Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma

10.18632/oncotarget.2372

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Main Authors:	Moore, N.F, Azarova, A.M, Bhatnagar, N, Ross, K.N, Drake, L.E, Frumm, S, Liu, Q.S, Christie, A.L, Sanda, T, Chesler, L, Kung, A.L, Gray, N.S, Stegmaier, K, George, R.E
Other Authors:	MEDICINE
Format:	Article
Published:	2020
Subjects:	2 morpholino 8 phenylchromone azd 8055 crizotinib dactolisib gedatolisib mammalian target of rapamycin inhibitor pictilisib torin 2 unclassified drug anaplastic lymphoma kinase antineoplastic agent mechanistic target of rapamycin complex 1 MTOR protein, human multiprotein complex MYCN protein, human nuclear protein oncoprotein phosphatidylinositol 3 kinase protein kinase B protein kinase inhibitor protein S6 protein tyrosine kinase pyrazole derivative pyridine derivative target of rapamycin kinase ALK gene animal experiment animal model antineoplastic activity Article controlled study down regulation drug cytotoxicity drug megadose drug potency drug potentiation enzyme activity gene expression profiling gene mutation human human cell molecularly targeted therapy mouse multiple cycle treatment MYCN gene neuroblastoma nonhuman oncogene protein phosphorylation signal transduction tumor volume tumor xenograft upregulation animal antagonists and inhibitors dose response drug effects drug resistance drug screening enzymology gene amplification genetic transfection genetics metabolism mutation nonobese diabetic mouse pathology phosphorylation RNA interference SCID mouse time tumor cell line Animals Antineoplastic Combined Chemotherapy Protocols Cell Line, Tumor Dose-Response Relationship, Drug Drug Resistance, Neoplasm Gene Amplification Humans Mice, Inbred NOD Mice, SCID Molecular Targeted Therapy Multiprotein Complexes Mutation Neuroblastoma Nuclear Proteins Oncogene Proteins Phosphatidylinositol 3-Kinase Phosphorylation Protein Kinase Inhibitors Proto-Oncogene Proteins c-akt Pyrazoles Pyridines Receptor Protein-Tyrosine Kinases Ribosomal Protein S6 RNA Interference Signal Transduction Time Factors TOR Serine-Threonine Kinases Transfection Xenograft Model Antitumor Assays
Online Access:	https://scholarbank.nus.edu.sg/handle/10635/181776
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Institution:	National University of Singapore

