Evidence map›Paper›PMID 24496096›Full record

ArticleCancer biology & therapy2014

Not so WEE: targeting G₂/M to kill mesothelioma cells.

Paul Dent

Open access · hybridAbstract readComment
In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 92% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Paul DentDepartment of Biochemistry and Molecular Biology; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.
University of Richmond · US

Funding

SIGNALING PATHWAYS REGULATING EPITHELIAL CELL SURVIVALR01DK052825 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENT, PAUL · 1999 to 2013
$3.3M
NIDDK NIH HHS R01 DK052825NIDDK NIH HHS R01 DK52825
6 · The paper itself

Abstract

It has been known for many years that manipulation of cell cycle checkpoint function represents one approach by which the toxicity of chemotherapy and of ionizing radiation can be increased in tumor cells. (1)(-) (3) In particular, abrogation of the G 2/M checkpoint has been shown to enhance the lethality of a wide range of toxic stresses. (1)(-) (3) Inhibition of the G 2/M checkpoint after chemotherapy/irradiation would result in tumor cells entering mitosis with damaged DNA, which would in turn result in loss of clonogenic survival (i.e., a lethal mitosis).

Indexed as

G2 Phase Cell Cycle CheckpointsAntineoplastic AgentsCell Cycle ProteinsCisplatinHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantNuclear ProteinsProtein-Tyrosine KinasesPyrazolesPyrimidinesPyrimidinonesadavosertibAntineoplastic AgentsCell Cycle ProteinsCisplatinNuclear ProteinsProtein-Tyrosine KinasesPyrazolesPyrimidinesPyrimidinonesWEE1 protein, humanapoptosisCDK1cisplatinG2/M checkpointmesotheliomaMK-1775WEE1

Identifiers

PMID24496096
PMCPMC3979810
OpenAlexW2032899952

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.