cancer stem cells through specific and stemness-related functions.
Sci Rep. 3:32302013. View Article : Google Scholar : PubMed/NCBI
|
47
|
Kingham E and Welham M: Distinct roles for
isoforms of the catalytic subunit of class-IA PI3K in the
regulation of behaviour of murine embryonic stem cells. J Cell Sci.
122:2311–2321. 2009. View Article : Google Scholar : PubMed/NCBI
|
48
|
Lathia JD, Mack SC, Mulkearns-Hubert EE,
Valentim CL and Rich JN: Cancer stem cells in glioblastoma. Genes
Dev. 29:1203–1217. 2015. View Article : Google Scholar : PubMed/NCBI
|
49
|
Zhang R, Banik NL and Ray SK: Differential
sensitivity of human glioblastoma LN18 (PTEN-positive) and A172
(PTEN-negative) cells to Taxol for apoptosis. Brain Res.
1239:216–225. 2008. View Article : Google Scholar : PubMed/NCBI
|
50
|
Meier TI, Cook JA, Thomas JE, Radding JA,
Horn C, Lingaraj T and Smith MC: Cloning, expression, purification,
and characterization of the human class Ia phosphoinositide
3-kinase isoforms. Protein Expr Purif. 35:218–224. 2004. View Article : Google Scholar : PubMed/NCBI
|
51
|
Beeton CA, Chance EM, Foukas LC and
Shepherd PR: Comparison of the kinetic properties of the lipid- and
protein-kinase activities of the p110alpha and p110beta catalytic
subunits of class-Ia phosphoinositide 3-kinases. Biochem J.
350:353–359. 2000. View Article : Google Scholar : PubMed/NCBI
|
52
|
Schwartz S, Wongvipat J, Trigwell CB,
Hancox U, Carver BS, Rodrik-Outmezguine V, Will M, Yellen P, de
Stanchina E, Baselga J, et al: Feedback suppression of PI3Kα
signaling in PTEN-mutated tumors is relieved by selective
inhibition of PI3Kβ. Cancer Cell. 27:109–122. 2015. View Article : Google Scholar
|
53
|
Costa C, Ebi H, Martini M, Beausoleil SA,
Faber AC, Jakubik CT, Huang A, Wang Y, Nishtala M, Hall B, et al:
Measurement of PIP3 levels reveals an unexpected role for p110β in
early adaptive responses to p110α-specific inhibitors in luminal
breast cancer. Cancer Cell. 27:97–108. 2015. View Article : Google Scholar
|
54
|
Sunayama J, Matsuda K, Sato A, Tachibana
K, Suzuki K, Narita Y, Shibui S, Sakurada K, Kayama T, Tomiyama A,
et al: Crosstalk between the PI3K/mTOR and MEK/ERK pathways
involved in the maintenance of self-renewal and tumorigenicity of
glioblastoma stem-like cells. Stem Cells. 28:1930–1939. 2010.
View Article : Google Scholar : PubMed/NCBI
|
55
|
Gough DJ, Koetz L and Levy DE: The MEK-ERK
pathway is necessary for serine phosphorylation of mitochondrial
STAT3 and Ras-mediated transformation. PLoS One. 8:e833952013.
View Article : Google Scholar : PubMed/NCBI
|
56
|
Soares HP, Ming M, Mellon M, Young SH, Han
L, Sinnet-Smith J and Rozengurt E: Dual PI3K/mTOR inhibitors induce
rapid overactivation of the MEK/ERK pathway in human pancreatic
cancer cells through suppression of mTORC2. Mol Cancer Ther.
14:1014–1023. 2015. View Article : Google Scholar : PubMed/NCBI
|
57
|
Toulany M, Minjgee M, Saki M, Holler M,
Meier F, Eicheler W and Rodemann HP: ERK2-dependent reactivation of
Akt mediates the limited response of tumor cells with constitutive
K-RAS activity to PI3K inhibition. Cancer Biol Ther. 15:317–328.
2014. View Article : Google Scholar :
|