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spelling	sg-nus-scholar.10635-1817762024-04-18T03:09:20Z Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma Moore, N.F Azarova, A.M Bhatnagar, N Ross, K.N Drake, L.E Frumm, S Liu, Q.S Christie, A.L Sanda, T Chesler, L Kung, A.L Gray, N.S Stegmaier, K George, R.E MEDICINE 2 morpholino 8 phenylchromone azd 8055 crizotinib dactolisib gedatolisib mammalian target of rapamycin inhibitor pictilisib torin 2 unclassified drug anaplastic lymphoma kinase antineoplastic agent crizotinib mechanistic target of rapamycin complex 1 MTOR protein, human multiprotein complex MYCN protein, human nuclear protein oncoprotein phosphatidylinositol 3 kinase protein kinase B protein kinase inhibitor protein S6 protein tyrosine kinase pyrazole derivative pyridine derivative target of rapamycin kinase ALK gene animal experiment animal model antineoplastic activity Article controlled study down regulation drug cytotoxicity drug megadose drug potency drug potentiation enzyme activity gene expression profiling gene mutation human human cell molecularly targeted therapy mouse multiple cycle treatment MYCN gene neuroblastoma nonhuman oncogene protein phosphorylation signal transduction tumor volume tumor xenograft upregulation animal antagonists and inhibitors dose response drug effects drug resistance drug screening enzymology gene amplification genetic transfection genetics metabolism mutation neuroblastoma nonobese diabetic mouse pathology phosphorylation RNA interference SCID mouse time tumor cell line Animals Antineoplastic Combined Chemotherapy Protocols Cell Line, Tumor Dose-Response Relationship, Drug Drug Resistance, Neoplasm Gene Amplification Humans Mice, Inbred NOD Mice, SCID Molecular Targeted Therapy Multiprotein Complexes Mutation Neuroblastoma Nuclear Proteins Oncogene Proteins Phosphatidylinositol 3-Kinase Phosphorylation Protein Kinase Inhibitors Proto-Oncogene Proteins c-akt Pyrazoles Pyridines Receptor Protein-Tyrosine Kinases Ribosomal Protein S6 RNA Interference Signal Transduction Time Factors TOR Serine-Threonine Kinases Transfection Xenograft Model Antitumor Assays 10.18632/oncotarget.2372 Oncotarget 5 18 8737-8749 2020-10-28T07:10:50Z 2020-10-28T07:10:50Z 2014 Article Moore, N.F, Azarova, A.M, Bhatnagar, N, Ross, K.N, Drake, L.E, Frumm, S, Liu, Q.S, Christie, A.L, Sanda, T, Chesler, L, Kung, A.L, Gray, N.S, Stegmaier, K, George, R.E (2014). Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma. Oncotarget 5 (18) : 8737-8749. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.2372 19492553 https://scholarbank.nus.edu.sg/handle/10635/181776 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Unpaywall 20201031
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	2 morpholino 8 phenylchromone azd 8055 crizotinib dactolisib gedatolisib mammalian target of rapamycin inhibitor pictilisib torin 2 unclassified drug anaplastic lymphoma kinase antineoplastic agent crizotinib mechanistic target of rapamycin complex 1 MTOR protein, human multiprotein complex MYCN protein, human nuclear protein oncoprotein phosphatidylinositol 3 kinase protein kinase B protein kinase inhibitor protein S6 protein tyrosine kinase pyrazole derivative pyridine derivative target of rapamycin kinase ALK gene animal experiment animal model antineoplastic activity Article controlled study down regulation drug cytotoxicity drug megadose drug potency drug potentiation enzyme activity gene expression profiling gene mutation human human cell molecularly targeted therapy mouse multiple cycle treatment MYCN gene neuroblastoma nonhuman oncogene protein phosphorylation signal transduction tumor volume tumor xenograft upregulation animal antagonists and inhibitors dose response drug effects drug resistance drug screening enzymology gene amplification genetic transfection genetics metabolism mutation neuroblastoma nonobese diabetic mouse pathology phosphorylation RNA interference SCID mouse time tumor cell line Animals Antineoplastic Combined Chemotherapy Protocols Cell Line, Tumor Dose-Response Relationship, Drug Drug Resistance, Neoplasm Gene Amplification Humans Mice, Inbred NOD Mice, SCID Molecular Targeted Therapy Multiprotein Complexes Mutation Neuroblastoma Nuclear Proteins Oncogene Proteins Phosphatidylinositol 3-Kinase Phosphorylation Protein Kinase Inhibitors Proto-Oncogene Proteins c-akt Pyrazoles Pyridines Receptor Protein-Tyrosine Kinases Ribosomal Protein S6 RNA Interference Signal Transduction Time Factors TOR Serine-Threonine Kinases Transfection Xenograft Model Antitumor Assays
spellingShingle	2 morpholino 8 phenylchromone azd 8055 crizotinib dactolisib gedatolisib mammalian target of rapamycin inhibitor pictilisib torin 2 unclassified drug anaplastic lymphoma kinase antineoplastic agent crizotinib mechanistic target of rapamycin complex 1 MTOR protein, human multiprotein complex MYCN protein, human nuclear protein oncoprotein phosphatidylinositol 3 kinase protein kinase B protein kinase inhibitor protein S6 protein tyrosine kinase pyrazole derivative pyridine derivative target of rapamycin kinase ALK gene animal experiment animal model antineoplastic activity Article controlled study down regulation drug cytotoxicity drug megadose drug potency drug potentiation enzyme activity gene expression profiling gene mutation human human cell molecularly targeted therapy mouse multiple cycle treatment MYCN gene neuroblastoma nonhuman oncogene protein phosphorylation signal transduction tumor volume tumor xenograft upregulation animal antagonists and inhibitors dose response drug effects drug resistance drug screening enzymology gene amplification genetic transfection genetics metabolism mutation neuroblastoma nonobese diabetic mouse pathology phosphorylation RNA interference SCID mouse time tumor cell line Animals Antineoplastic Combined Chemotherapy Protocols Cell Line, Tumor Dose-Response Relationship, Drug Drug Resistance, Neoplasm Gene Amplification Humans Mice, Inbred NOD Mice, SCID Molecular Targeted Therapy Multiprotein Complexes Mutation Neuroblastoma Nuclear Proteins Oncogene Proteins Phosphatidylinositol 3-Kinase Phosphorylation Protein Kinase Inhibitors Proto-Oncogene Proteins c-akt Pyrazoles Pyridines Receptor Protein-Tyrosine Kinases Ribosomal Protein S6 RNA Interference Signal Transduction Time Factors TOR Serine-Threonine Kinases Transfection Xenograft Model Antitumor Assays Moore, N.F Azarova, A.M Bhatnagar, N Ross, K.N Drake, L.E Frumm, S Liu, Q.S Christie, A.L Sanda, T Chesler, L Kung, A.L Gray, N.S Stegmaier, K George, R.E Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma
description	10.18632/oncotarget.2372
author2	MEDICINE
author_facet	MEDICINE Moore, N.F Azarova, A.M Bhatnagar, N Ross, K.N Drake, L.E Frumm, S Liu, Q.S Christie, A.L Sanda, T Chesler, L Kung, A.L Gray, N.S Stegmaier, K George, R.E
format	Article
author	Moore, N.F Azarova, A.M Bhatnagar, N Ross, K.N Drake, L.E Frumm, S Liu, Q.S Christie, A.L Sanda, T Chesler, L Kung, A.L Gray, N.S Stegmaier, K George, R.E
author_sort	Moore, N.F
title	Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma
title_short	Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma
title_full	Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma
title_fullStr	Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma
title_full_unstemmed	Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma
title_sort	molecular rationale for the use of pi3k/akt/mtor pathway inhibitors in combination with crizotinib in alk-mutated neuroblastoma
publishDate	2020
url	https://scholarbank.nus.edu.sg/handle/10635/181776
_version_	1800914651653865472

Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma

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