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CDK1 Is a Synthetic Lethal Target for KRAS Mutant Tumours
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scholarly article
1 reference
stated in
PubMed
PubMed ID
26881434
retrieved
13 November 2016
title
CDK1 Is a Synthetic Lethal Target for KRAS Mutant Tumours
(English)
1 reference
stated in
PubMed
PubMed ID
26881434
retrieved
13 November 2016
author
Alberto Bardelli
series ordinal
8
0 references
Alan Ashworth
series ordinal
11
0 references
James Campbell
series ordinal
5
object named as
James Campbell
0 references
Christopher J Lord
object named as
Christopher J Lord
series ordinal
10
0 references
Rachel Brough
series ordinal
2
object named as
Rachel Brough
0 references
Asha Konde
series ordinal
3
object named as
Asha Konde
0 references
Sara Costa-Cabral
series ordinal
1
object named as
Sara Costa-Cabral
0 references
Marieke Aarts
series ordinal
4
object named as
Marieke Aarts
0 references
Eliana Marinari
series ordinal
6
object named as
Eliana Marinari
0 references
Jenna L Riffell
series ordinal
7
object named as
Jenna Riffell
0 references
Christopher Torrance
series ordinal
9
object named as
Christopher Torrance
0 references
language of work or name
English
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publication date
2016
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published in
PLOS One
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volume
11
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issue
2
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page(s)
e0149099
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copyright license
Creative Commons Attribution 4.0 International
start time
16 February 2016
1 reference
stated in
April 2022 Public Data File from Crossref
copyright status
copyrighted
0 references
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K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
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Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models
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Cdc2: a monopotent or pluripotent CDK?
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A synthetic lethal interaction between K-Ras oncogenes and Cdk4 unveils a therapeutic strategy for non-small cell lung carcinoma.
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Replacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responses
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Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers
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KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer.
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Targeting RAS signalling pathways in cancer therapy
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RAS oncogenes: weaving a tumorigenic web
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Mammalian cells cycle without the D-type cyclin-dependent kinases Cdk4 and Cdk6
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Differential regulation of retinoblastoma protein function by specific Cdk phosphorylation sites
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ras oncogenes in human cancer: a review
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Dual blockade of lipid and cyclin-dependent kinases induces synthetic lethality in malignant glioma
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Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies
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MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition
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TAK1 inhibition promotes apoptosis in KRAS-dependent colon cancers.
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Functional viability profiles of breast cancer
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Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.
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Clinical relevance of KRAS in human cancers
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American Society of Clinical Oncology provisional clinical opinion: testing for KRAS gene mutations in patients with metastatic colorectal carcinoma to predict response to anti-epidermal growth factor receptor monoclonal antibody therapy
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Selective small-molecule inhibitor reveals critical mitotic functions of human CDK1
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Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts.
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Cdk1 is sufficient to drive the mammalian cell cycle
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A colon cancer cell line (LIM1215) derived from a patient with inherited nonpolyposis colorectal cancer.
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2 June 2018
Cdc2-cyclin E complexes regulate the G1/S phase transition
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21 January 2018
AZD5438, a potent oral inhibitor of cyclin-dependent kinases 1, 2, and 9, leads to pharmacodynamic changes and potent antitumor effects in human tumor xenografts.
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Genetic Interactions in Cancer Progression and Treatment
1 reference
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PubMed
reference URL
https://pubmed.ncbi.nlm.nih.gov/26881434
retrieved
12 December 2020
based on heuristic
inferred from PubMed ID database lookup
Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient
1 reference
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PubMed
reference URL
https://pubmed.ncbi.nlm.nih.gov/26881434
retrieved
12 December 2020
based on heuristic
inferred from PubMed ID database lookup
Identifiers
DOI
10.1371/JOURNAL.PONE.0149099
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
2260074
ADS bibcode
2016PLoSO..1149099C
0 references
OpenCitations bibliographic resource ID
2260074
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
2260074
PMCID
4755568
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
2260074
PubMed ID
26881434
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
2260074
ResearchGate publication ID
295100078
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