Evidence map›Paper›PMID 29769245›Full record

ReviewMolecular pharmacology2018

PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis.

Qiao Yi Chen, Max Costa

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
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  19. Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
  20. 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

2 authors at 1 institution in 1 country.

Qiao Yi ChenDepartment of Environmental Medicine, New York University School of Medicine, Tuxedo, New York.
Max CostaDepartment of Environmental Medicine, New York University School of Medicine, Tuxedo, New York Max.Costa@nyumc.org.
New York University · US

Funding

RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZELIKOFF, JUDITH TERRY · 1985 to 2020
$26.1M
TRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007324 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CUDDAPAH, SURESH · 1999 to 2025
$5.8M
SATB2 and Nickel CarcingenesisR01ES022935 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 2014 to 2018
$2.1M
Epigenetic Dysregulation by Oxidative Stress from Environmental InsultsR01ES023174 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX, CUDDAPAH, SURESH · 2013 to 2016
$2.0M
Arsenic Carcinogenesis and Interference With Histone mRNAR01ES026138 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX, JIN, CHUNYUAN · 2016 to 2020
$1.9M
NIEHS NIH HHS P30 ES000260NIEHS NIH HHS R01 ES022935NIEHS NIH HHS R01 ES023174NIEHS NIH HHS R01 ES026138NIEHS NIH HHS T32 ES007324
6 · The paper itself

Abstract

Arsenic is a naturally occurring, ubiquitous metalloid found in the Earth's crust. In its inorganic form, arsenic is highly toxic and carcinogenic and is widely found across the globe and throughout the environment. As an International Agency for Research on Cancer-defined class 1 human carcinogen, arsenic can cause multiple human cancers, including liver, lung, urinary bladder, skin, kidney, and prostate. Mechanisms of arsenic-induced carcinogenesis remain elusive, and this review focuses specifically on the role of the PI3K/AKT/mTOR pathway in promoting cancer development. In addition to exerting potent carcinogenic responses, arsenic is also known for its therapeutic effects against acute promyelocytic leukemia. Current literature suggests that arsenic can achieve both therapeutic as well as carcinogenic effects, and this review serves to examine the paradoxical effects of arsenic, specifically through the PI3K/AKT/mTOR pathway. Furthermore, a comprehensive review of current literature reveals an imperative need for future studies to establish and pinpoint the exact conditions for which arsenic can, and through what mechanisms it is able to, differentially regulate the PI3K/AKT/mTOR pathway to maximize the therapeutic and minimize the carcinogenic properties of arsenic.

Indexed as

AnimalsArsenicCarcinogenesisHumansLeukemia, Promyelocytic, AcutePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesArsenicPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID29769245
PMCPMC5994485
OpenAlexW2803640786

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.