Evidence map›Paper›PMID 24025257›Full record

ArticleCancer biology & therapy2013

Arsenic in leukemia: a RSKy business.

Paul Dent

Open access · hybridAbstract readComment
In one paragraph

Article in Cancer biology & therapy, 2013. 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
0.1field-weighted citation impact, top 44% 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, 3 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 Neurosurgery; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.
VCU Massey Comprehensive Cancer Center

Funding

SIGNALING PATHWAYS REGULATING EPITHELIAL CELL SURVIVALR01DK052825 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENT, PAUL · 1999 to 2013
$3.3M
Lapatinib and Obatoclax combination therapyR01CA150214 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENT, PAUL · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA150214NIDDK NIH HHS R01 DK052825
6 · The paper itself

Abstract

It has been known for many years that arsenic trioxide (As 2O 3; ATO) is an effective therapy for acute promyelocytic leukemia but has little activity against other forms of the disease. ATO has diverse modes of action, but is well known to generate high levels of reactive oxygen species in cells which are believed to be causal in many of its biologic actions. ROS can both activate and suppress signaling through multiple intracellular pathways based on the amount and duration of ROS production. As the basal activity of the MEK1/2-ERK1/2 pathway is often high in acute myeloid leukemias, and that ATO is known to stimulate MEK1/2-ERK1/2 signaling in leukemia, the authors investigated whether knock down of the downstream effector of ERK1/2, RSK1, could enhance the anti-leukemic activity of ATO.

Indexed as

ArsenicalsHumansLeukemia, Myeloid, AcuteOxidesRibosomal Protein S6 Kinases, 90-kDaArsenicalsOxidesRibosomal Protein S6 Kinases, 90-kDaarsenic trioxidekinaseleukemiamRNA translationmTORRSK signaling

Identifiers

PMID24025257
PMCPMC3926878
OpenAlexW1985302327

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.