Please use this identifier to cite or link to this item: https://doi.org/10.3389/fonc.2013.00093
Title: Dissecting the PI3K signaling axis in pediatric solid tumors: Novel targets for clinical integration
Authors: Loh, A.H 
Brennan, R.C
Lang, W.H
Hickey, R.J
Malkas, L.H
Sandoval, J.A
Keywords: 2 morpholino 8 phenylchromone
8 [4 (1 aminocyclobutyl) phenyl] 9 phenyl 1, 2, 4 triazolo [3, 4 f] [1, 6] naphthyridin 3 (2h) one
8 [4 (1 aminocyclobutyl)phenyl] 9 phenyl 1,2,4 triazolo[3,4 f][1,6]naphthyridin 3(2h) one
alendronic acid
buparlisib
cixutumumab
cyclophosphamide
dactolisib
dalotuzumab
doxorubicin
enzastaurin
etoposide
everolimus
irinotecan
lomustine
mammalian target of rapamycin
perifosine
phosphatidylinositol 3 kinase
phosphatidylinositol 3, 4, 5 trisphosphate 3 phosphatase
protein kinase B
protein tyrosine kinase
rapamycin
ridaforolimus
temozolomide
temsirolimus
topotecan
transcription factor FKHR
transcription factor FOXO
unclassified drug
unindexed drug
vinblastine
wortmannin
apoptosis
cancer inhibition
cancer recurrence
cancer survival
cell proliferation
child
childhood cancer
drug dose escalation
drug efficacy
drug tolerability
enzyme inhibition
Ewing sarcoma
febrile neutropenia
gene mutation
hematologic disease
human
mucosa inflammation
neuroblastoma
nonhuman
osteosarcoma
phase 1 clinical trial (topic)
phase 2 clinical trial (topic)
phase 3 clinical trial (topic)
protein expression
randomized controlled trial (topic)
review
rhabdomyosarcoma
signal transduction
single drug dose
solid tumor
thrombocytopenia
Issue Date: 2013
Citation: Loh, A.H, Brennan, R.C, Lang, W.H, Hickey, R.J, Malkas, L.H, Sandoval, J.A (2013). Dissecting the PI3K signaling axis in pediatric solid tumors: Novel targets for clinical integration. Frontiers in Oncology 43558 : Article 00093. ScholarBank@NUS Repository. https://doi.org/10.3389/fonc.2013.00093
Rights: Attribution 4.0 International
Abstract: Children with solid tumors represent a unique population. Recent improvements in pediatric solid tumor survival rates have been confined to low- and moderate-risk cancers, whereas minimal to no notable improvement in survival have been observed in high-risk and advanced-stage childhood tumors. Treatments for patients with advanced disease are rarely curative, and responses to therapy are often followed by relapse, which highlights the large unmet need for novel therapies. Recent advances in cancer treatment have focused on personalized therapy, whereby patients are treated with agents that best target the molecular drivers of their disease. Thus, a better understanding of the pathways that drive cancer or drug resistance is of critical importance. One such example is the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway, which is activated in many solid cancer patients and represents a target for therapy. PI3K/Akt/mTOR pathway activation has also been observed in tumors resistant to agents targeting upstream receptor tyrosine kinases (RTKs). Agents that target this pathway have the potential to shut down survival pathways, and are being explored both in the setting of pathway-activating mutations and for their ability to restore sensitivity to upstream signaling targeted agents. Here, we examine the role of the PI3K/Akt/mTOR pathway in pediatric solid tumors, review the novel agents being explored to target this pathway, and explore the potential role of the inhibition of this pathway in the clinical development of these agents in children. © 2013 Loh, Brennan, Lang, Hickey, Malkas and Sandoval.
Source Title: Frontiers in Oncology
URI: https://scholarbank.nus.edu.sg/handle/10635/183186
ISSN: 2234943X
DOI: 10.3389/fonc.2013.00093
Rights: Attribution 4.0 International
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