Evidence map›Paper›PMID 27655129›Full record

ArticleMolecular cancer research : MCR2016

MEK and TAK1 Regulate Apoptosis in Colon Cancer Cells with KRAS-Dependent Activation of Proinflammatory Signaling.

Kelsey L McNew, William J Whipple, Anita K Mehta, Trevor J Grant, Leah Ray, Connor Kenny, Anurag Singh

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Exome sequencing in 51 early onset non-familial CRC cases.Molecular genetics & genomic medicine · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kelsey L McNewDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts.
William J WhippleDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts.
Anita K MehtaDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts.
Trevor J GrantDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts.
Leah RayDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts.
Connor KennyDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts.
Anurag SinghDepartment of Pharmacology and Experimental Therapeutics, Center for Cancer Research, Boston University School of Medicine, Boston Massachusetts. asingh3@bu.edu.
Boston University · US

Funding

TRAINING IN BIOMOLECULAR PHARMACOLOGYT32GM008541 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FARB, DAVID H · 1997 to 2022
$5.2M
Defining lineage-specific determinants of K-Ras "addiction" in human cancersR00CA149169 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SINGH, ANURAG · 2012 to 2014
$710k
NCI NIH HHS R00 CA149169NIGMS NIH HHS T32 GM008541
6 · The paper itself

Abstract

MEK inhibitors have limited efficacy in treating RAS-RAF-MEK pathway-dependent cancers due to feedback pathway compensation and dose-limiting toxicities. Combining MEK inhibitors with other targeted agents may enhance efficacy. Here, codependencies of MEK, TAK1, and KRAS in colon cancer were investigated. Combined inhibition of MEK and TAK1 potentiates apoptosis in KRAS-dependent cells. Pharmacologic studies and cell-cycle analyses on a large panel of colon cancer cell lines demonstrate that MEK/TAK1 inhibition induces cell death, as assessed by sub-G IMPLICATIONS: This study describes a potential therapeutic strategy for a subset of colon cancers that are dependent on oncogenic KRAS signaling pathways, which are currently difficult to block with selective agents. Mol Cancer Res; 14(12); 1204-16. ©2016 AACR.

Indexed as

ApoptosisCell CycleCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsCytokinesGene Expression Regulation, NeoplasticHT29 CellsHumansMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)Signal TransductionCytokinesKRAS protein, humanMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)

Identifiers

PMID27655129
PMCPMC5136310
OpenAlexW2521184217

What OpenQuestion holds

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LicenceTDM
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.