Evidence map›Paper›PMID 32718025›Full record

ReviewBiology2020

The Intersection of DNA Damage Response and Ferroptosis-A Rationale for Combination Therapeutics.

Po-Han Chen, Watson Hua-Sheng Tseng, Jen-Tsan Chi

Open access · goldAbstract readReview
In one paragraph

Review in Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 46 citations in OpenAlex.

  1. The role of metals in cancer and the use of metal chelators as a potential treatment strategy.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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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 2 institutions in 2 countries.

Po-Han ChenDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.ORCID 0000-0002-9471-4471
Watson Hua-Sheng TsengDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Jen-Tsan ChiDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.ORCID 0000-0003-3433-903X
Duke University · USNational Yang Ming Chiao Tung University · TW

Funding

NIH HHS 1R01NS111588-01A1NIH HHS GM124062
6 · The paper itself

Abstract

Ferroptosis is a novel form of iron-dependent cell death characterized by lipid peroxidation. While the importance and disease relevance of ferroptosis are gaining recognition, much remains unknown about its interaction with other biological processes and pathways. Recently, several studies have identified intricate and complicated interplay between ferroptosis, ionizing radiation (IR), ATM (ataxia-telangiectasia mutated)/ATR (ATM and Rad3-related), and tumor suppressor p53, which signifies the participation of the DNA damage response (DDR) in iron-related cell death. DDR is an evolutionarily conserved response triggered by various DNA insults to attenuate proliferation, enable DNA repairs, and dispose of cells with damaged DNA to maintain genome integrity. Deficiency in proper DDR in many genetic disorders or tumors also highlights the importance of this pathway. In this review, we will focus on the biological crosstalk between DDR and ferroptosis, which is mediated mostly via noncanonical mechanisms. For clinical applications, we also discuss the potential of combining ionizing radiation and ferroptosis-inducers for synergistic effects. At last, various ATM/ATR inhibitors under clinical development may protect ferroptosis and treat many ferroptosis-related diseases to prevent cell death, delay disease progression, and improve clinical outcomes.

Indexed as

ATMATRDNA damageferroptosisMDM2MDMXp53

Identifiers

PMID32718025
PMCPMC7464484
OpenAlexW3044711546

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.