Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer

10.18632/oncotarget.8692

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Main Authors: Bhattacharya B., Low S.H.H., Chong M.L., Chia D., Koh K.X., Sapari N.S., Kaye S., Hung H., Benoukraf T., Soong R.
Other Authors: CANCER SCIENCE INSTITUTE OF SINGAPORE
Format: Article
Published: 2020
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Online Access:https://scholarbank.nus.edu.sg/handle/10635/174090
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spelling sg-nus-scholar.10635-1740902024-04-03T07:38:12Z Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer Bhattacharya B. Low S.H.H. Chong M.L. Chia D. Koh K.X. Sapari N.S. Kaye S. Hung H. Benoukraf T. Soong R. CANCER SCIENCE INSTITUTE OF SINGAPORE DEAN'S OFFICE (MEDICINE) PATHOLOGY buparlisib endothelin endothelin 1 selumetinib transforming growth factor beta2 antineoplastic agent mitogen activated protein kinase kinase kinase phosphatidylinositol 3 kinase protein kinase inhibitor acquired resistance animal experiment animal model animal tissue antineoplastic activity Article cancer combination chemotherapy cancer resistance cell stimulation colorectal cancer controlled study cross resistance drug efficacy drug potentiation EDN1 gene gene overexpression gene silencing genome analysis HCT116 cell line human human cell IC50 in vitro study in vivo study male mouse nonhuman phenotype signal transduction TGFB2 gene animal antagonists and inhibitors colorectal tumor drug potentiation drug resistance drug screening HCT 116 cell line pathology physiology SCID mouse Animals Antineoplastic Combined Chemotherapy Protocols Colorectal Neoplasms Drug Resistance, Neoplasm Drug Synergism HCT116 Cells Humans MAP Kinase Kinase Kinases Mice Mice, SCID Phosphatidylinositol 3-Kinases Protein Kinase Inhibitors Xenograft Model Antitumor Assays 10.18632/oncotarget.8692 Oncotarget 7 20 29187-29198 2020-09-03T10:27:48Z 2020-09-03T10:27:48Z 2016 Article Bhattacharya B., Low S.H.H., Chong M.L., Chia D., Koh K.X., Sapari N.S., Kaye S., Hung H., Benoukraf T., Soong R. (2016). Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer. Oncotarget 7 (20) : 29187-29198. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.8692 19492553 https://scholarbank.nus.edu.sg/handle/10635/174090 Unpaywall 20200831
institution National University of Singapore
building NUS Library
continent Asia
country Singapore
Singapore
content_provider NUS Library
collection ScholarBank@NUS
topic buparlisib
endothelin
endothelin 1
selumetinib
transforming growth factor beta2
antineoplastic agent
mitogen activated protein kinase kinase kinase
phosphatidylinositol 3 kinase
protein kinase inhibitor
acquired resistance
animal experiment
animal model
animal tissue
antineoplastic activity
Article
cancer combination chemotherapy
cancer resistance
cell stimulation
colorectal cancer
controlled study
cross resistance
drug efficacy
drug potentiation
EDN1 gene
gene overexpression
gene silencing
genome analysis
HCT116 cell line
human
human cell
IC50
in vitro study
in vivo study
male
mouse
nonhuman
phenotype
signal transduction
TGFB2 gene
animal
antagonists and inhibitors
colorectal tumor
drug potentiation
drug resistance
drug screening
HCT 116 cell line
pathology
physiology
SCID mouse
Animals
Antineoplastic Combined Chemotherapy Protocols
Colorectal Neoplasms
Drug Resistance, Neoplasm
Drug Synergism
HCT116 Cells
Humans
MAP Kinase Kinase Kinases
Mice
Mice, SCID
Phosphatidylinositol 3-Kinases
Protein Kinase Inhibitors
Xenograft Model Antitumor Assays
spellingShingle buparlisib
endothelin
endothelin 1
selumetinib
transforming growth factor beta2
antineoplastic agent
mitogen activated protein kinase kinase kinase
phosphatidylinositol 3 kinase
protein kinase inhibitor
acquired resistance
animal experiment
animal model
animal tissue
antineoplastic activity
Article
cancer combination chemotherapy
cancer resistance
cell stimulation
colorectal cancer
controlled study
cross resistance
drug efficacy
drug potentiation
EDN1 gene
gene overexpression
gene silencing
genome analysis
HCT116 cell line
human
human cell
IC50
in vitro study
in vivo study
male
mouse
nonhuman
phenotype
signal transduction
TGFB2 gene
animal
antagonists and inhibitors
colorectal tumor
drug potentiation
drug resistance
drug screening
HCT 116 cell line
pathology
physiology
SCID mouse
Animals
Antineoplastic Combined Chemotherapy Protocols
Colorectal Neoplasms
Drug Resistance, Neoplasm
Drug Synergism
HCT116 Cells
Humans
MAP Kinase Kinase Kinases
Mice
Mice, SCID
Phosphatidylinositol 3-Kinases
Protein Kinase Inhibitors
Xenograft Model Antitumor Assays
Bhattacharya B.
Low S.H.H.
Chong M.L.
Chia D.
Koh K.X.
Sapari N.S.
Kaye S.
Hung H.
Benoukraf T.
Soong R.
Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer
description 10.18632/oncotarget.8692
author2 CANCER SCIENCE INSTITUTE OF SINGAPORE
author_facet CANCER SCIENCE INSTITUTE OF SINGAPORE
Bhattacharya B.
Low S.H.H.
Chong M.L.
Chia D.
Koh K.X.
Sapari N.S.
Kaye S.
Hung H.
Benoukraf T.
Soong R.
format Article
author Bhattacharya B.
Low S.H.H.
Chong M.L.
Chia D.
Koh K.X.
Sapari N.S.
Kaye S.
Hung H.
Benoukraf T.
Soong R.
author_sort Bhattacharya B.
title Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer
title_short Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer
title_full Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer
title_fullStr Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer
title_full_unstemmed Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer
title_sort acquired resistance to combination treatment through loss of synergy with mek and pi3k inhibitors in colorectal cancer
publishDate 2020
url https://scholarbank.nus.edu.sg/handle/10635/174090
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