Evidence map›Paper›PMID 31929855›Full record

ReviewOxidative medicine and cellular longevity2019

Understanding of ROS-Inducing Strategy in Anticancer Therapy.

Su Ji Kim, Hyun Soo Kim, Young Rok Seo

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 2 pooled it
22.3field-weighted citation impact, top 1% 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

202 citing papers in PubMed, 2 syntheses or guidelines pooled it, 397 citations in OpenAlex.

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  18. Iranian journal of basic medical sciences · 2026
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142 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Su Ji KimInstitute of Environmental Medicine for Green Chemistry, Dongguk University Biomedi Campus, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10326, Republic of Korea.ORCID https://orcid.org/0000-0001-9050-5851
Hyun Soo KimInstitute of Environmental Medicine for Green Chemistry, Dongguk University Biomedi Campus, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10326, Republic of Korea.ORCID https://orcid.org/0000-0001-7805-4429
Young Rok SeoInstitute of Environmental Medicine for Green Chemistry, Dongguk University Biomedi Campus, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10326, Republic of Korea.ORCID https://orcid.org/0000-0002-4093-4073
Dongguk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Redox homeostasis is essential for the maintenance of diverse cellular processes. Cancer cells have higher levels of reactive oxygen species (ROS) than normal cells as a result of hypermetabolism, but the redox balance is maintained in cancer cells due to their marked antioxidant capacity. Recently, anticancer therapies that induce oxidative stress by increasing ROS and/or inhibiting antioxidant processes have received significant attention. The acceleration of accumulative ROS disrupts redox homeostasis and causes severe damage in cancer cells. In this review, we describe ROS-inducing cancer therapy and the anticancer mechanism employed by prooxidative agents. To understand the comprehensive biological response to certain prooxidative anticancer drugs such as 2-methoxyestradiol, buthionine sulfoximine, cisplatin, doxorubicin, imexon, and motexafin gadolinium, we propose and visualize the drug-gene, drug-cell process, and drug-disease interactions involved in oxidative stress induction and antioxidant process inhibition as well as specific side effects of these drugs using pathway analysis with a big data-based text-mining approach. Our review will be helpful to improve the therapeutic effects of anticancer drugs by providing information about biological changes that occur in response to prooxidants. For future directions, there is still a need for pharmacogenomic studies on prooxidative agents as well as the molecular mechanisms underlying the effects of the prooxidants and/or antioxidant-inhibitor agents for effective anticancer therapy through selective killing of cancer cells.

Indexed as

2-MethoxyestradiolAnimalsAntineoplastic AgentsHomeostasisHumansNeoplasmsOxidantsOxidation-ReductionOxidative StressReactive Oxygen Species2-MethoxyestradiolAntineoplastic AgentsOxidantsReactive Oxygen Species

Identifiers

PMID31929855
PMCPMC6939418
OpenAlexW2995708286

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.